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human myocardial cell line ac16  (ATCC)


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    Structured Review

    ATCC human myocardial cell line ac16
    The effect of miR-143-5p on LPS-induced <t>AC16</t> injury. a The miR-143-5p was downregulated in LPS-induced AC16. b - d Overexpressed miR-143-5p could promote ( b ) the cell viability, suppress ( c ) the apoptosis, and ( d ) the inflammatory cytokines (TNF-α, IL-6) of LPS-induced AC16. ns: no significance, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Statistical tests: one-way ANOVA with post hoc Tukey’s test
    Human Myocardial Cell Line Ac16, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 335 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+myocardial+cell+line+ac16/AC16/pmc12801460-80-0-5
    Average 97 stars, based on 335 article reviews
    human myocardial cell line ac16 - by Bioz Stars, 2026-10
    97/100 stars

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    1) Product Images from "MiR-143-5p serves as a diagnostic biomarker in patients with sepsis and regulates sepsis-induced inflammation and cardiac dysfunction"

    Article Title: MiR-143-5p serves as a diagnostic biomarker in patients with sepsis and regulates sepsis-induced inflammation and cardiac dysfunction

    Journal: Hereditas

    doi: 10.1186/s41065-025-00623-0

    The effect of miR-143-5p on LPS-induced AC16 injury. a The miR-143-5p was downregulated in LPS-induced AC16. b - d Overexpressed miR-143-5p could promote ( b ) the cell viability, suppress ( c ) the apoptosis, and ( d ) the inflammatory cytokines (TNF-α, IL-6) of LPS-induced AC16. ns: no significance, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Statistical tests: one-way ANOVA with post hoc Tukey’s test
    Figure Legend Snippet: The effect of miR-143-5p on LPS-induced AC16 injury. a The miR-143-5p was downregulated in LPS-induced AC16. b - d Overexpressed miR-143-5p could promote ( b ) the cell viability, suppress ( c ) the apoptosis, and ( d ) the inflammatory cytokines (TNF-α, IL-6) of LPS-induced AC16. ns: no significance, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Statistical tests: one-way ANOVA with post hoc Tukey’s test

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    ATCC human myocardial cell line ac16
    The effect of miR-143-5p on LPS-induced <t>AC16</t> injury. a The miR-143-5p was downregulated in LPS-induced AC16. b - d Overexpressed miR-143-5p could promote ( b ) the cell viability, suppress ( c ) the apoptosis, and ( d ) the inflammatory cytokines (TNF-α, IL-6) of LPS-induced AC16. ns: no significance, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Statistical tests: one-way ANOVA with post hoc Tukey’s test
    Human Myocardial Cell Line Ac16, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+myocardial+cell+line+ac16/AC16/pmc12801460-80-0-5
    Average 97 stars, based on 1 article reviews
    human myocardial cell line ac16 - by Bioz Stars, 2026-10
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      Buy from Supplier

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    Yeasen Biotechnology human myocardial cell lines ac16
    The effect of miR-143-5p on LPS-induced <t>AC16</t> injury. a The miR-143-5p was downregulated in LPS-induced AC16. b - d Overexpressed miR-143-5p could promote ( b ) the cell viability, suppress ( c ) the apoptosis, and ( d ) the inflammatory cytokines (TNF-α, IL-6) of LPS-induced AC16. ns: no significance, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Statistical tests: one-way ANOVA with post hoc Tukey’s test
    Human Myocardial Cell Lines Ac16, supplied by Yeasen Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC ac16 human ventricular myocardial cell lines
    The effect of miR-143-5p on LPS-induced <t>AC16</t> injury. a The miR-143-5p was downregulated in LPS-induced AC16. b - d Overexpressed miR-143-5p could promote ( b ) the cell viability, suppress ( c ) the apoptosis, and ( d ) the inflammatory cytokines (TNF-α, IL-6) of LPS-induced AC16. ns: no significance, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Statistical tests: one-way ANOVA with post hoc Tukey’s test
    Ac16 Human Ventricular Myocardial Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC human myocardial cell line ac16 cells
    The effect of miR-143-5p on LPS-induced <t>AC16</t> injury. a The miR-143-5p was downregulated in LPS-induced AC16. b - d Overexpressed miR-143-5p could promote ( b ) the cell viability, suppress ( c ) the apoptosis, and ( d ) the inflammatory cytokines (TNF-α, IL-6) of LPS-induced AC16. ns: no significance, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Statistical tests: one-way ANOVA with post hoc Tukey’s test
    Human Myocardial Cell Line Ac16 Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+myocardial+cell+line+ac16/AC16/pmc10011218-48-0-9
    Average 97 stars, based on 1 article reviews
    human myocardial cell line ac16 cells - by Bioz Stars, 2026-10
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    ATCC human myocardial cell lines
    Figure 2. Ang II induced the down-regulation of NBR2 in cardiomyocytes and aggravated <t>myocardial</t> hypertrophy A: Immunofluorescence staining results of HCM and <t>AC16</t> cells. Cell size was measured for two groups of 50 randomized cells (n = 3 for each independent experiment; nuclei was blue; α-actinin was green). B: The mRNA expression of ANP, BNP and β-MHC in HCM and AC16 cells after 48 hours of Ang II treatment was monitored by RT-qPCR C: RT-qPCR was implemented to examine the relative levels of NBR2 in HCM and AC16 cells after 48 hours of treatment with Ang II. Data were expressed as mean ±SD (n = 3). *P < 0.01, ***P < 0.001(vs.Con).
    Human Myocardial Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+myocardial+cell+line+ac16/AC16/pm35703318-47-0-11
    Average 97 stars, based on 1 article reviews
    human myocardial cell lines - by Bioz Stars, 2026-10
    97/100 stars
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    ATCC human myocardial cell lines ac16
    Figure 2. Ang II induced the down-regulation of NBR2 in cardiomyocytes and aggravated <t>myocardial</t> hypertrophy A: Immunofluorescence staining results of HCM and <t>AC16</t> cells. Cell size was measured for two groups of 50 randomized cells (n = 3 for each independent experiment; nuclei was blue; α-actinin was green). B: The mRNA expression of ANP, BNP and β-MHC in HCM and AC16 cells after 48 hours of Ang II treatment was monitored by RT-qPCR C: RT-qPCR was implemented to examine the relative levels of NBR2 in HCM and AC16 cells after 48 hours of treatment with Ang II. Data were expressed as mean ±SD (n = 3). *P < 0.01, ***P < 0.001(vs.Con).
    Human Myocardial Cell Lines Ac16, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+myocardial+cell+line+ac16/AC16/pm34843094-30-0-8
    Average 97 stars, based on 1 article reviews
    human myocardial cell lines ac16 - by Bioz Stars, 2026-10
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      Buy from Supplier

    Image Search Results


    The effect of miR-143-5p on LPS-induced AC16 injury. a The miR-143-5p was downregulated in LPS-induced AC16. b - d Overexpressed miR-143-5p could promote ( b ) the cell viability, suppress ( c ) the apoptosis, and ( d ) the inflammatory cytokines (TNF-α, IL-6) of LPS-induced AC16. ns: no significance, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Statistical tests: one-way ANOVA with post hoc Tukey’s test

    Journal: Hereditas

    Article Title: MiR-143-5p serves as a diagnostic biomarker in patients with sepsis and regulates sepsis-induced inflammation and cardiac dysfunction

    doi: 10.1186/s41065-025-00623-0

    Figure Lengend Snippet: The effect of miR-143-5p on LPS-induced AC16 injury. a The miR-143-5p was downregulated in LPS-induced AC16. b - d Overexpressed miR-143-5p could promote ( b ) the cell viability, suppress ( c ) the apoptosis, and ( d ) the inflammatory cytokines (TNF-α, IL-6) of LPS-induced AC16. ns: no significance, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Statistical tests: one-way ANOVA with post hoc Tukey’s test

    Article Snippet: Human myocardial cell line AC16 (ATCC, USA).

    Techniques:

    Figure 2. Ang II induced the down-regulation of NBR2 in cardiomyocytes and aggravated myocardial hypertrophy A: Immunofluorescence staining results of HCM and AC16 cells. Cell size was measured for two groups of 50 randomized cells (n = 3 for each independent experiment; nuclei was blue; α-actinin was green). B: The mRNA expression of ANP, BNP and β-MHC in HCM and AC16 cells after 48 hours of Ang II treatment was monitored by RT-qPCR C: RT-qPCR was implemented to examine the relative levels of NBR2 in HCM and AC16 cells after 48 hours of treatment with Ang II. Data were expressed as mean ±SD (n = 3). *P < 0.01, ***P < 0.001(vs.Con).

    Journal: Bioengineered

    Article Title: lncRNA NBR2 attenuates angiotensin II-induced myocardial hypertrophy through repressing ER stress via activating LKB1/AMPK/Sirt1 pathway.

    doi: 10.1080/21655979.2022.2062527

    Figure Lengend Snippet: Figure 2. Ang II induced the down-regulation of NBR2 in cardiomyocytes and aggravated myocardial hypertrophy A: Immunofluorescence staining results of HCM and AC16 cells. Cell size was measured for two groups of 50 randomized cells (n = 3 for each independent experiment; nuclei was blue; α-actinin was green). B: The mRNA expression of ANP, BNP and β-MHC in HCM and AC16 cells after 48 hours of Ang II treatment was monitored by RT-qPCR C: RT-qPCR was implemented to examine the relative levels of NBR2 in HCM and AC16 cells after 48 hours of treatment with Ang II. Data were expressed as mean ±SD (n = 3). *P < 0.01, ***P < 0.001(vs.Con).

    Article Snippet: Human myocardial cell lines (HCM and AC16) were bought from the American Type Culture Collection Center (ATCC).

    Techniques: Immunofluorescence, Staining, Expressing, Quantitative RT-PCR

    Figure 3. Overexpressing NBR2 dramatically suppressed Ang II–induced myocardial hypertrophy A: Relative levels of NBR2 in HCM and AC16 cells transfected with NBR2 overexpression plasmid for 48 hours were testified by RT-qPCR. B: Changes in surface area of cells treated with Ang II in the presence or absence of NBR2 overexpression plasmids (n = 3 for each independent experiment; nuclear was blue; α actin was green). (Scale, 50 μM). C: ANP, BNP and β-MHC mRNA expression levels were measured with RT-qPCR in Ang II-stimulated HCM and AC16 cardiomyocytes after NBR2 overexpression plasmid transfection. Data were expressed as mean ±SD (n = 3). **P < 0.01, ***P < 0.001(vs.Con). &P < 0.05, &&P < 0.01, &&&P < 0.001(vs.Vector+Ang-II).

    Journal: Bioengineered

    Article Title: lncRNA NBR2 attenuates angiotensin II-induced myocardial hypertrophy through repressing ER stress via activating LKB1/AMPK/Sirt1 pathway.

    doi: 10.1080/21655979.2022.2062527

    Figure Lengend Snippet: Figure 3. Overexpressing NBR2 dramatically suppressed Ang II–induced myocardial hypertrophy A: Relative levels of NBR2 in HCM and AC16 cells transfected with NBR2 overexpression plasmid for 48 hours were testified by RT-qPCR. B: Changes in surface area of cells treated with Ang II in the presence or absence of NBR2 overexpression plasmids (n = 3 for each independent experiment; nuclear was blue; α actin was green). (Scale, 50 μM). C: ANP, BNP and β-MHC mRNA expression levels were measured with RT-qPCR in Ang II-stimulated HCM and AC16 cardiomyocytes after NBR2 overexpression plasmid transfection. Data were expressed as mean ±SD (n = 3). **P < 0.01, ***P < 0.001(vs.Con). &P < 0.05, &&P < 0.01, &&&P < 0.001(vs.Vector+Ang-II).

    Article Snippet: Human myocardial cell lines (HCM and AC16) were bought from the American Type Culture Collection Center (ATCC).

    Techniques: Transfection, Over Expression, Plasmid Preparation, Quantitative RT-PCR, Expressing

    Figure 7. Dampening the LKB1/AMPK/Sirt1 pathway weakened the inhibitory effect of NBR2 on myocardial hypertrophy and ER stress lncRNA NBR2 overexpression plasmids were co-transfected with shRNA of LKB1 into Ang II-treated HCM and AC16 cardiomyocytes. A: WB was conducted to evaluate the LKB1/AMPK/SIRT1 expression in HCM and AC16 cells. B: The mRNA expression of ANP, BNP and β-MHC in HCM and AC16 cells was checked by RT-qPCR. C: Cellular immunofluorescence staining was adopted for assaying surface area changes of HCM and AC16 cells (n = 3 for each independent experiment; nuclear was blue; α-actin was green). (Scale, 50 μM). D. WB was conducted to measure ER stress protein expression in HCM and AC16 cardiomyocytes E: Flow cytometry showed that inhibiting LKB1 hindered the anti-apoptotic impact of NBR2 on HCM and AC16 cells. Data were expressed as mean ±SD (n = 3). *P < 0.05, **P < 0.01, ***P < 0.001(vs.Con). & P < 0.05, && P < 0.01, &&& P < 0.001 (vs.lncRNA NBR2+ Ang-II).

    Journal: Bioengineered

    Article Title: lncRNA NBR2 attenuates angiotensin II-induced myocardial hypertrophy through repressing ER stress via activating LKB1/AMPK/Sirt1 pathway.

    doi: 10.1080/21655979.2022.2062527

    Figure Lengend Snippet: Figure 7. Dampening the LKB1/AMPK/Sirt1 pathway weakened the inhibitory effect of NBR2 on myocardial hypertrophy and ER stress lncRNA NBR2 overexpression plasmids were co-transfected with shRNA of LKB1 into Ang II-treated HCM and AC16 cardiomyocytes. A: WB was conducted to evaluate the LKB1/AMPK/SIRT1 expression in HCM and AC16 cells. B: The mRNA expression of ANP, BNP and β-MHC in HCM and AC16 cells was checked by RT-qPCR. C: Cellular immunofluorescence staining was adopted for assaying surface area changes of HCM and AC16 cells (n = 3 for each independent experiment; nuclear was blue; α-actin was green). (Scale, 50 μM). D. WB was conducted to measure ER stress protein expression in HCM and AC16 cardiomyocytes E: Flow cytometry showed that inhibiting LKB1 hindered the anti-apoptotic impact of NBR2 on HCM and AC16 cells. Data were expressed as mean ±SD (n = 3). *P < 0.05, **P < 0.01, ***P < 0.001(vs.Con). & P < 0.05, && P < 0.01, &&& P < 0.001 (vs.lncRNA NBR2+ Ang-II).

    Article Snippet: Human myocardial cell lines (HCM and AC16) were bought from the American Type Culture Collection Center (ATCC).

    Techniques: Over Expression, Transfection, shRNA, Expressing, Quantitative RT-PCR, Immunofluorescence, Staining, Flow Cytometry