ArticleThe Journal of biological chemistry2010
Loss of beta1-integrin enhances TGF-beta1-induced collagen expression in epithelial cells via increased alphavbeta3-integrin and Rac1 activity.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Plerixafor Engages β-Arrestin-Dependent CXCR4 Signaling to Promote Melanogenesis via β-Catenin-MITF Activation.Current issues in molecular biology · 2026Article
- Applying dendrimer nanoprobes to the diagnosis and evaluation of kidney fibrosis.Nanomedicine (London, England) · 2026Review
- Aberrant localization of β1 integrin in podocyte cytoplasm of primary FSGS with cellular lesion.Virchows Archiv : an international journal of pathology · 2025Article
- Decellularized Disc Hydrogels for hBMSCs tissue-specific differentiation and tissue regeneration.Bioactive materials · 2021Article
- Targeting transforming growth factor-β signaling for enhanced cancer chemotherapy.Theranostics · 2021Review
- The effect of bone marrow mesenchymal stem cells on highly metastatic MHCC97-H hepatocellular carcinoma cells following OPN and TGFβ1 gene silencing.Experimental and therapeutic medicine · 2020Article
- Integrin Crosstalk Contributes to the Complexity of Signalling and Unpredictable Cancer Cell Fates.Cancers · 2020Review
- Effect of integrin β1 in the treatment of stress urinary incontinence by electrical stimulation.Molecular medicine reports · 2019Article
- HACE1 is a potential tumor suppressor in osteosarcoma.Cell death & disease · 2019Article
- Deletion of β1-integrin in collecting duct principal cells leads to tubular injury and renal medullary fibrosis.American journal of physiology. Renal physiology · 2017Article
- Fibrillar Type I Collagen Enhances the Differentiation and Proliferation of Myofibroblasts by LoweringBioMed research international · 2017Article
- Podocyte injury-driven intracapillary plasminogen activator inhibitor type 1 accelerates podocyte loss via uPAR-mediated β1-integrin endocytosis.American journal of physiology. Renal physiology · 2015Article
- Integrin-mediated type II TGF-β receptor tyrosine dephosphorylation controls SMAD-dependent profibrotic signaling.The Journal of clinical investigation · 2014Article
- Expression and activity of Rac1 is negatively affected in the dehydroepiandrosterone induced polycystic ovary of mouse.Journal of ovarian research · 2014Article
- Serine-204 in the linker region of Smad3 mediates the collagen-I response to TGF-β in a cell phenotype-specific manner.Experimental cell research · 2013Article
- Cell-matrix adhesion of podocytes in physiology and disease.Nature reviews. Nephrology · 2013Review
- Divergent roles of Smad3 and PI3-kinase in murine adriamycin nephropathy indicate distinct mechanisms of proteinuria and fibrogenesis.Kidney international · 2012Article
- Beta 1 integrin predicts survival in breast cancer: a clinicopathological and immunohistochemical study.Diagnostic pathology · 2012Article
- Matrix-dependent perturbation of TGFβ signaling and disease.FEBS letters · 2012Review
- Serial non-invasive monitoring of renal disease following immune-mediated injury using near-infrared optical imaging.PloS one · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Transforming growth factor β (TGF-β) promotes tissue fibrosis via the receptor-specific Smad pathway and non-canonical pathways. We recently reported that TGF-β1-stimulated collagen expression by cultured kidney cells requires integrin-dependent activation of focal adhesion kinase (FAK) and consequent ERK MAP kinase activity leading to Smad3 linker region phosphorylation. Here, we defined a role for αvβ3-integrin in this non-canonical pathway. A human kidney tubular cell line in which β1-integrin was knocked down (β1-k/d) demonstrated enhanced type I collagen mRNA expression and promoter activity. A second shRNA to either αv-integrin or β3-integrin, but not to another αv-binding partner, β6-integrin, abrogated the enhanced COL1A2 promoter activity in β1-k/d cells. Although αvβ3-integrin surface expression levels were not different, αvβ3-integrins colocalized with sites of focal adhesion significantly more in β1-k/d cells, and activated αvβ3-integrin was detected only in β1-k/d cells. Further, the collagen response was decreased by a function-blocking antibody or a peptide inhibitor of αvβ3-integrin. In cells lacking αvβ3-integrin, the responses were attenuated, whereas the response was enhanced in αvβ3-overexpressing cells. Rac1 and ERK, previously defined mediators for this non-canonical pathway, showed increased activities in β1-k/d cells. Finally, inhibition of αvβ3-integrin decreased Rac1 activity and COL1A2 promoter activity in β1-k/d cells. Together, our results indicate that decreasing β1 chain causes αvβ3-integrin to become functionally dominant and promotes renal cell fibrogenesis via Rac1-mediated ERK activity.
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