ArticleThe American journal of pathology2001
High glucose-induced hypertrophy of mesangial cells requires p27(Kip1), an inhibitor of cyclin-dependent kinases.
Article in The American journal of pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 113 citations in OpenAlex.
- Article
- Immunomodulation effects of collagen hydrogel encapsulating extracellular vesicles derived from calcium silicate stimulated-adipose mesenchymal stem cells for diabetic healing.Journal of nanobiotechnology · 2025Article
- Diabetic condition induces hypertrophy and vacuolization in glomerular parietal epithelial cells.Scientific reports · 2021Article
- Depletion of cyclic-GMP levels and inhibition of cGMP-dependent protein kinase activate p21FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Flaming the fight against cancer cells: the role of microRNA-93.Cancer cell international · 2020Review
- Review
- LincRNA-p21 sponges miR-18b to promote the progression of diabetic nephropathy.American journal of translational research · 2018Article
- The cellular selection between apoptosis and autophagy: roles of vitamin D, glucose and immune response in diabetic nephropathy.Endocrine · 2017Article
- Cinaciguat ameliorates glomerular damage by reducing ERK1/2 activity and TGF-ß expression in type-1 diabetic rats.Scientific reports · 2017Article
- Effects of Dangguibuxue decoction on rat glomerular mesangial cells cultured under high glucose conditions.BMC complementary and alternative medicine · 2017Article
- Article
- Cellular senescence in renal ageing and disease.Nature reviews. Nephrology · 2017Review
- New Altered Non-Fibrillar Collagens in Human Dilated Cardiomyopathy: Role in the Remodeling Process.PloS one · 2016Article
- TGF-beta induced RBL2 expression in renal cancer cells by down-regulating miR-93.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2014Article
- The influence of high glucose on the Cip/Kip family expression profiles in HRECs.Journal of molecular histology · 2013Article
- Retinoic acid improves morphology of cultured peritoneal mesothelial cells from patients undergoing dialysis.PloS one · 2013Article
- Article
- Epac1-mediated, high glucose-induced renal proximal tubular cells hypertrophy via the Akt/p21 pathway.The American journal of pathology · 2011Article
- Pathophysiology of the diabetic kidney.Comprehensive Physiology · 2011Review
- Type VIII collagen modulates TGF-β1-induced proliferation of mesangial cells.Journal of the American Society of Nephrology : JASN · 2011Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Hypertrophy of mesangial cells is one of the earliest morphological alterations in the kidney after the onset of diabetes mellitus. We have previously shown that cultured mesangial cells exposed to high ambient glucose arrest in the G1 phase of the cell cycle and that this is associated with an increased expression of inhibitors of the cyclin-dependent kinase (CDK)-inhibitors p21(Cip) and p27(Kip1). To further investigate a potential role of p27Kip1 in the development of glucose-induced hypertrophy, mesangial cells from p27Kip1 wild-type (+/+) and knockout (-/-) mice were established. High glucose medium (450 mg/dl) increased p21(Cip1) protein in p27Kip1+/+ and -/- mesangial cells, and increased p27Kip1 protein levels in p27Kip1+/+ cells. In contrast to high glucose increasing de novo protein synthesis in p27Kip1+/+ cells, high glucose did not increase protein synthesis in p27Kip1-/- cells. High glucose also reduced DNA synthesis and caused cell cycle arrest in p27Kip1+/+ cells. In contrast, despite an increase in transforming growth factor (TGF)-beta mRNA and protein expression, DNA synthesis and cell cycle progression were increased by high glucose in p27Kip1-/- cells. Exogenous TGF-beta comparably induced fibronectin mRNA in p27Kip1+/+ and -/- cells suggesting intact TGF-beta receptor transduction. In addition, high glucose failed to increase the total protein/cell number ratio in p27Kip1-/- cells. However, in the presence of high glucose, reconstituting p27Kip1 expression by transient or stable transfection in p27Kip1-/- cells, using an inducible expression system, increased the de novo protein synthesis and restored G1-phase arrest. These results show that p27Kip1 is required for glucose-induced mesangial cell hypertrophy and cell cycle arrest.
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