Glucose-induced protein kinase C activity regulates arachidonic acid release and eicosanoid production by cultured glomerular mesangial cells - PubMed (original) (raw)
Glucose-induced protein kinase C activity regulates arachidonic acid release and eicosanoid production by cultured glomerular mesangial cells
B Williams et al. J Clin Invest. 1993 Dec.
Abstract
Changes in glomerular eicosanoid production have been implicated in the development of diabetes-induced glomerular hyperfiltration and glomerular mesangial cells (GMC) are major eicosanoid-producing cells within the glomerulus. However, the mechanism for the effect of diabetes mellitus on glomerular mesangial eicosanoid production is unknown. The present study therefore examined whether elevated glucose concentrations activate protein kinase C (PKC) in GMC and whether this PKC activation mediates an effect of elevated glucose concentrations to increase the release of arachidonic acid and eicosanoid production by GMC. The percentage of [3H]arachidonic acid release per 30 min by preloaded GMC monolayers was significantly increased after 3-h exposure to high glucose (20 mM) medium (177% vs control medium) and this increase was sustained after 24-h exposure to high glucose concentrations. 3-h and 24-h exposure to high glucose medium also increased PGE2, 6-keto-PGF1 alpha, and thromboxane (TXB2) production by GMC. High glucose medium (20 mM) increased PKC activity in GMC at 3 and 24 h (168% vs control). In contrast, osmotic control media containing either L-glucose or mannitol did not increase arachidonic acid release, eicosanoid production, or PKC activity in GMC. Inhibiting glucose-induced PKC activation with either H-7 (50 microM) or staurosporine (1 microM) prevented glucose-induced increases in arachidonic acid release and eicosanoid production by GMC. These data demonstrate that elevated extracellular glucose concentrations directly increase the release of endogenous arachidonic acid and eicosanoids by GMC via mechanisms dependent on glucose-induced PKC activation.
Similar articles
- Fibronectin-induced increase in mesangial cell prostaglandin release. Effect of hyperglycemia and PKC inhibition.
Dunlop M, Keogh R, Larkins RG. Dunlop M, et al. Diabetes. 1993 Jan;42(1):183-90. doi: 10.2337/diab.42.1.183. Diabetes. 1993. PMID: 8420816 - Endotoxin-induced arachidonic acid metabolism requires de novo protein synthesis and protein kinase C activation.
Geisel J, Cook JA, Coffee KA, Wise WC, Halushka PV. Geisel J, et al. Biochim Biophys Acta. 1991 Aug 20;1085(1):15-20. doi: 10.1016/0005-2760(91)90226-8. Biochim Biophys Acta. 1991. PMID: 1909897 - Role of protein kinase C and cyclic AMP/protein kinase A in high glucose-stimulated transcriptional activation of collagen alpha 1 (IV) in glomerular mesangial cells.
Ziyadeh FN, Fumo P, Rodenberger CH, Kuncio GS, Neilson EG. Ziyadeh FN, et al. J Diabetes Complications. 1995 Oct-Dec;9(4):255-61. doi: 10.1016/1056-8727(95)80016-8. J Diabetes Complications. 1995. PMID: 8573741 Review. - Activation of protein kinase C in glomerular cells in diabetes. Mechanisms and potential links to the pathogenesis of diabetic glomerulopathy.
Derubertis FR, Craven PA. Derubertis FR, et al. Diabetes. 1994 Jan;43(1):1-8. doi: 10.2337/diab.43.1.1. Diabetes. 1994. PMID: 8262306 Review.
Cited by
- The pericyte connectome: spatial precision of neurovascular coupling is driven by selective connectivity maps of pericytes and endothelial cells and is disrupted in diabetes.
Kovacs-Oller T, Ivanova E, Bianchimano P, Sagdullaev BT. Kovacs-Oller T, et al. Cell Discov. 2020 Jun 16;6:39. doi: 10.1038/s41421-020-0180-0. eCollection 2020. Cell Discov. 2020. PMID: 32566247 Free PMC article. - Diabetic Kidney Disease: Pathophysiology and Therapeutic Targets.
Toth-Manikowski S, Atta MG. Toth-Manikowski S, et al. J Diabetes Res. 2015;2015:697010. doi: 10.1155/2015/697010. Epub 2015 Apr 30. J Diabetes Res. 2015. PMID: 26064987 Free PMC article. Review. - COX-2 but not mPGES-1 contributes to renal PGE2 induction and diabetic proteinuria in mice with type-1 diabetes.
Jia Z, Sun Y, Liu S, Liu Y, Yang T. Jia Z, et al. PLoS One. 2014 Jul 1;9(7):e93182. doi: 10.1371/journal.pone.0093182. eCollection 2014. PLoS One. 2014. PMID: 24984018 Free PMC article. - Gap junctions in the control of vascular function.
Figueroa XF, Duling BR. Figueroa XF, et al. Antioxid Redox Signal. 2009 Feb;11(2):251-66. doi: 10.1089/ars.2008.2117. Antioxid Redox Signal. 2009. PMID: 18831678 Free PMC article. Review.
References
- J Clin Invest. 1985 Feb;75(2):404-12 - PubMed
- Br Med J (Clin Res Ed). 1982 Apr 24;284(6324):1215-7 - PubMed
- J Clin Endocrinol Metab. 1985 Jun;60(6):1231-6 - PubMed
- Anal Chem. 1985 Jun;57(7):1170-3 - PubMed
- J Biol Chem. 1985 Oct 15;260(23):12484-91 - PubMed
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources