ArticleGrowth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society2005
Insulin-like growth factor binding protein-3 mediates cytokine-induced mesangial cell apoptosis.
Article in Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 39 citations in OpenAlex.
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- ROS- and HIF1α-dependent IGFBP3 upregulation blocks IGF1 survival signaling and thereby mediates high-glucose-induced cardiomyocyte apoptosis.Journal of cellular physiology · 2019Article
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- Cornea and ocular surface disease: application of cutting-edge optometric research.Optometry and vision science : official publication of the American Academy of Optometry · 2014Review
- IGFBP-3 and TNF-α regulate retinal endothelial cell apoptosis.Investigative ophthalmology & visual science · 2013Article
- Compound 49b prevents diabetes-induced apoptosis through increased IGFBP-3 levels.Investigative ophthalmology & visual science · 2012Article
- Elevated IGFBP3 levels in diabetic tears: a negative regulator of IGF-1 signaling in the corneal epithelium.The ocular surface · 2012Article
- The insulin-like growth factor system in chronic kidney disease: Pathophysiology and therapeutic opportunities.Kidney research and clinical practice · 2012Review
- Increased tumor necrosis factor-α, cleaved caspase 3 levels and insulin receptor substrate-1 phosphorylation in the β₁-adrenergic receptor knockout mouse.Molecular vision · 2011Article
- Role of growth hormone, insulin-like growth factor 1 and insulin-like growth factor-binding protein 3 in development of non-alcoholic fatty liver disease.Hepatology international · 2007Article
- Novel roles of the IGF-IGFBP axis in etiopathophysiology of diabetic nephropathy.Diabetes research and clinical practice · 2007Review
- Novel actions of IGFBP-3 on intracellular signaling pathways of insulin-secreting cells.Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society · 2006Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Mesangial cells are critical for glomerular filtration. Mesangial cell dysfunction, the hallmark of diabetic nephropathy, results from disordered mesangial growth induced by cytokines, abnormal hemodynamic influence, and metabolic factors associated with chronic hyperglycemia. Insulin-like growth factors (IGFs) and their high affinity binding proteins (IGFBPs) exert major actions on mesangial cell survival, but their underlying mechanisms remain unclear. In light of emerging IGF-independent roles for IGFBP-3, we investigated IGFBP-3 actions during mesangial cell apoptosis induced by cytokine or high glucose concentration. Quantified by DNA fragmentation ELISA and Annexin V flow cytometry, apoptosis occurred in rat mesangial cells (RMC) exposed to 2 microg/mL IGFBP-3 for 24 h under high ambient or standard glucose. Anti-sense IGFBP-3 oligo at 10 microg/mL significantly inhibited apoptosis induced by 100 ng/mL TNF-alpha, serum-free conditions, or high (25 mM) glucose. Increased IGFBP-3 release associated with high ambient glucose or TNF-alpha was inhibited by pre-treatment with anti-sense oligo. Under serum-free conditions, recombinant human IGFBP-3 blocked Akt phosphorylation at threonine 308 (pThr308), whereas anti-sense oligo treatment was associated with enhanced pThr308 activity. In summary, these data support a novel mechanism for TNF-alpha-induced mesangial cell apoptosis mediated by IGFBP-3 and present regulation of pThr308 activity as a novel mechanism underlying IGFBP-3 action.
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