ab81887 rabbit polyclonal anti col1 proteintech  (Proteintech)

Journal: iScience

Article Title: Targeting endometrial inflammation in intrauterine adhesion ameliorates endometrial fibrosis by priming MSCs to secrete C1INH

doi: 10.1016/j.isci.2023.107201

Figure Lengend Snippet:

Article Snippet: Rabbit polyclonal anti-Col1 , Proteintech , Cat# 14695-1-AP; RRID: AB_2082037.

Techniques: Staining, Recombinant, Cell Counting, Enzyme-linked Immunosorbent Assay, Western Blot, Software

Journal: Stem Cell Research & Therapy

Article Title: C/EBPα regulates the fate of bone marrow mesenchymal stem cells and steroid-induced avascular necrosis of the femoral head by targeting the PPARγ signalling pathway

doi: 10.1186/s13287-022-03027-3

Figure Lengend Snippet: Establishment and evaluation of SANFH rat models. a Scheme of animal treatments. b The coronal (COR), transverse (TRA) and sagittal (SAG) sections of the femoral head were reconstructed by the micro-CT images in the control and model groups. c Quantitative analysis of related parameters of micro-CT. d H&E staining of the femoral head after decalcification, with black arrows indicating trabecular bone, red arrows indicating fat vacuoles, and yellow arrows indicating empty bone lacunae. e, f IHC staining of COL1 in the femoral head and quantitative analysis showed the IOD in the control and model groups. g The expression levels of femoral head-related proteins in the control and model groups were detected by western blotting, and β-actin was used for normalization and quantitative analysis by ImageJ. *** P < 0.001, ** P < 0.01, * P < 0.05

Article Snippet: The remaining femoral head sections were dewaxed, antigen recovered, incubated with the primary antibody (rabbit polyclonal anti-type 1 collagen (COL1) and anti-PPARγ, Proteintech Group, Inc.), and then incubated with the appropriate horseradish peroxide-coupled secondary antibody.

Techniques: Micro-CT, Control, Staining, Immunohistochemistry, Expressing, Western Blot

Journal: Molecular Medicine Reports

Article Title: Interleukin-10 promotes proliferation and migration, and inhibits tendon differentiation via the JAK/Stat3 pathway in tendon-derived stem cells in vitro

doi: 10.3892/mmr.2018.9547

Figure Lengend Snippet: Primers used for reverse transcription-quantitative polymerase chain reaction.

Article Snippet: Cells were then incubated overnight at 4°C with primary rabbit anti-Col1 antibodies (1:100; cat. no. 14695-1-AP; ProteinTech Group, Inc., Chicago, IL, USA) and subsequently incubated with tetramethylrhodamine-tagged goat anti-rabbit IgG secondary antibodies (1:100; cat. no. HA1016; Hangzhou HuaAn Biotechnology Co., Ltd., Hangzhou, China) for 2 h at room temperature.

Techniques:

Journal: Molecular Medicine Reports

Article Title: Interleukin-10 promotes proliferation and migration, and inhibits tendon differentiation via the JAK/Stat3 pathway in tendon-derived stem cells in vitro

doi: 10.3892/mmr.2018.9547

Figure Lengend Snippet: IL-10 inhibits spontaneous tenogenic differentiation. Tendon-derived stem cells were treated with the indicated concentrations of IL-10 for 3 days and subjected to quantitative polymerase chain reaction to detect the gene expression of (A) Scx and (B) Col1. (C) Representative images of the morphological alterations in control and IL-10-treated TDSCs (magnification, ×100). Data are expressed as the mean ± standard error of the mean. *P<0.05, **P<0.01 vs. control cells. IL-10, interleukin-10; Col1, collagen type 1; Scx, scleraxis.

Article Snippet: Cells were then incubated overnight at 4°C with primary rabbit anti-Col1 antibodies (1:100; cat. no. 14695-1-AP; ProteinTech Group, Inc., Chicago, IL, USA) and subsequently incubated with tetramethylrhodamine-tagged goat anti-rabbit IgG secondary antibodies (1:100; cat. no. HA1016; Hangzhou HuaAn Biotechnology Co., Ltd., Hangzhou, China) for 2 h at room temperature.

Techniques: Derivative Assay, Real-time Polymerase Chain Reaction, Gene Expression, Control

Journal: Molecular Medicine Reports

Article Title: Interleukin-10 promotes proliferation and migration, and inhibits tendon differentiation via the JAK/Stat3 pathway in tendon-derived stem cells in vitro

doi: 10.3892/mmr.2018.9547

Figure Lengend Snippet: IL-10 alters the mRNA and protein expression levels tendon-associated molecules in TDSCs. (A) The mRNA expression Tnmd, Col3, Mkx, Egr1, Fmod and Lum was altered by IL-10 treatment. (B) Fluorescent staining of Col1 expression following treatment with IL-10 for 3 days. (C) Rat TDSCs were treated with the indicated concentrations of IL-10 for 3 days and subjected to western blot analysis for Scx, Col1, Tnmd and Col3 protein expression. (D) Densitometric analysis of the western blotting results. Data are expressed as the mean ± standard error of the mean. *P<0.05, **P<0.01 vs. control cells. IL-10, interleukin-10; TDSCs, tendon-derived stem cells; Tnmd, tenomodulin; Col3, collagen type 3; Mkx, mohawk; Egr1, early growth response gene 1; Fmod, fibromodulin; Lum, lumican; Dcn, decorin; Bgn, biglycan.

Article Snippet: Cells were then incubated overnight at 4°C with primary rabbit anti-Col1 antibodies (1:100; cat. no. 14695-1-AP; ProteinTech Group, Inc., Chicago, IL, USA) and subsequently incubated with tetramethylrhodamine-tagged goat anti-rabbit IgG secondary antibodies (1:100; cat. no. HA1016; Hangzhou HuaAn Biotechnology Co., Ltd., Hangzhou, China) for 2 h at room temperature.

Techniques: Expressing, Staining, Western Blot, Control, Derivative Assay

Journal: Molecular Medicine Reports

Article Title: Interleukin-10 promotes proliferation and migration, and inhibits tendon differentiation via the JAK/Stat3 pathway in tendon-derived stem cells in vitro

doi: 10.3892/mmr.2018.9547

Figure Lengend Snippet: IL-10 activates Stat3 but has no effect on Akt expression in TDSCs. (A) Rat TDSCs were treated with the indicated concentrations of IL-10 and were subjected to western blot analysis to detect p-Stat3, Stat3, p-Akt and Akt protein expression. (B) TDSCs were treated with the indicated concentrations of IL-10 with or without the Stat3 inhibitor WP1066 and subjected to western blot analysis for Col1, Tnmd and Col3 protein expression. Data are expressed as the mean ± standard error of the mean. *P<0.05, **P<0.01 vs. 10 ng/ml IL-10. IL-10, interleukin-10; TDSCs, tendon-derived stem cells; p-, phosphorylated; Stat3, Signal transducer and activator of transcription 3; Akt, protein kinase B; Tnmd, tenomodulin; Col3, collagen type 3.

Article Snippet: Cells were then incubated overnight at 4°C with primary rabbit anti-Col1 antibodies (1:100; cat. no. 14695-1-AP; ProteinTech Group, Inc., Chicago, IL, USA) and subsequently incubated with tetramethylrhodamine-tagged goat anti-rabbit IgG secondary antibodies (1:100; cat. no. HA1016; Hangzhou HuaAn Biotechnology Co., Ltd., Hangzhou, China) for 2 h at room temperature.

Techniques: Expressing, Western Blot, Derivative Assay

Journal: PLoS ONE

Article Title: CXCL12/CXCR4 Axis Activation Mediates Prostate Myofibroblast Phenoconversion through Non-Canonical EGFR/MEK/ERK Signaling

doi: 10.1371/journal.pone.0159490

Figure Lengend Snippet: ( A ) N1 fibroblasts were treated with vehicle (DMSO) or EGFR inhibitor (AG1478, 500 nM) prior to CXCL12 treatment. Phosphorylation of EGFR, Akt, Smad and ERK1/2 were assessed via western blot. ( B ) qRT-PCR analysis of myofibroblast marker expression after CXCL12 (100pM) treatment in the presence or absence of AG1478 (500 nM). Expression levels of α-smooth muscle actin (ACTA2) and collagen 1α1 (COL1α1) were analyzed over the course of 24 hours of treatment. Treatment with AG1478 reduced or ablated the CXCL12/CXCR4 -mediated stimulation of both the ACTA2 and COL1α1 genes. ( C ) Western blot analysis of fibroblast markers, α-smooth muscle actin and collagen 1, at 24 and 48 hours after CXCL12 treatment. Secretion and incorporation of collagen 1 was inhibited in the presence of AG1478, α-smooth muscle actin production was inhibited as well. ( D ) Signal intensity quantification for 7 and collagen 1 western blots. * = p-value < 0.05. Error bars, SE.

Article Snippet: Primary antibodies were diluted in blocking solution and included 1:200 dilution FITC-conjugated mouse monoclonal anti-α-smooth muscle actin (α SMA), and 1:100 dilution biotin-conjugated rabbit polyclonal anti-collagen type 1 (COL1) (Rockland Immunochemicals, Gilbertsville, PA).

Techniques: Phospho-proteomics, Western Blot, Quantitative RT-PCR, Marker, Expressing

Journal: PLoS ONE

Article Title: CXCL12/CXCR4 Axis Activation Mediates Prostate Myofibroblast Phenoconversion through Non-Canonical EGFR/MEK/ERK Signaling

doi: 10.1371/journal.pone.0159490

Figure Lengend Snippet: ( A ) Immunofluorescence analysis of N1 fibroblasts left untreated (-CXCL12) or treated with 100pM CXCL12 (CXCL12) for 48 hours in the absence or presence of CXCR4 (250 μM AMD3100), EGFR (250 uM AG1478), ALK-5 (TGFβRII) (20μM A-83-01) small molecular inhibitors or an antibody against TGFβRII (200 ng/ml TGFβ MAb). Figure depicts photomicrographs images of cells stained for α-smooth muscle actin (green) or collagen 1 (red) proteins or DAPI (blue nuclear stain); orange color indicates α-smooth muscle actin and collagen 1 colocalization in the merged image. ( B ) Western blot analysis of fibroblast markers, α-smooth muscle actin and collagen 1 at 24, 48 and 72 hours after CXCL12 (100pM) of scramble, anti-CXCR4, and anti-TGFβRI siRNAs transfected fibroblasts. CXCL12-driven expression of myofibroblasts markers does not require the presence or activation of TGFβRI. ( C ) Quantification of western blot images for myofibroblast markers.

Article Snippet: Primary antibodies were diluted in blocking solution and included 1:200 dilution FITC-conjugated mouse monoclonal anti-α-smooth muscle actin (α SMA), and 1:100 dilution biotin-conjugated rabbit polyclonal anti-collagen type 1 (COL1) (Rockland Immunochemicals, Gilbertsville, PA).

Techniques: Immunofluorescence, Staining, Western Blot, Transfection, Expressing, Activation Assay

Journal: PLoS ONE

Article Title: Resveratrol-Mediated Repression and Reversion of Prostatic Myofibroblast Phenoconversion

doi: 10.1371/journal.pone.0158357

Figure Lengend Snippet: N1 immortalized or primary prostate fibroblasts were seeded, switched to SF media, then treated as indicated below. After fixation, cells were incubated against antibodies to detect COL1 (PE-cy5-conjugated Ab, red) or α SMA (fluorescein-conjugated Ab, green), then counterstained with DAPI to image nuclei using immunofluorescence. The images were then merged, and co-expression of COL1 and α SMA proteins became evident as orange immunofluorescence. Untreated N1 or primary cells express very low basal levels of COL1 or α SMA, whereas cells treated with either CXCL12 or TGF β co-express high levels of both proteins. Cells treated with either CXCL12 ( A ) or TGF β ( B ) for 24 hr then supplemented (post-treated) with 50 μM Resveratrol for an additional 24 hr demonstrate very little co-expression of COL1 and α SMA, though higher levels are observed for TGF β -treated cells. Lastly, cells pre-treated with 50 μM Resveratrol for 2 hr followed by supplementation with either CXCL12 ( A ) or TGF β ( B ) for 48 hr demonstrate dramatically reduced levels of COL1 and α SMA compared to non-Resveratrol treated cells.

Article Snippet: Cells were plated on chamber slides coated with 10 μg/ml fibronectin (Sigma-Aldrich, St. Louis, MO), then treated as above and subjected to immunofluorescence as previously described using FITC-conjugated mouse monoclonal anti-α-smooth muscle actin ( α SMA) (Sigma-Aldrich, St. Louis, MO), and biotin conjugated rabbit polyclonal anti-collagen type 1 (COL1) (Rockland Immunochemicals, Gilbertsville, PA), PE-Cy 5 streptavidin (BD Pharmingen San Diego, CA) secondary antibodies, and control mouse IgG2a (Sigma-Aldrich, St. Louis, MO), and rabbit IgG biotin conjugate (Rockland Immunochemicals, Gilbertsville, PA) [ ].

Techniques: Incubation, Immunofluorescence, Expressing

Journal: PLoS ONE

Article Title: Resveratrol-Mediated Repression and Reversion of Prostatic Myofibroblast Phenoconversion

doi: 10.1371/journal.pone.0158357

Figure Lengend Snippet: Primary lung fibroblasts from a patient with clinically significant idiopathic pulmonary fibrosis (IPF) were grown ex vivo. After fixation, cells were incubated against antibodies to detect COL1 (PE-cy5-conjugated Ab, red) or α SMA (fluorescein-conjugated Ab, green), then counterstained with DAPI to image nuclei. The images were then merged, and co-expression of COL1 and α SMA proteins became evident as orange immunofluorescence. Untreated IPF fibroblasts express very low levels of COL1 or α SMA, whereas cells treated with either CXCL12 ( A ) or TGF β ( B ) co-express high levels of both proteins. Cells treated with either CXCL12 ( A ) or TGF β ( B ) for 24hr then supplemented (post-treated) with 50 μM Resveratrol for an additional 24 hr express reduced but clearly detectable levels of COL1 and α SMA. Cells pre-treated with 50 μM Resveratrol for 2 hr followed by supplementation with either CXCL12 or TGF β for 48 hr also demonstrate reduced but clearly detectable levels of COL1 and α SMA. Finally, cells pre- or post-treated with 100 μM Resveratrol and TGF β ( C ) demonstrate nearly ablated levels of COL1 and α SMA proteins.

Article Snippet: Cells were plated on chamber slides coated with 10 μg/ml fibronectin (Sigma-Aldrich, St. Louis, MO), then treated as above and subjected to immunofluorescence as previously described using FITC-conjugated mouse monoclonal anti-α-smooth muscle actin ( α SMA) (Sigma-Aldrich, St. Louis, MO), and biotin conjugated rabbit polyclonal anti-collagen type 1 (COL1) (Rockland Immunochemicals, Gilbertsville, PA), PE-Cy 5 streptavidin (BD Pharmingen San Diego, CA) secondary antibodies, and control mouse IgG2a (Sigma-Aldrich, St. Louis, MO), and rabbit IgG biotin conjugate (Rockland Immunochemicals, Gilbertsville, PA) [ ].

Techniques: Ex Vivo, Incubation, Expressing, Immunofluorescence