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Proteintech vimentin

circSMAD4 drives tumor-educated M2-like polarization of macrophages and promotes tumor-cell aggressiveness. (A) Workflow for generating TC-hMDMs and TC-BMDMs, circSMAD4 knockdown, and downstream functional assays. (B) RT–qPCR analysis of M1-associated markers (MHC-II [HLA-DRA in TC-hMDMs; H2-Ab1 in TC-BMDMs], NOS2, and CD86) and M2-associated markers (CD163, CD206, and ARG1) in TC-hMDMs and TC-BMDMs. (C) Representative flow-cytometry histograms for HLA-DR, iNOS, CD86, CD163, CD206, and ARG1 in TC-hMDMs. Gating strategy and marker thresholds were defined based on FMO controls (see ). (D) Flow-cytometry quantification of marker-positive cells in TC-hMDMs and TC-BMDMs. (E) ELISA of IL-10, TGF-β, and iNOS in culture supernatants. (F) CCK-8 assays of A549 and LLC cells. (G) Colony-formation assays of A549 and LLC cells with quantification. (H) Bioluminescence-based growth readouts of patient-derived LUAD organoids (PDO #1 and PDO #2) after co-culture with TC-hMDMs. (I) Immunoblot analysis of EMT-related <t>proteins</t> <t>(E-cadherin,</t> N-cadherin, <t>Vimentin)</t> in A549 and LLC cells. (J) Transwell migration and invasion assays of A549 and LLC cells with quantification. Scale bar, 50 μm. ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001; ∗∗∗∗P < 0.0001; ns, not significant.

Vimentin, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 2444 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/vim/Vimentin+Antibody/pmc13050104-89-17-18
Average 96 stars, based on 2444 article reviews

vimentin - by Bioz Stars, 2026-09

96/100 stars

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1) Product Images from "CircSMAD4 shapes matrix-remodeling TAMs in lung adenocarcinoma"

Article Title: CircSMAD4 shapes matrix-remodeling TAMs in lung adenocarcinoma

Journal: Non-coding RNA Research

doi: 10.1016/j.ncrna.2026.03.003

Figure Legend Snippet: circSMAD4 drives tumor-educated M2-like polarization of macrophages and promotes tumor-cell aggressiveness. (A) Workflow for generating TC-hMDMs and TC-BMDMs, circSMAD4 knockdown, and downstream functional assays. (B) RT–qPCR analysis of M1-associated markers (MHC-II [HLA-DRA in TC-hMDMs; H2-Ab1 in TC-BMDMs], NOS2, and CD86) and M2-associated markers (CD163, CD206, and ARG1) in TC-hMDMs and TC-BMDMs. (C) Representative flow-cytometry histograms for HLA-DR, iNOS, CD86, CD163, CD206, and ARG1 in TC-hMDMs. Gating strategy and marker thresholds were defined based on FMO controls (see ). (D) Flow-cytometry quantification of marker-positive cells in TC-hMDMs and TC-BMDMs. (E) ELISA of IL-10, TGF-β, and iNOS in culture supernatants. (F) CCK-8 assays of A549 and LLC cells. (G) Colony-formation assays of A549 and LLC cells with quantification. (H) Bioluminescence-based growth readouts of patient-derived LUAD organoids (PDO #1 and PDO #2) after co-culture with TC-hMDMs. (I) Immunoblot analysis of EMT-related proteins (E-cadherin, N-cadherin, Vimentin) in A549 and LLC cells. (J) Transwell migration and invasion assays of A549 and LLC cells with quantification. Scale bar, 50 μm. ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001; ∗∗∗∗P < 0.0001; ns, not significant.

Techniques Used: Knockdown, Functional Assay, Quantitative RT-PCR, Flow Cytometry, Marker, Enzyme-linked Immunosorbent Assay, CCK-8 Assay, Derivative Assay, Co-Culture Assay, Western Blot, Migration

circSMAD4 depletion in macrophages restrains LUAD growth and metastasis in vivo. (A) Schematic of orthotopic lung implantation and experimental metastasis models using LLC cells mixed with BMDMs expressing shNC or sh-circSMAD4. (B) Representative images of orthotopic lung tumors. (C) Tumor weight of orthotopic implants. (D) Overall survival of mice bearing orthotopic tumors. (E) Immunofluorescence showing F4/80 and circSMAD4 signals in tumor tissues. Scale bar, 50 μm. (F, G) Representative Ki-67 IHC staining and quantification in orthotopic tumors. Scale bar, 50 μm. (H) Representative bioluminescence images of lung tumor burden in the metastasis model. (I) Tumor weight in the metastasis model. (J) Overall survival of mice in the metastasis model. (K–M) Representative IHC staining and quantification of E-cadherin and vimentin in tumors. Scale bar, 50 μm. ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001; ∗∗∗∗P < 0.0001; ns, not significant.

Figure Legend Snippet: circSMAD4 depletion in macrophages restrains LUAD growth and metastasis in vivo. (A) Schematic of orthotopic lung implantation and experimental metastasis models using LLC cells mixed with BMDMs expressing shNC or sh-circSMAD4. (B) Representative images of orthotopic lung tumors. (C) Tumor weight of orthotopic implants. (D) Overall survival of mice bearing orthotopic tumors. (E) Immunofluorescence showing F4/80 and circSMAD4 signals in tumor tissues. Scale bar, 50 μm. (F, G) Representative Ki-67 IHC staining and quantification in orthotopic tumors. Scale bar, 50 μm. (H) Representative bioluminescence images of lung tumor burden in the metastasis model. (I) Tumor weight in the metastasis model. (J) Overall survival of mice in the metastasis model. (K–M) Representative IHC staining and quantification of E-cadherin and vimentin in tumors. Scale bar, 50 μm. ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001; ∗∗∗∗P < 0.0001; ns, not significant.

Techniques Used: In Vivo, Expressing, Immunofluorescence, Immunohistochemistry

Immunohistochemistry:

Article Title: Machine learning-based integration develops a hypoxia-derived signature for improving outcomes in glioma
Article Snippet: .. IHC assays were conducted utilizing primary antibodies targeting CD8 (Proteintech, China), PD-1 (Proteintech, China), HIF1A (CST, United States), Ki67(CST, United States), STAT3 (Proteintech, China), VIM (Proteintech, China), P65 (Proteintech, China), PD-L1 (CST, United States), and CD163 (Proteintech, China). ..

Western Blot:

Article Title: PPP1CA promotes hepatocellular carcinoma progression in a YAP1-dependent way.
Article Snippet: Hepatocellular carcinoma (HCC) exhibits high incidence, malignancy, and mortality rates.. Inactivation of the Hippo pathway has been implicated in the acquisition of malignant characteristics in HCC.. The present study identifies upregulation of protein phosphatase 1 catalytic subunit alpha (PPP1CA) in HCC tissues, with elevated PPP1CA expression correlating with poor prognosis in patients with HCC.

Incubation:

Article Title: Transcriptomic comparison of avian auditory and vestibular sensory epithelia
Article Snippet: .. The samples were immersed in a blocking buffer containing 1% BSA for 30 minutes, followed by an overnight incubation with primary antibodies (MYO7A (1:500, Proteus Biosciences), VIM (1:200, Proteintech), and SOX2 (1:200, Santa Cruz Biotechnology)) at 4°C with gentle rotation. ..

Article Title: Lactate production by tumor-resident Staphylococcus promotes metastatic colonization in lung adenocarcinoma.
Article Snippet: .. Following blocking, the membranes were incubated overnight at 4◦C with the primary antibodies: NDRG1 (Proteintech, 26902-1-AP), MCT1 (Proteintech, 20139-1-AP), Tubulin (Abcam, ab-7291), Lamin-B1 (Proteintech, 12987), LDHA (Proteintech, 19987), VIM (Proteintech, 10366), ENO1 (Proteintech, 11204), SNAI1 (Proteintech, 13099), Cortactin (Proteintech, 11381) and anti-beta actin monoclonal antibody (Proteintech, 20536). ..

Article Title: Integrated Multi‐Omics and Experimental Validation Unveil the GZMK/NF‐κB Axis Driving Inflammation and Fibroblast Proliferation in Rosacea: A Novel Drug Target Selection Strategy
Article Snippet: .. For immunofluorescence staining, the slice was incubated in a solution containing primary antibodies of Ki67 (Proteintech, 84 432–1- RR, China) and Vim (Proteintech, 10 366–1- AP, China), or CD31 (Proteintech, 65 058–1- Ig, China) overnight at 4°C and then incubated with Alexa Fluor 488- labeled or Alexa Fluor 594- labeled secondary antibodies, respectively. ..

Blocking Assay:

Gentle:

Immunofluorescence:

Staining:

Labeling:

Image Search Results

iNOS increases sensitivity to cisplatin in ovarian cancer (A) The cell viability of OVCAR8 cells was assessed using RealTime-Glo MT Cell Viability Assay after culturing in increasing concentrations of cisplatin for 72 h. (B) OVCAR8 cells incubated with or without L-NMMA for 48 h, measured by RealTime-Glo MT Cell Viability Assay. (C) Cell viability after either no treatment (control), cisplatin, and a combination of cisplatin and L-NMMA by RealTime-Glo MT Cell Viability Assay. (D) Western blot analysis of vimentin protein expression in ovarian cancer cell lines. (E) Ovarian cancer cell lines were analyzed for VIM mRNA levels by qPCR. (F) OVCAR8 cells were treated with or without L-NMMA (4, 6, 8, and 10 mM) for 48 h, and western blot was used to analyze the effect of L-NMMA on the vimentin protein expression. B-actin was used as a loading control. Band densities were quantified using ImageJ analysis. Error bars, SEM. ∗ p < 0.05; ∗∗ p < 0.01 (compared with the control group, using two-way ANOVA). All experiments were independently repeated three times.

Journal: Molecular Therapy. Nucleic Acids

Article Title: Nitric oxide-dependent stabilization of vimentin confers chemoresistance in ovarian cancer

doi: 10.1016/j.omtn.2026.102924

Figure Lengend Snippet: iNOS increases sensitivity to cisplatin in ovarian cancer (A) The cell viability of OVCAR8 cells was assessed using RealTime-Glo MT Cell Viability Assay after culturing in increasing concentrations of cisplatin for 72 h. (B) OVCAR8 cells incubated with or without L-NMMA for 48 h, measured by RealTime-Glo MT Cell Viability Assay. (C) Cell viability after either no treatment (control), cisplatin, and a combination of cisplatin and L-NMMA by RealTime-Glo MT Cell Viability Assay. (D) Western blot analysis of vimentin protein expression in ovarian cancer cell lines. (E) Ovarian cancer cell lines were analyzed for VIM mRNA levels by qPCR. (F) OVCAR8 cells were treated with or without L-NMMA (4, 6, 8, and 10 mM) for 48 h, and western blot was used to analyze the effect of L-NMMA on the vimentin protein expression. B-actin was used as a loading control. Band densities were quantified using ImageJ analysis. Error bars, SEM. ∗ p < 0.05; ∗∗ p < 0.01 (compared with the control group, using two-way ANOVA). All experiments were independently repeated three times.

Article Snippet: The following primers for TaqMan Gene Expression Assay were purchased from Thermo Fisher Scientific; human VIM (Cat. #Hs00958111_m1) and human NOS2 (Cat. #Hs01075529_m1).

Techniques: Viability Assay, Incubation, Control, Western Blot, Expressing

iNOS knockout increased chemosensitivity and impaired cell motility and migration of ovarian cancer cells (A) Immunoblotting showing reduced iNOS (left) and vimentin (right) expression levels following NOS2 knockdown in the OVCAR8 cells. (B) NOS2 knockdown sensitized OVCAR8 cells to cisplatin, reducing its IC 50 value. Log-logistic model was used to analyze the data. The group comparison between control group and KO-1 had a p value = 8.98e-07. The comparison between control and KO-2 had a p value = 0.0132. The detected EC50 for control group was 0.8554, for KO-1 was 0.6037, for KO2 was 0.7688. (C and D) Analysis of reduced protein (left) and mRNA (right) expression of iNOS and vimentin following siRNA transfection in OVCAR8 and A2780cis cells for 72 h, assessed by western blot and RT-qPCR. (E) OVCAR8 cells were transfected with 2 different siRNAs or the scramble siRNA and were assessed for migration using the scratch wound assay. The area of the wound was measured at 0, 12, 24, and 36 h by the IncuCyte live-cell analysis system. Two-way repeated measures ANOVA was used to analyze the data. After 6 h, siRNA1 had p value = 1, siRNA2 had p value = 0.23. After 12 h, siRNA1 had p value = 0.71 and siRNA 2 had p value = 0.16. After 24 h, siRNA1 had a p value = 0.39 and siRNA2 had a p value = 0.05. After 36 h, siRNA1 had a p value = 0.86 and siRNA2 had a p value = 0.04. (F) NOS2 KO-1 and KO-2 OVCAR8 cells formed significantly fewer colonies compared to parental OVCAR8. The experiment was performed in triplicate with three biological replicates. Statistical analysis was conducted with two-way ANOVA. ∗ p < 0.05 and ∗∗ p < 0.01. (G) Silencing of NOS2 by two different siRNAs significantly reduced the number of colonies formed by OVCAR8 cells. Clonogenic growth was measured after 10 days, quantified using ImageJ, and represented as a bar graph (mean ± SEM). The experiment was performed in triplicate with three biological replicates. Statistical analysis was conducted with two-way ANOVA. ∗ p < 0.05 and ∗∗ p < 0.01. All experiments were independently repeated two to three times.

Journal: Molecular Therapy. Nucleic Acids

Article Title: Nitric oxide-dependent stabilization of vimentin confers chemoresistance in ovarian cancer

doi: 10.1016/j.omtn.2026.102924

Figure Lengend Snippet: iNOS knockout increased chemosensitivity and impaired cell motility and migration of ovarian cancer cells (A) Immunoblotting showing reduced iNOS (left) and vimentin (right) expression levels following NOS2 knockdown in the OVCAR8 cells. (B) NOS2 knockdown sensitized OVCAR8 cells to cisplatin, reducing its IC 50 value. Log-logistic model was used to analyze the data. The group comparison between control group and KO-1 had a p value = 8.98e-07. The comparison between control and KO-2 had a p value = 0.0132. The detected EC50 for control group was 0.8554, for KO-1 was 0.6037, for KO2 was 0.7688. (C and D) Analysis of reduced protein (left) and mRNA (right) expression of iNOS and vimentin following siRNA transfection in OVCAR8 and A2780cis cells for 72 h, assessed by western blot and RT-qPCR. (E) OVCAR8 cells were transfected with 2 different siRNAs or the scramble siRNA and were assessed for migration using the scratch wound assay. The area of the wound was measured at 0, 12, 24, and 36 h by the IncuCyte live-cell analysis system. Two-way repeated measures ANOVA was used to analyze the data. After 6 h, siRNA1 had p value = 1, siRNA2 had p value = 0.23. After 12 h, siRNA1 had p value = 0.71 and siRNA 2 had p value = 0.16. After 24 h, siRNA1 had a p value = 0.39 and siRNA2 had a p value = 0.05. After 36 h, siRNA1 had a p value = 0.86 and siRNA2 had a p value = 0.04. (F) NOS2 KO-1 and KO-2 OVCAR8 cells formed significantly fewer colonies compared to parental OVCAR8. The experiment was performed in triplicate with three biological replicates. Statistical analysis was conducted with two-way ANOVA. ∗ p < 0.05 and ∗∗ p < 0.01. (G) Silencing of NOS2 by two different siRNAs significantly reduced the number of colonies formed by OVCAR8 cells. Clonogenic growth was measured after 10 days, quantified using ImageJ, and represented as a bar graph (mean ± SEM). The experiment was performed in triplicate with three biological replicates. Statistical analysis was conducted with two-way ANOVA. ∗ p < 0.05 and ∗∗ p < 0.01. All experiments were independently repeated two to three times.

Article Snippet: The following primers for TaqMan Gene Expression Assay were purchased from Thermo Fisher Scientific; human VIM (Cat. #Hs00958111_m1) and human NOS2 (Cat. #Hs01075529_m1).

Techniques: Knock-Out, Migration, Western Blot, Expressing, Knockdown, Comparison, Control, Transfection, Quantitative RT-PCR, Scratch Wound Assay Assay, Cell Analysis

L-NMMA promotes vimentin destabilization by enhancing its ubiquitination (A) CHX chase assay showing vimentin protein levels in OVCAR8 cells treated with 10 mM L-NMMA at different time points. (B) Vimentin ubiquitination was assessed in OVCAR8 cells treated with L-NMMA for 24 h, in the presence of the proteasome inhibitor MG-132 (10 μM) for the final 4 h, followed by immunoprecipitation and western blot using an anti-ubiquitin antibody. (C) Measurement of vimentin S-nitrosylation levels was performed by immunoprecipitation in OVCAR8 cells. (D) Western blot analysis of vimentin expression in OVCAR8 cells treated with 10 mM L-NMMA alone or in combination with MG132 at 1, 5, or 10 μM. (E) Tumor growth and proliferation were monitored in mice bearing parental and NOS2 KO OVCAR8 tumors, evaluated by ROI measurements every 4 days ( n = 6). (F) Kaplan-Meier survival curves of mice bearing parental and NOS2 KO OVCAR8 tumors following cisplatin treatment ( n = 6). Data are presented as mean ± SEM. Statistical analysis was performed using two-way ANOVA for growth curves and the Kaplan-Meier method for survival analysis ( p < 0.05, ∗ p < 0.01). Experiments were performed in duplicate or triplicate.

Journal: Molecular Therapy. Nucleic Acids

Article Title: Nitric oxide-dependent stabilization of vimentin confers chemoresistance in ovarian cancer

doi: 10.1016/j.omtn.2026.102924

Figure Lengend Snippet: L-NMMA promotes vimentin destabilization by enhancing its ubiquitination (A) CHX chase assay showing vimentin protein levels in OVCAR8 cells treated with 10 mM L-NMMA at different time points. (B) Vimentin ubiquitination was assessed in OVCAR8 cells treated with L-NMMA for 24 h, in the presence of the proteasome inhibitor MG-132 (10 μM) for the final 4 h, followed by immunoprecipitation and western blot using an anti-ubiquitin antibody. (C) Measurement of vimentin S-nitrosylation levels was performed by immunoprecipitation in OVCAR8 cells. (D) Western blot analysis of vimentin expression in OVCAR8 cells treated with 10 mM L-NMMA alone or in combination with MG132 at 1, 5, or 10 μM. (E) Tumor growth and proliferation were monitored in mice bearing parental and NOS2 KO OVCAR8 tumors, evaluated by ROI measurements every 4 days ( n = 6). (F) Kaplan-Meier survival curves of mice bearing parental and NOS2 KO OVCAR8 tumors following cisplatin treatment ( n = 6). Data are presented as mean ± SEM. Statistical analysis was performed using two-way ANOVA for growth curves and the Kaplan-Meier method for survival analysis ( p < 0.05, ∗ p < 0.01). Experiments were performed in duplicate or triplicate.

Article Snippet: The following primers for TaqMan Gene Expression Assay were purchased from Thermo Fisher Scientific; human VIM (Cat. #Hs00958111_m1) and human NOS2 (Cat. #Hs01075529_m1).

Techniques: Ubiquitin Proteomics, Immunoprecipitation, Western Blot, Expressing

Journal: Non-coding RNA Research

Article Title: CircSMAD4 shapes matrix-remodeling TAMs in lung adenocarcinoma

doi: 10.1016/j.ncrna.2026.03.003

Figure Lengend Snippet: circSMAD4 drives tumor-educated M2-like polarization of macrophages and promotes tumor-cell aggressiveness. (A) Workflow for generating TC-hMDMs and TC-BMDMs, circSMAD4 knockdown, and downstream functional assays. (B) RT–qPCR analysis of M1-associated markers (MHC-II [HLA-DRA in TC-hMDMs; H2-Ab1 in TC-BMDMs], NOS2, and CD86) and M2-associated markers (CD163, CD206, and ARG1) in TC-hMDMs and TC-BMDMs. (C) Representative flow-cytometry histograms for HLA-DR, iNOS, CD86, CD163, CD206, and ARG1 in TC-hMDMs. Gating strategy and marker thresholds were defined based on FMO controls (see ). (D) Flow-cytometry quantification of marker-positive cells in TC-hMDMs and TC-BMDMs. (E) ELISA of IL-10, TGF-β, and iNOS in culture supernatants. (F) CCK-8 assays of A549 and LLC cells. (G) Colony-formation assays of A549 and LLC cells with quantification. (H) Bioluminescence-based growth readouts of patient-derived LUAD organoids (PDO #1 and PDO #2) after co-culture with TC-hMDMs. (I) Immunoblot analysis of EMT-related proteins (E-cadherin, N-cadherin, Vimentin) in A549 and LLC cells. (J) Transwell migration and invasion assays of A549 and LLC cells with quantification. Scale bar, 50 μm. ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001; ∗∗∗∗P < 0.0001; ns, not significant.

Article Snippet: Sections were incubated with primary antibodies against Ki-67 (Servicebio, Cat# GB111499 ), E-cadherin (Proteintech, Cat# 20874-1-AP), and Vimentin (Proteintech, Cat# 10366-1-AP).

Techniques: Knockdown, Functional Assay, Quantitative RT-PCR, Flow Cytometry, Marker, Enzyme-linked Immunosorbent Assay, CCK-8 Assay, Derivative Assay, Co-Culture Assay, Western Blot, Migration

Journal: Non-coding RNA Research

Article Title: CircSMAD4 shapes matrix-remodeling TAMs in lung adenocarcinoma

doi: 10.1016/j.ncrna.2026.03.003

Figure Lengend Snippet: circSMAD4 depletion in macrophages restrains LUAD growth and metastasis in vivo. (A) Schematic of orthotopic lung implantation and experimental metastasis models using LLC cells mixed with BMDMs expressing shNC or sh-circSMAD4. (B) Representative images of orthotopic lung tumors. (C) Tumor weight of orthotopic implants. (D) Overall survival of mice bearing orthotopic tumors. (E) Immunofluorescence showing F4/80 and circSMAD4 signals in tumor tissues. Scale bar, 50 μm. (F, G) Representative Ki-67 IHC staining and quantification in orthotopic tumors. Scale bar, 50 μm. (H) Representative bioluminescence images of lung tumor burden in the metastasis model. (I) Tumor weight in the metastasis model. (J) Overall survival of mice in the metastasis model. (K–M) Representative IHC staining and quantification of E-cadherin and vimentin in tumors. Scale bar, 50 μm. ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001; ∗∗∗∗P < 0.0001; ns, not significant.

Techniques: In Vivo, Expressing, Immunofluorescence, Immunohistochemistry

MSC-mt alleviates oxidative stress and promote tissue regeneration during wound healing (A) In vivo imaging showing the spatial–temporal persistence of fluorescently labeled MSC-mt (mtH) at the wound site at indicated time point, indicating transient but sustained early presence after topical application. (B) Measurement of ATP levels in peri-wound tissues on PWD8 showed enhanced local metabolic activity following mtH treatment. n = 5 ∼ 6 per group. (C) Quantification of malondialdehyde (MDA) levels in peri-wound tissues on PWD8 indicated reduced lipid peroxidation and oxidative stress in both MSC-mt–treated wounds. n = 5 ∼ 6 per group. (D) Laser speckle contrast imaging of blood perfusion at the wound site on PWD8 showed improved microvascular perfusion following mtH treatment. n = 5 per group. (E) Representative immunofluorescence images and quantification of CD31 expression in peri-wound tissues on PWD8, indicating enhanced angiogenesis in mtH–treated wounds. n = 6 per group. (F) Quantitative PCR analysis of angiogenesis-related gene expression in peri-wound tissues on PWD8, indicating transcriptional activation of pro-angiogenic programs following mtH treatment. n = 3 ∼ 5 per group. (G-H) Representative immunohistochemical staining and quantification of Col1a1 in wound tissues on PWD8, showing increased collagen synthesis and matrix remodeling in mtH–treated wounds. n = 6 per group. Scale bar = 100 μm. (I-J) Representative immunofluorescence staining and quantification of Vimentin and TUNEL in wound tissues on PWD8, indicating reduced fibroblast apoptosis following mtH treatment. n = 6 per group. Scale bar = 20 μm. (K-L) Representative immunofluorescence staining and quantification of Vimentin and 8-hydroxyguanosine (8-OHG) in wound tissues on PWD8, indicating attenuated oxidative DNA damage in fibroblasts following mtH treatment. n = 6 per group. Scale bar = 20 μm. Data are presented as mean ± SEM. ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001; ns, not significant.

Journal: Materials Today Bio

Article Title: Extracellular biogenic nanoscale mitochondria reprogram the wound microenvironment via ROS scavenging independent of cellular uptake

doi: 10.1016/j.mtbio.2026.103023

Figure Lengend Snippet: MSC-mt alleviates oxidative stress and promote tissue regeneration during wound healing (A) In vivo imaging showing the spatial–temporal persistence of fluorescently labeled MSC-mt (mtH) at the wound site at indicated time point, indicating transient but sustained early presence after topical application. (B) Measurement of ATP levels in peri-wound tissues on PWD8 showed enhanced local metabolic activity following mtH treatment. n = 5 ∼ 6 per group. (C) Quantification of malondialdehyde (MDA) levels in peri-wound tissues on PWD8 indicated reduced lipid peroxidation and oxidative stress in both MSC-mt–treated wounds. n = 5 ∼ 6 per group. (D) Laser speckle contrast imaging of blood perfusion at the wound site on PWD8 showed improved microvascular perfusion following mtH treatment. n = 5 per group. (E) Representative immunofluorescence images and quantification of CD31 expression in peri-wound tissues on PWD8, indicating enhanced angiogenesis in mtH–treated wounds. n = 6 per group. (F) Quantitative PCR analysis of angiogenesis-related gene expression in peri-wound tissues on PWD8, indicating transcriptional activation of pro-angiogenic programs following mtH treatment. n = 3 ∼ 5 per group. (G-H) Representative immunohistochemical staining and quantification of Col1a1 in wound tissues on PWD8, showing increased collagen synthesis and matrix remodeling in mtH–treated wounds. n = 6 per group. Scale bar = 100 μm. (I-J) Representative immunofluorescence staining and quantification of Vimentin and TUNEL in wound tissues on PWD8, indicating reduced fibroblast apoptosis following mtH treatment. n = 6 per group. Scale bar = 20 μm. (K-L) Representative immunofluorescence staining and quantification of Vimentin and 8-hydroxyguanosine (8-OHG) in wound tissues on PWD8, indicating attenuated oxidative DNA damage in fibroblasts following mtH treatment. n = 6 per group. Scale bar = 20 μm. Data are presented as mean ± SEM. ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001; ns, not significant.

Article Snippet: Sections were incubated overnight at 4 °C with primary antibodies against CD31 (Servicebio, Cat# GB120005 , 1:200), Vimentin (CST, Cat# 5741, 1:200), and 8-hydroxyguanosine (8-OHG, Rockland, Cat# 200-301-A99, 1:200).

Techniques: In Vivo Imaging, Labeling, Activity Assay, Imaging, Immunofluorescence, Expressing, Real-time Polymerase Chain Reaction, Gene Expression, Activation Assay, Immunohistochemical staining, Staining, TUNEL Assay

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vimentin (Proteintech)

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1) Product Images from "CircSMAD4 shapes matrix-remodeling TAMs in lung adenocarcinoma"

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