ArticleAmerican journal of physiology. Renal physiology2009
C-peptide reverses TGF-beta1-induced changes in renal proximal tubular cells: implications for treatment of diabetic nephropathy.
Article in American journal of physiology. Renal physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 71 citations in OpenAlex.
- An Updated Review on Diabetic Nephropathy: Potential Mechanisms, Biomarkers, Therapeutic Targets and Interventional Therapies.Current diabetes reviews · 2025Review
- Renoprotective Effect of Liraglutide Is Mediated via the Inhibition of TGF-Beta 1 in an LLC-PK1 Cell Model of Diabetic Nephropathy.Current issues in molecular biology · 2022Article
- Streptozotocin-Induced Diabetes in a Mouse Model (BALB/c) Is Not an Effective Model for Research on Transplantation Procedures in the Treatment of Type 1 Diabetes.Biomedicines · 2021Article
- Duck enteritis virus infection suppresses viability and induces apoptosis and endoplasmic reticulum stress in duck embryo fibroblast cells via the regulation of CaThe Journal of veterinary medical science · 2021Article
- C-peptide corrects hepatocellular dysfunction in a rat model of type 1 diabetes.Journal of physiology and biochemistry · 2020Article
- Renal Benefits of SGLT 2 Inhibitors and GLP-1 Receptor Agonists: Evidence Supporting a Paradigm Shift in the Medical Management of Type 2 Diabetes.International journal of molecular sciences · 2019Review
- Molecular mechanisms involved in podocyte EMT and concomitant diabetic kidney diseases: an update.Renal failure · 2017Review
- Identification of urinary exosomal noncoding RNAs as novel biomarkers in chronic kidney disease.RNA (New York, N.Y.) · 2017Article
- Role of Epigenetic Histone Modifications in Diabetic Kidney Disease Involving Renal Fibrosis.Journal of diabetes research · 2017Review
- Anthocyanins inhibit high-glucose-induced cholesterol accumulation and inflammation by activating LXRα pathway in HK-2 cells.Drug design, development and therapy · 2015Article
- Sphingosine-1-phosphate induces differentiation of cultured renal tubular epithelial cells under Rho kinase activation via the S1P2 receptor.Clinical and experimental nephrology · 2014Article
- Physiological effects and therapeutic potential of proinsulin C-peptide.American journal of physiology. Endocrinology and metabolism · 2014Review
- L1 cell adhesion molecule expression is associated with pelvic lymph node metastasis and advanced stage in diabetic patients with endometrial cancer: a matched case control study.Journal of cancer prevention · 2014Article
- Effects of Chinese Medicine Tong xinluo on Diabetic Nephropathy via Inhibiting TGF- β 1-Induced Epithelial-to-Mesenchymal Transition.Evidence-based complementary and alternative medicine : eCAM · 2014Article
- Hypoxia-inducible factor prolyl-hydroxylase-2 mediates transforming growth factor beta 1-induced epithelial-mesenchymal transition in renal tubular cells.Biochimica et biophysica acta · 2013Article
- Correlation of high urinary Smad1 level with glomerular hyperfiltration in type 2 diabetes mellitus.Endocrine · 2013Article
- Article
- Renoprotective effects of C-peptide in the Dahl salt-sensitive rat.American journal of physiology. Renal physiology · 2012Article
- Review
- TGFβ modulates cell-to-cell communication in early epithelial-to-mesenchymal transition.Diabetologia · 2012Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The crucial pathology underlying progressive chronic kidney disease in diabetes is tubulointerstitial fibrosis. Central to this process is epithelial-mesenchymal transformation (EMT) of proximal tubular epithelial cells driven by maladaptive transforming growth factor-beta1 (TGF-beta1) signaling. Novel signaling roles for C-peptide have recently been discovered with evidence emerging that C-peptide may mitigate microvascular complications of diabetes. We studied the potential for C-peptide to interrupt injurious TGF-beta1 signaling pathways and thus block development of EMT in HK2 human kidney proximal tubular cells. Cells were incubated with TGF-beta1 either alone or with C-peptide in low or high glucose. Changes in cell morphology, TGF-beta1 receptor expression, vimentin, E-cadherin, and phosphorylated Smads were assessed. Luciferase reporters were used to assess Smad activity. The cytoskeleton was visualized by TRITC-phalloidin staining. The typical TGF-beta1-stimulated, EMT-associated morphological alterations of proximal tubular cells, including increased vimentin expression, decreased E-cadherin expression, and cytoskeletal rearrangements, were prevented by C-peptide treatment. C-peptide also blocked TGF-beta1-induced upregulation of expression of both type I and type II TGF-beta1 receptors and attenuated TGF-beta1-mediated Smad phosphorylation and Smad transcriptional activity. These effects of C-peptide were inhibited by pertussis toxin. The results demonstrate that C-peptide almost completely reversed the morphological changes in PT cells induced by TGF-beta1 and suggest a role or C-peptide as a renoprotective agent in diabetic nephropathy.
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