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tm4 sertoli cell line  (ATCC)


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    Structured Review

    ATCC tm4 sertoli cell line
    Tm4 Sertoli Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 532 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/tm4+sertoli+cell+line/TM4/pm42314964-70-4-8
    Average 96 stars, based on 532 article reviews
    tm4 sertoli cell line - by Bioz Stars, 2026-09
    96/100 stars

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    Related Articles

    Derivative Assay:

    Article Title: Development of a model for studying the developmental consequences of oxidative sperm DNA damage by targeting redox-cycling naphthoquinones to the Sertoli cell population.
    Article Snippet: .. Specifically, we used the TM4 Sertoli cell line, originally purchased from ATCC (derived from 11 to 14 day old murine testis) and which has been shown in other studies to express the FSH receptor [29]. .. According to ATCC (https://www.atcc.org/), the TM4 cell line is reported to respond to FSH with an increase in cAMP production.

    Article Title: Melatonin improves oxidative state and lactate metabolism in rodent Sertoli cells.
    Article Snippet: Antioxidant actions of melatonin and its impact on testicular function and fertility have already been described.. Considering that Sertoli cells contribute to provide structural support and nutrition to germ cells, we evaluated the effect of melatonin on oxidative state and lactate metabolism in the immature murine TM4 cell line and in immature hamster Sertoli cells.. A prooxidant stimulus applied to rodent Sertoli cells expressing MT1/MT2 receptors, increased lipid peroxidation whereas decreased antioxidant enzymes (superoxide dismutase 1, catalase, peroxiredoxin 1) expression and catalase activity.

    Article Title: Reactive oxygen species (ROS) production triggered by prostaglandin D2 (PGD2) regulates lactate dehydrogenase (LDH) expression/activity in TM4 Sertoli cells.
    Article Snippet: Please cite this article as: Rossi, S.P., Windschuettl, S., Matzkin, M.E., Rey-Ares, V., Terradas, C., Ponzio, R., Puigdomenech, E., Levalle, O., Calandra, R.S., Mayerhofer, A., Frungieri, M.B., Reactive oxygen species (ROS) production triggered by prostaglandin D2 (PGD2) regulates lactate dehydrogenase (LDH) expression/activity in TM4 Sertoli cells, Molecular and Cellular Endocrinology (2016), doi: 10.1016/j.mce.2016.06.021.

    Article Title: Furan impairs cell function by inducing oxidative stress, DNA damage and apoptosis in mouse Sertoli cells in vitro .
    Article Snippet: Research on heat-induced food contaminants, such as furan, has shown its harmful effects on various systems. however, the impact of furan on sertoli cells, a crucial male reproductive system cell, has not been studied. the investigation involved the treatment of furan to tM4 sertoli cells at various concentrations (750, 1500, and 3000 μM) over a period of 24 h. this in vitro study determined that furan causes a decrease in sertoli cell viability and an increase in lactate dehydrogenase activity, leading to cytotoxicity. additionally, we observed an increase in MDa, one of the oxidative stress markers, in sertoli cells, indicating that furan exposure leads to lipid peroxidation. it was determined that enzyme activities in the antioxidant defense system in sertoli cells decreased after furan exposure. the findings indicate that furan induces oxidative damage in sertoli cells by impairing the activity of antioxidant enzymes and promoting the production of ROs. this study discovered that furan triggers apoptosis in sertoli cells by damaging DNa and altering the expression levels of apoptotic genes.. Moreover, results suggest that furan causes cellular toxicity and apoptosis, leading to damage to sertoli cells and thus causing male infertility.

    Cell Culture:

    Article Title: Oleanolic acid causes reversible contraception in male mice by increasing the permeability of the germinal epithelium
    Article Snippet: The effects of oleanolic acid (OA) on the fertility ofmalemicewere investigated using both in vivo and in vitro experimental models.. The experimental group (n1⁄4 12) was treated with a daily dose of 30 mgOA kg 1 bodyweight (i.p.), while the control group (n1⁄4 6) received a daily dose of 10%ethanol solution (1mLkg 1 bodyweight).. The effect of OAon the permeability status of TM4 Sertoli monolayers was investigated by measuring the transepithelial electrical resistance (TER), intracellular electrical resistance and semiquantitative RT–PCR.

    Article Title: Dose-dependent modulation of mitochondrial physiology and nutrient secretion in Sertoli cells by l-carnitine.
    Article Snippet: .. Cell Culture Conditions The TM4 Sertoli cell line (ATCC, Manassas, VA, USA), a mouse Sertoli-like cell line (mSCs), was used in this study. .. Cells were cultured and handled according to ATCC protocols.

    Article Title: Reactive oxygen species (ROS) production triggered by prostaglandin D2 (PGD2) regulates lactate dehydrogenase (LDH) expression/activity in TM4 Sertoli cells.
    Article Snippet: Please cite this article as: Rossi, S.P., Windschuettl, S., Matzkin, M.E., Rey-Ares, V., Terradas, C., Ponzio, R., Puigdomenech, E., Levalle, O., Calandra, R.S., Mayerhofer, A., Frungieri, M.B., Reactive oxygen species (ROS) production triggered by prostaglandin D2 (PGD2) regulates lactate dehydrogenase (LDH) expression/activity in TM4 Sertoli cells, Molecular and Cellular Endocrinology (2016), doi: 10.1016/j.mce.2016.06.021.

    Article Title: Metabolomics and exploratory mendelian randomization identify indole-3-propionic acid associated with doxorubicin-induced testicular injury.
    Article Snippet: Doxorubicin (DOX) exhibits severe side effects that restrict its clinical application.. In the testes, DOX triggers apoptosis and excessive oxidative stress.. Modulation of the metabolic microenvironment may contribute to the amelioration of testicular injury.

    Isolation:

    Article Title: Furan impairs cell function by inducing oxidative stress, DNA damage and apoptosis in mouse Sertoli cells in vitro .
    Article Snippet: Research on heat-induced food contaminants, such as furan, has shown its harmful effects on various systems. however, the impact of furan on sertoli cells, a crucial male reproductive system cell, has not been studied. the investigation involved the treatment of furan to tM4 sertoli cells at various concentrations (750, 1500, and 3000 μM) over a period of 24 h. this in vitro study determined that furan causes a decrease in sertoli cell viability and an increase in lactate dehydrogenase activity, leading to cytotoxicity. additionally, we observed an increase in MDa, one of the oxidative stress markers, in sertoli cells, indicating that furan exposure leads to lipid peroxidation. it was determined that enzyme activities in the antioxidant defense system in sertoli cells decreased after furan exposure. the findings indicate that furan induces oxidative damage in sertoli cells by impairing the activity of antioxidant enzymes and promoting the production of ROs. this study discovered that furan triggers apoptosis in sertoli cells by damaging DNa and altering the expression levels of apoptotic genes.. Moreover, results suggest that furan causes cellular toxicity and apoptosis, leading to damage to sertoli cells and thus causing male infertility.

    In Vitro:

    Article Title: Furan impairs cell function by inducing oxidative stress, DNA damage and apoptosis in mouse Sertoli cells in vitro .
    Article Snippet: Research on heat-induced food contaminants, such as furan, has shown its harmful effects on various systems. however, the impact of furan on sertoli cells, a crucial male reproductive system cell, has not been studied. the investigation involved the treatment of furan to tM4 sertoli cells at various concentrations (750, 1500, and 3000 μM) over a period of 24 h. this in vitro study determined that furan causes a decrease in sertoli cell viability and an increase in lactate dehydrogenase activity, leading to cytotoxicity. additionally, we observed an increase in MDa, one of the oxidative stress markers, in sertoli cells, indicating that furan exposure leads to lipid peroxidation. it was determined that enzyme activities in the antioxidant defense system in sertoli cells decreased after furan exposure. the findings indicate that furan induces oxidative damage in sertoli cells by impairing the activity of antioxidant enzymes and promoting the production of ROs. this study discovered that furan triggers apoptosis in sertoli cells by damaging DNa and altering the expression levels of apoptotic genes.. Moreover, results suggest that furan causes cellular toxicity and apoptosis, leading to damage to sertoli cells and thus causing male infertility.

    Modification:

    Article Title: Furan impairs cell function by inducing oxidative stress, DNA damage and apoptosis in mouse Sertoli cells in vitro .
    Article Snippet: Research on heat-induced food contaminants, such as furan, has shown its harmful effects on various systems. however, the impact of furan on sertoli cells, a crucial male reproductive system cell, has not been studied. the investigation involved the treatment of furan to tM4 sertoli cells at various concentrations (750, 1500, and 3000 μM) over a period of 24 h. this in vitro study determined that furan causes a decrease in sertoli cell viability and an increase in lactate dehydrogenase activity, leading to cytotoxicity. additionally, we observed an increase in MDa, one of the oxidative stress markers, in sertoli cells, indicating that furan exposure leads to lipid peroxidation. it was determined that enzyme activities in the antioxidant defense system in sertoli cells decreased after furan exposure. the findings indicate that furan induces oxidative damage in sertoli cells by impairing the activity of antioxidant enzymes and promoting the production of ROs. this study discovered that furan triggers apoptosis in sertoli cells by damaging DNa and altering the expression levels of apoptotic genes.. Moreover, results suggest that furan causes cellular toxicity and apoptosis, leading to damage to sertoli cells and thus causing male infertility.

    Incubation:

    Article Title: Furan impairs cell function by inducing oxidative stress, DNA damage and apoptosis in mouse Sertoli cells in vitro .
    Article Snippet: Research on heat-induced food contaminants, such as furan, has shown its harmful effects on various systems. however, the impact of furan on sertoli cells, a crucial male reproductive system cell, has not been studied. the investigation involved the treatment of furan to tM4 sertoli cells at various concentrations (750, 1500, and 3000 μM) over a period of 24 h. this in vitro study determined that furan causes a decrease in sertoli cell viability and an increase in lactate dehydrogenase activity, leading to cytotoxicity. additionally, we observed an increase in MDa, one of the oxidative stress markers, in sertoli cells, indicating that furan exposure leads to lipid peroxidation. it was determined that enzyme activities in the antioxidant defense system in sertoli cells decreased after furan exposure. the findings indicate that furan induces oxidative damage in sertoli cells by impairing the activity of antioxidant enzymes and promoting the production of ROs. this study discovered that furan triggers apoptosis in sertoli cells by damaging DNa and altering the expression levels of apoptotic genes.. Moreover, results suggest that furan causes cellular toxicity and apoptosis, leading to damage to sertoli cells and thus causing male infertility.

    In Vivo:

    Article Title: Furan impairs cell function by inducing oxidative stress, DNA damage and apoptosis in mouse Sertoli cells in vitro .
    Article Snippet: Research on heat-induced food contaminants, such as furan, has shown its harmful effects on various systems. however, the impact of furan on sertoli cells, a crucial male reproductive system cell, has not been studied. the investigation involved the treatment of furan to tM4 sertoli cells at various concentrations (750, 1500, and 3000 μM) over a period of 24 h. this in vitro study determined that furan causes a decrease in sertoli cell viability and an increase in lactate dehydrogenase activity, leading to cytotoxicity. additionally, we observed an increase in MDa, one of the oxidative stress markers, in sertoli cells, indicating that furan exposure leads to lipid peroxidation. it was determined that enzyme activities in the antioxidant defense system in sertoli cells decreased after furan exposure. the findings indicate that furan induces oxidative damage in sertoli cells by impairing the activity of antioxidant enzymes and promoting the production of ROs. this study discovered that furan triggers apoptosis in sertoli cells by damaging DNa and altering the expression levels of apoptotic genes.. Moreover, results suggest that furan causes cellular toxicity and apoptosis, leading to damage to sertoli cells and thus causing male infertility.

    Control:

    Article Title: Furan impairs cell function by inducing oxidative stress, DNA damage and apoptosis in mouse Sertoli cells in vitro .
    Article Snippet: Research on heat-induced food contaminants, such as furan, has shown its harmful effects on various systems. however, the impact of furan on sertoli cells, a crucial male reproductive system cell, has not been studied. the investigation involved the treatment of furan to tM4 sertoli cells at various concentrations (750, 1500, and 3000 μM) over a period of 24 h. this in vitro study determined that furan causes a decrease in sertoli cell viability and an increase in lactate dehydrogenase activity, leading to cytotoxicity. additionally, we observed an increase in MDa, one of the oxidative stress markers, in sertoli cells, indicating that furan exposure leads to lipid peroxidation. it was determined that enzyme activities in the antioxidant defense system in sertoli cells decreased after furan exposure. the findings indicate that furan induces oxidative damage in sertoli cells by impairing the activity of antioxidant enzymes and promoting the production of ROs. this study discovered that furan triggers apoptosis in sertoli cells by damaging DNa and altering the expression levels of apoptotic genes.. Moreover, results suggest that furan causes cellular toxicity and apoptosis, leading to damage to sertoli cells and thus causing male infertility.



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    PFOA altered the expression of glycolysis-related genes. Based on RNA-seq analysis, the total RNA expression profiles of testicular tissues in the control and 5 mg/kg/day PFOA-exposed groups were compared ( A ). KEGG pathway enrichment ( B ) and GO functional enrichment analyses ( C ) of differentially expressed genes revealed that the glycolysis pathway served as a key target of PFOA. After 24 h of PFOA treatment in <t>TM4</t> cells, cell viability was decreased ( D ), accompanied by significant changes in the expression of glycolysis-related genes ( E ). ( n = 3, * p < 0.05; ** p < 0.01; *** p < 0.001, * vs. control group).
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    AMPK inhibition-induced Angiogenin is accompanied by alteration of tRFs profile in vitro. A Western blot results of proteins related with AMPK-mTOR pathways in TM3, <t>TM4,</t> and NIH/3T3 cell lines using compound C (CC), rapamycin (Rapa), and MHY1485 (MHY) in TM3, TM4, and NIH/3T3 cell lines (left to right). The number represents the densiometric comparison of the expression of pAMPK and pmTOR proteins against AMPK and mTOR, respectively. B Angiogenin gene expression. Gene expression was quantified after 12 h of treatment. mRNA expression level was normalized to Actin . Data are represented as mean ± standard deviation. Statistical analysis was performed using One-way ANOVA with Tukey post-hoc test. Different letters are significantly different. C Northern blot results of tRF3-Pro and Val in mouse testis cell lines. Each sample RNAs were extracted from both TM3 and TM4 cells with CC treatment and overexpression of Angiogenin (Ang OE). Each intact tRNA was shown as a control. Band intensities of Northern blot are represented as bar graph after quantification using Image J software. Data are presented as mean ± standard deviation. One-way ANOVA was used for statistical analysis, and the different alphabets with Tukey post-hoc test. D Distribution of read counts based on small RNA type. E Distribution of reads assigned to GtRNAdb in tRF subtypes. The total bar height is proportional to the total read count for each group. Percentages indicate the relative proportion of each tRF subtype within the corresponding group, and n represents the actual read count number for each subtype. tRF5, reads derived from tRNA 5′ end among reads aligned to GtRNAdb; tRF3, reads derived from tRNA 3′ end among reads aligned to GtRNAdb; other, not included in the previous two groups. F Histogram showing the distribution of log 2 (Fold change) using reads aligned to GtRNAdb. Green, CC-treated versus non-treated; Yellow, ANG overexpression versus control. G Volcano plot depicting significantly changed tRFs in TM4 cell lines. Results from CC-treated versus non-treated are represented as circles, and results from ANG overexpression versus control are represented as triangles. n = 2 for each group.
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    AMPK inhibition-induced Angiogenin is accompanied by alteration of tRFs profile in vitro. A Western blot results of proteins related with AMPK-mTOR pathways in TM3, <t>TM4,</t> and NIH/3T3 cell lines using compound C (CC), rapamycin (Rapa), and MHY1485 (MHY) in TM3, TM4, and NIH/3T3 cell lines (left to right). The number represents the densiometric comparison of the expression of pAMPK and pmTOR proteins against AMPK and mTOR, respectively. B Angiogenin gene expression. Gene expression was quantified after 12 h of treatment. mRNA expression level was normalized to Actin . Data are represented as mean ± standard deviation. Statistical analysis was performed using One-way ANOVA with Tukey post-hoc test. Different letters are significantly different. C Northern blot results of tRF3-Pro and Val in mouse testis cell lines. Each sample RNAs were extracted from both TM3 and TM4 cells with CC treatment and overexpression of Angiogenin (Ang OE). Each intact tRNA was shown as a control. Band intensities of Northern blot are represented as bar graph after quantification using Image J software. Data are presented as mean ± standard deviation. One-way ANOVA was used for statistical analysis, and the different alphabets with Tukey post-hoc test. D Distribution of read counts based on small RNA type. E Distribution of reads assigned to GtRNAdb in tRF subtypes. The total bar height is proportional to the total read count for each group. Percentages indicate the relative proportion of each tRF subtype within the corresponding group, and n represents the actual read count number for each subtype. tRF5, reads derived from tRNA 5′ end among reads aligned to GtRNAdb; tRF3, reads derived from tRNA 3′ end among reads aligned to GtRNAdb; other, not included in the previous two groups. F Histogram showing the distribution of log 2 (Fold change) using reads aligned to GtRNAdb. Green, CC-treated versus non-treated; Yellow, ANG overexpression versus control. G Volcano plot depicting significantly changed tRFs in TM4 cell lines. Results from CC-treated versus non-treated are represented as circles, and results from ANG overexpression versus control are represented as triangles. n = 2 for each group.
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    AMPK inhibition-induced Angiogenin is accompanied by alteration of tRFs profile in vitro. A Western blot results of proteins related with AMPK-mTOR pathways in TM3, <t>TM4,</t> and NIH/3T3 cell lines using compound C (CC), rapamycin (Rapa), and MHY1485 (MHY) in TM3, TM4, and NIH/3T3 cell lines (left to right). The number represents the densiometric comparison of the expression of pAMPK and pmTOR proteins against AMPK and mTOR, respectively. B Angiogenin gene expression. Gene expression was quantified after 12 h of treatment. mRNA expression level was normalized to Actin . Data are represented as mean ± standard deviation. Statistical analysis was performed using One-way ANOVA with Tukey post-hoc test. Different letters are significantly different. C Northern blot results of tRF3-Pro and Val in mouse testis cell lines. Each sample RNAs were extracted from both TM3 and TM4 cells with CC treatment and overexpression of Angiogenin (Ang OE). Each intact tRNA was shown as a control. Band intensities of Northern blot are represented as bar graph after quantification using Image J software. Data are presented as mean ± standard deviation. One-way ANOVA was used for statistical analysis, and the different alphabets with Tukey post-hoc test. D Distribution of read counts based on small RNA type. E Distribution of reads assigned to GtRNAdb in tRF subtypes. The total bar height is proportional to the total read count for each group. Percentages indicate the relative proportion of each tRF subtype within the corresponding group, and n represents the actual read count number for each subtype. tRF5, reads derived from tRNA 5′ end among reads aligned to GtRNAdb; tRF3, reads derived from tRNA 3′ end among reads aligned to GtRNAdb; other, not included in the previous two groups. F Histogram showing the distribution of log 2 (Fold change) using reads aligned to GtRNAdb. Green, CC-treated versus non-treated; Yellow, ANG overexpression versus control. G Volcano plot depicting significantly changed tRFs in TM4 cell lines. Results from CC-treated versus non-treated are represented as circles, and results from ANG overexpression versus control are represented as triangles. n = 2 for each group.
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    Fluoride impairs male reproductive capacity by differentially regulating autophagy of testicular somatic cells in mice. (A to F) Six-week-old male mice freely drank distilled water with or without 100 mg/l NaF for 18 weeks. (A) Representative images of H&E staining on testis. Scale bars, 100 μm (left) and 50 μm (right). (B) Representative microscopic views of sperm morphology. Scale bars, 50 μm. (C) Sperm quality. (D and E) Representative transmission electron microscopy images of autophagosomes in (D) Leydig cells and (E) Sertoli cells [scale bars, 2 μm (bottom) and 1 μm (top)], with red arrows indicating autophagosomes. (F) Immunohistochemistry was used to detect the protein expression of LC3B and p62 in Leydig cells and Sertoli cells. (G and H) Testicular somatic cells were treated with various concentrations of NaF for 24 h. The relative expression of LC3B and p62 proteins in (G) TM3 cells, (H) <t>TM4</t> cells, and (I) TM4 cells cotreated with 20 μM chloroquine. Cell viability of (J) TM3 and (K) TM4 cells that were treated with 0.25 mM NaF and 20 μM chloroquine for 24 h or pretreated with 20 nM rapamycin for 1 h. All values in the figure are means ± SEM. n ≥ 3. * P < 0.05, ** P < 0.01 versus control; # P < 0.05, ## P < 0.01 versus chloroquine.
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    Procell Inc mouse sertoli cell line tm4 gnm41
    Cd exposure activates autophagy in Sertoli cells. A - G The male mice were injected (i.p.) with 2.0 mg/kg CdCl 2 or vehicle, respectively. Mouse testes were collected at 0, 2, 8, 24, 48, and 72 h after Cd treatment. A , B Representative images and quantification of autophagosomes in mice Sertoli cells detected by transmission electron microscopy. The yellow arrows represent the autophagosomes. C - E The expression of ATG5 and LC3B-II/I was detected by western blotting. F , G Representative images and quantification of mIHC assay. White arrows denoted the LC3B puncta surrounding WT1. Scale bar: 50 μm. H - J <t>TM4</t> cells were exposed to Cd for 0, 2, 8, and 24 h, respectively. H - J The expression of ATG5 and LC3B-II/I was detected by western blotting. Data were displayed as mean ± SEM . n = 3- 6. * P < 0.05, ** P < 0.01 vs 0 h group
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    Image Search Results


    PFOA altered the expression of glycolysis-related genes. Based on RNA-seq analysis, the total RNA expression profiles of testicular tissues in the control and 5 mg/kg/day PFOA-exposed groups were compared ( A ). KEGG pathway enrichment ( B ) and GO functional enrichment analyses ( C ) of differentially expressed genes revealed that the glycolysis pathway served as a key target of PFOA. After 24 h of PFOA treatment in TM4 cells, cell viability was decreased ( D ), accompanied by significant changes in the expression of glycolysis-related genes ( E ). ( n = 3, * p < 0.05; ** p < 0.01; *** p < 0.001, * vs. control group).

    Journal: Toxics

    Article Title: PFOA Damages Blood–Testis Barrier Integrity in Mice by Inhibited Glycolysis Caused H3K18 Lactylation Modification Impairment

    doi: 10.3390/toxics14050399

    Figure Lengend Snippet: PFOA altered the expression of glycolysis-related genes. Based on RNA-seq analysis, the total RNA expression profiles of testicular tissues in the control and 5 mg/kg/day PFOA-exposed groups were compared ( A ). KEGG pathway enrichment ( B ) and GO functional enrichment analyses ( C ) of differentially expressed genes revealed that the glycolysis pathway served as a key target of PFOA. After 24 h of PFOA treatment in TM4 cells, cell viability was decreased ( D ), accompanied by significant changes in the expression of glycolysis-related genes ( E ). ( n = 3, * p < 0.05; ** p < 0.01; *** p < 0.001, * vs. control group).

    Article Snippet: This experiment utilized a mouse testicular sertoli cell line (TM4) obtained from the ATCC cell bank in the United States.

    Techniques: Expressing, RNA Sequencing, RNA Expression, Control, Functional Assay

    PFOA inhibited the expression of glycolysis and BTB-related molecules in TM4 cells and mouse testicular tissues. In PFOA-treated TM4 cells, the protein levels of key glycolytic molecules, including HK1 ( B ), GLUT1 ( C ) and LDHA ( D ), were downregulated ( A – D ), accompanied by reduced production of lactate ( E ) and ATP ( F ). Meanwhile, both the gene ( G ) and protein ( H ) expression of BTB-related factors were decreased in TM4 cells. Consistent with the cellular results, the mRNA ( I ) and protein ( J ) levels of glycolysis-related molecules were also suppressed in mouse testis, along with a decline in lactate concentration ( K ). ( n = 3, * p < 0.05; ** p < 0.01; *** p < 0.001, * vs. control group).

    Journal: Toxics

    Article Title: PFOA Damages Blood–Testis Barrier Integrity in Mice by Inhibited Glycolysis Caused H3K18 Lactylation Modification Impairment

    doi: 10.3390/toxics14050399

    Figure Lengend Snippet: PFOA inhibited the expression of glycolysis and BTB-related molecules in TM4 cells and mouse testicular tissues. In PFOA-treated TM4 cells, the protein levels of key glycolytic molecules, including HK1 ( B ), GLUT1 ( C ) and LDHA ( D ), were downregulated ( A – D ), accompanied by reduced production of lactate ( E ) and ATP ( F ). Meanwhile, both the gene ( G ) and protein ( H ) expression of BTB-related factors were decreased in TM4 cells. Consistent with the cellular results, the mRNA ( I ) and protein ( J ) levels of glycolysis-related molecules were also suppressed in mouse testis, along with a decline in lactate concentration ( K ). ( n = 3, * p < 0.05; ** p < 0.01; *** p < 0.001, * vs. control group).

    Article Snippet: This experiment utilized a mouse testicular sertoli cell line (TM4) obtained from the ATCC cell bank in the United States.

    Techniques: Expressing, Concentration Assay, Control

    Effects of PFOA on H3K18 lactylation and the transcriptional regulation of key genes involved in glycolysis. PFOA exposure reduced the modification levels of Pan-Kla and H3K18la in TM4 cells ( A ) and mouse testicular tissues ( B ). ChIP-qPCR results further demonstrated that PFOA altered the binding of H3K18la to glycolytic genes, thereby regulating their transcription ( C ). ( n = 3, * p < 0.05; ** p < 0.01; *** p < 0.001, * vs. control group).

    Journal: Toxics

    Article Title: PFOA Damages Blood–Testis Barrier Integrity in Mice by Inhibited Glycolysis Caused H3K18 Lactylation Modification Impairment

    doi: 10.3390/toxics14050399

    Figure Lengend Snippet: Effects of PFOA on H3K18 lactylation and the transcriptional regulation of key genes involved in glycolysis. PFOA exposure reduced the modification levels of Pan-Kla and H3K18la in TM4 cells ( A ) and mouse testicular tissues ( B ). ChIP-qPCR results further demonstrated that PFOA altered the binding of H3K18la to glycolytic genes, thereby regulating their transcription ( C ). ( n = 3, * p < 0.05; ** p < 0.01; *** p < 0.001, * vs. control group).

    Article Snippet: This experiment utilized a mouse testicular sertoli cell line (TM4) obtained from the ATCC cell bank in the United States.

    Techniques: Modification, ChIP-qPCR, Binding Assay, Control

    Protective effects of Nala against PFOA-induced reproductive damage. Gradient Nala treatment for 24 h significantly elevated the levels of Pan-Kla and H3K18la in TM4 cells ( A ). After co-treatment with 30 mM Nala and 400 μM PFOA for 24 h, the PFOA-mediated reductions in Pan-Kla and H3K18la were notably restored ( B ). The decreased expression of Hk1, Glut1 and Ldha was partially rescued ( C ), and the downregulated mRNA ( D ) and protein ( E ) levels of BTB-related molecules were also markedly recovered. ( n = 3, * p < 0.05; ** p < 0.01; *** p < 0.001; * vs. control group. # p < 0.05; ## p < 0.01; ### p < 0.001; # vs. PFOA group).

    Journal: Toxics

    Article Title: PFOA Damages Blood–Testis Barrier Integrity in Mice by Inhibited Glycolysis Caused H3K18 Lactylation Modification Impairment

    doi: 10.3390/toxics14050399

    Figure Lengend Snippet: Protective effects of Nala against PFOA-induced reproductive damage. Gradient Nala treatment for 24 h significantly elevated the levels of Pan-Kla and H3K18la in TM4 cells ( A ). After co-treatment with 30 mM Nala and 400 μM PFOA for 24 h, the PFOA-mediated reductions in Pan-Kla and H3K18la were notably restored ( B ). The decreased expression of Hk1, Glut1 and Ldha was partially rescued ( C ), and the downregulated mRNA ( D ) and protein ( E ) levels of BTB-related molecules were also markedly recovered. ( n = 3, * p < 0.05; ** p < 0.01; *** p < 0.001; * vs. control group. # p < 0.05; ## p < 0.01; ### p < 0.001; # vs. PFOA group).

    Article Snippet: This experiment utilized a mouse testicular sertoli cell line (TM4) obtained from the ATCC cell bank in the United States.

    Techniques: Expressing, Control

    AMPK inhibition-induced Angiogenin is accompanied by alteration of tRFs profile in vitro. A Western blot results of proteins related with AMPK-mTOR pathways in TM3, TM4, and NIH/3T3 cell lines using compound C (CC), rapamycin (Rapa), and MHY1485 (MHY) in TM3, TM4, and NIH/3T3 cell lines (left to right). The number represents the densiometric comparison of the expression of pAMPK and pmTOR proteins against AMPK and mTOR, respectively. B Angiogenin gene expression. Gene expression was quantified after 12 h of treatment. mRNA expression level was normalized to Actin . Data are represented as mean ± standard deviation. Statistical analysis was performed using One-way ANOVA with Tukey post-hoc test. Different letters are significantly different. C Northern blot results of tRF3-Pro and Val in mouse testis cell lines. Each sample RNAs were extracted from both TM3 and TM4 cells with CC treatment and overexpression of Angiogenin (Ang OE). Each intact tRNA was shown as a control. Band intensities of Northern blot are represented as bar graph after quantification using Image J software. Data are presented as mean ± standard deviation. One-way ANOVA was used for statistical analysis, and the different alphabets with Tukey post-hoc test. D Distribution of read counts based on small RNA type. E Distribution of reads assigned to GtRNAdb in tRF subtypes. The total bar height is proportional to the total read count for each group. Percentages indicate the relative proportion of each tRF subtype within the corresponding group, and n represents the actual read count number for each subtype. tRF5, reads derived from tRNA 5′ end among reads aligned to GtRNAdb; tRF3, reads derived from tRNA 3′ end among reads aligned to GtRNAdb; other, not included in the previous two groups. F Histogram showing the distribution of log 2 (Fold change) using reads aligned to GtRNAdb. Green, CC-treated versus non-treated; Yellow, ANG overexpression versus control. G Volcano plot depicting significantly changed tRFs in TM4 cell lines. Results from CC-treated versus non-treated are represented as circles, and results from ANG overexpression versus control are represented as triangles. n = 2 for each group.

    Journal: Molecular Metabolism

    Article Title: AMPK inhibition and elevated angiogenin are associated with tRNA fragmentation in the male germline exposed to a high-fat diet

    doi: 10.1016/j.molmet.2026.102350

    Figure Lengend Snippet: AMPK inhibition-induced Angiogenin is accompanied by alteration of tRFs profile in vitro. A Western blot results of proteins related with AMPK-mTOR pathways in TM3, TM4, and NIH/3T3 cell lines using compound C (CC), rapamycin (Rapa), and MHY1485 (MHY) in TM3, TM4, and NIH/3T3 cell lines (left to right). The number represents the densiometric comparison of the expression of pAMPK and pmTOR proteins against AMPK and mTOR, respectively. B Angiogenin gene expression. Gene expression was quantified after 12 h of treatment. mRNA expression level was normalized to Actin . Data are represented as mean ± standard deviation. Statistical analysis was performed using One-way ANOVA with Tukey post-hoc test. Different letters are significantly different. C Northern blot results of tRF3-Pro and Val in mouse testis cell lines. Each sample RNAs were extracted from both TM3 and TM4 cells with CC treatment and overexpression of Angiogenin (Ang OE). Each intact tRNA was shown as a control. Band intensities of Northern blot are represented as bar graph after quantification using Image J software. Data are presented as mean ± standard deviation. One-way ANOVA was used for statistical analysis, and the different alphabets with Tukey post-hoc test. D Distribution of read counts based on small RNA type. E Distribution of reads assigned to GtRNAdb in tRF subtypes. The total bar height is proportional to the total read count for each group. Percentages indicate the relative proportion of each tRF subtype within the corresponding group, and n represents the actual read count number for each subtype. tRF5, reads derived from tRNA 5′ end among reads aligned to GtRNAdb; tRF3, reads derived from tRNA 3′ end among reads aligned to GtRNAdb; other, not included in the previous two groups. F Histogram showing the distribution of log 2 (Fold change) using reads aligned to GtRNAdb. Green, CC-treated versus non-treated; Yellow, ANG overexpression versus control. G Volcano plot depicting significantly changed tRFs in TM4 cell lines. Results from CC-treated versus non-treated are represented as circles, and results from ANG overexpression versus control are represented as triangles. n = 2 for each group.

    Article Snippet: The mouse testicular TM3 cell line and TM4 Sertoli cell line were purchased from the Korean Cell Line Bank (Seoul, Korea).

    Techniques: Inhibition, In Vitro, Western Blot, Comparison, Expressing, Gene Expression, Standard Deviation, Northern Blot, Over Expression, Control, Software, Derivative Assay

    Fluoride impairs male reproductive capacity by differentially regulating autophagy of testicular somatic cells in mice. (A to F) Six-week-old male mice freely drank distilled water with or without 100 mg/l NaF for 18 weeks. (A) Representative images of H&E staining on testis. Scale bars, 100 μm (left) and 50 μm (right). (B) Representative microscopic views of sperm morphology. Scale bars, 50 μm. (C) Sperm quality. (D and E) Representative transmission electron microscopy images of autophagosomes in (D) Leydig cells and (E) Sertoli cells [scale bars, 2 μm (bottom) and 1 μm (top)], with red arrows indicating autophagosomes. (F) Immunohistochemistry was used to detect the protein expression of LC3B and p62 in Leydig cells and Sertoli cells. (G and H) Testicular somatic cells were treated with various concentrations of NaF for 24 h. The relative expression of LC3B and p62 proteins in (G) TM3 cells, (H) TM4 cells, and (I) TM4 cells cotreated with 20 μM chloroquine. Cell viability of (J) TM3 and (K) TM4 cells that were treated with 0.25 mM NaF and 20 μM chloroquine for 24 h or pretreated with 20 nM rapamycin for 1 h. All values in the figure are means ± SEM. n ≥ 3. * P < 0.05, ** P < 0.01 versus control; # P < 0.05, ## P < 0.01 versus chloroquine.

    Journal: Research

    Article Title: Environmental Fluoride Compromises Male Fertility: Differentially Modulated miR-34a-5p Targets REST to Regulate Autophagy in Testicular Somatic Cells

    doi: 10.34133/research.1113

    Figure Lengend Snippet: Fluoride impairs male reproductive capacity by differentially regulating autophagy of testicular somatic cells in mice. (A to F) Six-week-old male mice freely drank distilled water with or without 100 mg/l NaF for 18 weeks. (A) Representative images of H&E staining on testis. Scale bars, 100 μm (left) and 50 μm (right). (B) Representative microscopic views of sperm morphology. Scale bars, 50 μm. (C) Sperm quality. (D and E) Representative transmission electron microscopy images of autophagosomes in (D) Leydig cells and (E) Sertoli cells [scale bars, 2 μm (bottom) and 1 μm (top)], with red arrows indicating autophagosomes. (F) Immunohistochemistry was used to detect the protein expression of LC3B and p62 in Leydig cells and Sertoli cells. (G and H) Testicular somatic cells were treated with various concentrations of NaF for 24 h. The relative expression of LC3B and p62 proteins in (G) TM3 cells, (H) TM4 cells, and (I) TM4 cells cotreated with 20 μM chloroquine. Cell viability of (J) TM3 and (K) TM4 cells that were treated with 0.25 mM NaF and 20 μM chloroquine for 24 h or pretreated with 20 nM rapamycin for 1 h. All values in the figure are means ± SEM. n ≥ 3. * P < 0.05, ** P < 0.01 versus control; # P < 0.05, ## P < 0.01 versus chloroquine.

    Article Snippet: Murine Leydig cell line (TM3) and murine Sertoli cell line (TM4) were purchased from the American Type Culture Collection (ATCC) (Manassas, USA).

    Techniques: Staining, Transmission Assay, Electron Microscopy, Immunohistochemistry, Expressing, Control

    miR-34a-5p was selected as the key miRNA in the differential regulation of autophagy in testicular somatic cells by fluoride. (A) Network toxicological analysis results of miRNAs related to fluoride-induced male reproductive injury. (B) HAMDB database analysis results of autophagy-related candidate miRNAs. (C and D) qRT-PCR revealed autophagy-related candidate miRNA expression changes in (C) TM3 and (D) TM4 cells after fluoride treatment. (E) FISH of miR-34a-5p in the testis of control and fluoride-treated mice (dashed areas indicate Leydig cells, and white arrows indicate Sertoli cells). All values in the figure are means ± SEM. n = 3. * P < 0.05, ** P < 0.01.

    Journal: Research

    Article Title: Environmental Fluoride Compromises Male Fertility: Differentially Modulated miR-34a-5p Targets REST to Regulate Autophagy in Testicular Somatic Cells

    doi: 10.34133/research.1113

    Figure Lengend Snippet: miR-34a-5p was selected as the key miRNA in the differential regulation of autophagy in testicular somatic cells by fluoride. (A) Network toxicological analysis results of miRNAs related to fluoride-induced male reproductive injury. (B) HAMDB database analysis results of autophagy-related candidate miRNAs. (C and D) qRT-PCR revealed autophagy-related candidate miRNA expression changes in (C) TM3 and (D) TM4 cells after fluoride treatment. (E) FISH of miR-34a-5p in the testis of control and fluoride-treated mice (dashed areas indicate Leydig cells, and white arrows indicate Sertoli cells). All values in the figure are means ± SEM. n = 3. * P < 0.05, ** P < 0.01.

    Article Snippet: Murine Leydig cell line (TM3) and murine Sertoli cell line (TM4) were purchased from the American Type Culture Collection (ATCC) (Manassas, USA).

    Techniques: Quantitative RT-PCR, Expressing, Control

    Fluoride differentially regulates miR-34a-5p to modulate autophagy in testicular somatic cells. (A to F) Testicular somatic cells were treated with lentiviruses expressing miR-34a-5p/miR-NC and Inhibitor-miR-34a-5p/Inhibitor-NC. (A and D) Relative expression of miR-34a-5p. (B, C, E, and F) Relative expression of LC3B and p62 proteins. (G to I) miR-34a-5p overexpression rescued fluoride-treated TM3 cells. (G) Relative expression of miR-34a-5p. (H and I) Relative expression of LC3B and p62 proteins. (J to L) miR-34a-5p knockdown rescued fluoride-treated TM4 cells. (J) Relative expression of miR-34a-5p. (K and L) Relative expression of LC3B and p62 proteins. All values in the figure are means ± SEM. n = 3. * P < 0.05, ** P < 0.01 versus control, miR-NC, or Inhibitor-NC; # P < 0.05, ## P < 0.01 versus 0.25 mM NaF.

    Journal: Research

    Article Title: Environmental Fluoride Compromises Male Fertility: Differentially Modulated miR-34a-5p Targets REST to Regulate Autophagy in Testicular Somatic Cells

    doi: 10.34133/research.1113

    Figure Lengend Snippet: Fluoride differentially regulates miR-34a-5p to modulate autophagy in testicular somatic cells. (A to F) Testicular somatic cells were treated with lentiviruses expressing miR-34a-5p/miR-NC and Inhibitor-miR-34a-5p/Inhibitor-NC. (A and D) Relative expression of miR-34a-5p. (B, C, E, and F) Relative expression of LC3B and p62 proteins. (G to I) miR-34a-5p overexpression rescued fluoride-treated TM3 cells. (G) Relative expression of miR-34a-5p. (H and I) Relative expression of LC3B and p62 proteins. (J to L) miR-34a-5p knockdown rescued fluoride-treated TM4 cells. (J) Relative expression of miR-34a-5p. (K and L) Relative expression of LC3B and p62 proteins. All values in the figure are means ± SEM. n = 3. * P < 0.05, ** P < 0.01 versus control, miR-NC, or Inhibitor-NC; # P < 0.05, ## P < 0.01 versus 0.25 mM NaF.

    Article Snippet: Murine Leydig cell line (TM3) and murine Sertoli cell line (TM4) were purchased from the American Type Culture Collection (ATCC) (Manassas, USA).

    Techniques: Expressing, Over Expression, Knockdown, Control

    miR-34a-5p targets REST in testicular somatic cells exposed to fluoride. (A) Expression changes of p62 mRNA in TM3 and TM4 cells after fluoride treatment and overexpression or knockdown of miR-34a-5p. (B) Prediction results of miR-34a-5p target genes by miRWalk combined with ChEA3 database. (C and F) Differential expression of the top 15 predicted target genes after fluoride treatment in (C) TM3 and (F) TM4 cells. (D, E, G, and H) Relative mRNA expression of Elf1 , Foxo1 , Foxp1 , Klf10 , Mef2a , Rest , Smad5 , and Yy1 . (I) Schematic showing the targeted binding sites of miR-34a-5p to FOXO1 and REST 3′ UTR. (J and K) The histogram shows the relative fluorescence intensity of each group. (L) FISH of miR-34a-5p and Rest mRNA in testicular tissue from control mice (white arrow indicates the positive area within the Sertoli cells or Leydig cells). (M and N) Differential expression of REST protein in testicular somatic cells after overexpression or knockdown of miR-34a-5p. All values in the figure are means ± SEM. n = 3. * P < 0.05, ** P < 0.01.

    Journal: Research

    Article Title: Environmental Fluoride Compromises Male Fertility: Differentially Modulated miR-34a-5p Targets REST to Regulate Autophagy in Testicular Somatic Cells

    doi: 10.34133/research.1113

    Figure Lengend Snippet: miR-34a-5p targets REST in testicular somatic cells exposed to fluoride. (A) Expression changes of p62 mRNA in TM3 and TM4 cells after fluoride treatment and overexpression or knockdown of miR-34a-5p. (B) Prediction results of miR-34a-5p target genes by miRWalk combined with ChEA3 database. (C and F) Differential expression of the top 15 predicted target genes after fluoride treatment in (C) TM3 and (F) TM4 cells. (D, E, G, and H) Relative mRNA expression of Elf1 , Foxo1 , Foxp1 , Klf10 , Mef2a , Rest , Smad5 , and Yy1 . (I) Schematic showing the targeted binding sites of miR-34a-5p to FOXO1 and REST 3′ UTR. (J and K) The histogram shows the relative fluorescence intensity of each group. (L) FISH of miR-34a-5p and Rest mRNA in testicular tissue from control mice (white arrow indicates the positive area within the Sertoli cells or Leydig cells). (M and N) Differential expression of REST protein in testicular somatic cells after overexpression or knockdown of miR-34a-5p. All values in the figure are means ± SEM. n = 3. * P < 0.05, ** P < 0.01.

    Article Snippet: Murine Leydig cell line (TM3) and murine Sertoli cell line (TM4) were purchased from the American Type Culture Collection (ATCC) (Manassas, USA).

    Techniques: Expressing, Over Expression, Knockdown, Quantitative Proteomics, Binding Assay, Fluorescence, Control

    miR-34a-5p targets REST to regulate autophagy in testicular somatic cells. (A to F) TM3 and TM4 cells were treated with lentivirus expressing OE-REST, si-REST, OE-NC, or si-NC. (A and D) Relative Rest mRNA expression. (B, C, E, and F) Relative LC3B, p62, and REST protein expression. (G to K) REST overexpression rescued TM3 and TM4 cells overexpressing miR-34a-5p. (G and H) Relative miR-34a-5p, Rest , and p62 mRNA expression. (I to K) Relative REST, LC3B, and p62 protein levels. All values in the figure are means ± SEM. n = 3. ns indicates not significant; * P < 0.05, ** P < 0.01 versus control; # P < 0.05, ## P < 0.01 versus miR-34a-5p.

    Journal: Research

    Article Title: Environmental Fluoride Compromises Male Fertility: Differentially Modulated miR-34a-5p Targets REST to Regulate Autophagy in Testicular Somatic Cells

    doi: 10.34133/research.1113

    Figure Lengend Snippet: miR-34a-5p targets REST to regulate autophagy in testicular somatic cells. (A to F) TM3 and TM4 cells were treated with lentivirus expressing OE-REST, si-REST, OE-NC, or si-NC. (A and D) Relative Rest mRNA expression. (B, C, E, and F) Relative LC3B, p62, and REST protein expression. (G to K) REST overexpression rescued TM3 and TM4 cells overexpressing miR-34a-5p. (G and H) Relative miR-34a-5p, Rest , and p62 mRNA expression. (I to K) Relative REST, LC3B, and p62 protein levels. All values in the figure are means ± SEM. n = 3. ns indicates not significant; * P < 0.05, ** P < 0.01 versus control; # P < 0.05, ## P < 0.01 versus miR-34a-5p.

    Article Snippet: Murine Leydig cell line (TM3) and murine Sertoli cell line (TM4) were purchased from the American Type Culture Collection (ATCC) (Manassas, USA).

    Techniques: Expressing, Over Expression, Control

    Fluoride differentially regulates REST to modulate autophagy in testicular somatic cells. (A) Representative image of Rest mRNA FISH in testes from control and fluoride-treated mice. (B) Representative immunofluorescence staining of REST proteins in testes from control and fluoride-treated mice. Dashed areas indicate Leydig cells, and white arrows indicate Sertoli cells. (C and D) Relative REST protein expression in testicular somatic cells treated with fluoride. (E to G) REST knockdown rescued fluoride-treated TM3 cells. (E) Relative expression of Rest mRNA. (F and G) Relative expression of REST, p62, and LC3B proteins. (H to J) REST overexpression rescued fluoride-treated TM4 cells. (H) Relative expression of Rest mRNA. (I and J) Relative expression of REST, p62, and LC3B proteins. All values in the figure are means ± SEM. n = 3. * P < 0.05, ** P < 0.01 versus control, si-NC, or OE-NC; # P < 0.05, ## P < 0.01 versus 0.25 mM NaF.

    Journal: Research

    Article Title: Environmental Fluoride Compromises Male Fertility: Differentially Modulated miR-34a-5p Targets REST to Regulate Autophagy in Testicular Somatic Cells

    doi: 10.34133/research.1113

    Figure Lengend Snippet: Fluoride differentially regulates REST to modulate autophagy in testicular somatic cells. (A) Representative image of Rest mRNA FISH in testes from control and fluoride-treated mice. (B) Representative immunofluorescence staining of REST proteins in testes from control and fluoride-treated mice. Dashed areas indicate Leydig cells, and white arrows indicate Sertoli cells. (C and D) Relative REST protein expression in testicular somatic cells treated with fluoride. (E to G) REST knockdown rescued fluoride-treated TM3 cells. (E) Relative expression of Rest mRNA. (F and G) Relative expression of REST, p62, and LC3B proteins. (H to J) REST overexpression rescued fluoride-treated TM4 cells. (H) Relative expression of Rest mRNA. (I and J) Relative expression of REST, p62, and LC3B proteins. All values in the figure are means ± SEM. n = 3. * P < 0.05, ** P < 0.01 versus control, si-NC, or OE-NC; # P < 0.05, ## P < 0.01 versus 0.25 mM NaF.

    Article Snippet: Murine Leydig cell line (TM3) and murine Sertoli cell line (TM4) were purchased from the American Type Culture Collection (ATCC) (Manassas, USA).

    Techniques: Control, Immunofluorescence, Staining, Expressing, Knockdown, Over Expression

    Cd exposure activates autophagy in Sertoli cells. A - G The male mice were injected (i.p.) with 2.0 mg/kg CdCl 2 or vehicle, respectively. Mouse testes were collected at 0, 2, 8, 24, 48, and 72 h after Cd treatment. A , B Representative images and quantification of autophagosomes in mice Sertoli cells detected by transmission electron microscopy. The yellow arrows represent the autophagosomes. C - E The expression of ATG5 and LC3B-II/I was detected by western blotting. F , G Representative images and quantification of mIHC assay. White arrows denoted the LC3B puncta surrounding WT1. Scale bar: 50 μm. H - J TM4 cells were exposed to Cd for 0, 2, 8, and 24 h, respectively. H - J The expression of ATG5 and LC3B-II/I was detected by western blotting. Data were displayed as mean ± SEM . n = 3- 6. * P < 0.05, ** P < 0.01 vs 0 h group

    Journal: Cell Biology and Toxicology

    Article Title: ATG5-dependent autophagy in Sertoli cells protects against cadmium-disrupted blood-testis barrier via perturbing CXCL2/CXCR2 axis

    doi: 10.1007/s10565-025-10089-5

    Figure Lengend Snippet: Cd exposure activates autophagy in Sertoli cells. A - G The male mice were injected (i.p.) with 2.0 mg/kg CdCl 2 or vehicle, respectively. Mouse testes were collected at 0, 2, 8, 24, 48, and 72 h after Cd treatment. A , B Representative images and quantification of autophagosomes in mice Sertoli cells detected by transmission electron microscopy. The yellow arrows represent the autophagosomes. C - E The expression of ATG5 and LC3B-II/I was detected by western blotting. F , G Representative images and quantification of mIHC assay. White arrows denoted the LC3B puncta surrounding WT1. Scale bar: 50 μm. H - J TM4 cells were exposed to Cd for 0, 2, 8, and 24 h, respectively. H - J The expression of ATG5 and LC3B-II/I was detected by western blotting. Data were displayed as mean ± SEM . n = 3- 6. * P < 0.05, ** P < 0.01 vs 0 h group

    Article Snippet: The mouse Sertoli cell line TM4 (GNM41) was obtained from Procell Life Science & Technology(Li et al. ).

    Techniques: Injection, Transmission Assay, Electron Microscopy, Expressing, Western Blot