High glucose level inhibits capacitative Ca2 + influx in cultured rat mesangial cells by a protein kinase C-dependent mechanism
暂无分享,去创建一个
Giuseppe Pugliese | Francesco Pugliese | Flavia Pricci | F. Pricci | Paolo Menè | U. Di Mario | Giulio A. Cinotti | P. Menè | G. Cinotti | U. Mario | G. Pugliese | F. Pricci | F. Pugliese
[1] A. Sbarbati,et al. De novo synthesis of diacylglycerol from glucose. A new pathway of signal transduction in human neutrophils stimulated during phagocytosis of beta-glucan particles. , 1991, The Journal of biological chemistry.
[2] B. Chavers,et al. Mesangial Expansion as a Central Mechanism for Loss of Kidney Function in Diabetic Patients , 1989, Diabetes.
[3] K. Sharma,et al. High glucose-induced proliferation in mesangial cells is reversed by autocrine TGF-β , 1992 .
[4] G. Dubyak,et al. Phospholipase C activation by prostaglandins and thromboxane A2 in cultured mesangial cells. , 1988, The American journal of physiology.
[5] K. Sharma,et al. Stimulation of collagen gene expression and protein synthesis in murine mesangial cells by high glucose is mediated by autocrine activation of transforming growth factor-beta. , 1994, The Journal of clinical investigation.
[6] M. Dunn,et al. Phospholipids in signal transduction of mesangial cells. , 1989, The American journal of physiology.
[7] F. DeRubertis,et al. Sequential alterations in glomerular prostaglandin and thromboxane synthesis in diabetic rats: relationship to the hyperfiltration of early diabetes. , 1987, Metabolism: clinical and experimental.
[8] T. Faraggiana,et al. Identification and characteristics of a Na+/Ca2+ exchanger in cultured human mesangial cells. , 1990, Kidney international.
[9] F. Pugliese,et al. Regulation of capacitative calcium influx in cultured human mesangial cells: roles of protein kinase C and calmodulin. , 1996, Journal of the American Society of Nephrology : JASN.
[10] D. Giugliano,et al. Does a Common Mechanism Induce Diverse Complications of Diabetes? , 1988, Diabetes Care.
[11] J. Sowers,et al. Diabetes mellitus: a disease of abnormal cellular calcium metabolism? , 1994, The American journal of medicine.
[12] D. Troyer,et al. High glucose increases diacylglycerol mass and activates protein kinase C in mesangial cell cultures. , 1991, The American journal of physiology.
[13] F. Thaiss,et al. Hyperglycaemia--pathophysiological aspects at the cellular level. , 1995, Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association.
[14] B. Williams,et al. Glucose-induced protein kinase C activity regulates arachidonic acid release and eicosanoid production by cultured glomerular mesangial cells. , 1993, The Journal of clinical investigation.
[15] R. Marchase,et al. Hyperglycemia alters cytoplasmic Ca2+ responses to capacitative Ca2+ influx in rat aortic smooth muscle cells. , 1995, The American journal of physiology.
[16] R. Tsien,et al. Degradation of a Calcium Influx Factor (CIF) Can Be Blocked by Phosphatase Inhibitors or Chelation of Ca(*) , 1995, The Journal of Biological Chemistry.
[17] B. Williams,et al. Effect of elevated extracellular glucose concentrations on calcium ion uptake by cultured rat vascular smooth muscle cells. , 1992, Mineral and electrolyte metabolism.
[18] N. Nahman,et al. Effects of high glucose on cellular proliferation and fibronectin production by cultured human mesangial cells. , 1992, Kidney international.
[19] Roger Y. Tsien,et al. Emptying of intracellular Ca2+ stores releases a novel small messenger that stimulates Ca2+ influx , 1993, Nature.
[20] J. Putney. Capacitative calcium entry revisited. , 1990, Cell calcium.
[21] F. Crews,et al. Effects of glucose on receptor-mediated phosphoinositide hydrolysis and second messenger generation in rat glomerular mesangial cells. , 1991, Journal of the American Society of Nephrology : JASN.
[22] C. Whiteside,et al. Diabetic rat glomerular mesangial cells display normal inositol trisphosphate and calcium release. , 1992, The American journal of physiology.
[23] F. DeRubertis,et al. Protein kinase C is activated in glomeruli from streptozotocin diabetic rats. Possible mediation by glucose. , 1989, The Journal of clinical investigation.
[24] B. Williams,et al. Effect of elevated extracellular glucose concentrations on transmembrane calcium ion fluxes in cultured rat VSMC. , 1993, Kidney international.
[25] F. Luft,et al. High glucose concentrations and protein kinase C isoforms in vascular smooth muscle cells. , 1995, Kidney international.
[26] M. Haneda,et al. Impaired contractile responsiveness of diabetic glomeruli to angiotensin II: a possible indication of mesangial dysfunction in diabetes mellitus. , 1986, Biochemical and biophysical research communications.
[27] B. Brenner,et al. Prevention of diabetic glomerulopathy by pharmacological amelioration of glomerular capillary hypertension. , 1986, The Journal of clinical investigation.
[28] Y. Nishizuka. Intracellular signaling by hydrolysis of phospholipids and activation of protein kinase C. , 1992, Science.
[29] D. Eaton,et al. Role of growth factors in mesangial cell ion channel regulation. , 1995, Kidney international.
[30] T. Hallam,et al. Influx of bivalent cations can be independent of receptor stimulation in human endothelial cells. , 1989, The Biochemical journal.
[31] N. Bank. Mechanisms of diabetic hyperfiltration. , 1991, Kidney international.
[32] A. Winegrad. Banting Lecture 1986: Does a Common Mechanism Induce the Diverse Complications of Diabetes? , 1987, Diabetes.
[33] M. Berridge,et al. The regulation of capacitative calcium entry by calcium and protein kinase C in Xenopus oocytes. , 1994, The Journal of biological chemistry.
[34] B. Williams. Glucose-induced vascular smooth muscle dysfunction: the role of protein kinase C. , 1995, Journal of hypertension.
[35] R. Tsien,et al. A new generation of Ca2+ indicators with greatly improved fluorescence properties. , 1985, The Journal of biological chemistry.
[36] G. Pugliese,et al. High glucose inhibits cytosolic calcium signaling in cultured rat mesangial cells. , 1993, Kidney international.
[37] F. Pugliese,et al. Regulation of Na(+)-Ca2+ exchange in cultured human mesangial cells. , 1991, The American journal of physiology.
[38] J. Kreisberg,et al. Increased extracellular matrix synthesis and mRNA in mesangial cells grown in high-glucose medium. , 1991, The American journal of physiology.
[39] R. Penner,et al. Depletion of intracellular calcium stores activates a calcium current in mast cells , 1992, Nature.
[40] A. Teti,et al. Calcium release-activated calcium influx in cultured human mesangial cells. , 1994, Kidney international.
[41] M. Hanley,et al. Evaluation of Calcium Influx Factors from Stimulated Jurkat T-lymphocytes by Microinjection into Xenopus Oocytes(*) , 1995, The Journal of Biological Chemistry.
[42] Walter Stühmer,et al. Depletion of InsP3 stores activates a Ca2+ and K+ current by means of a phosphatase and a diffusible messenger , 1993, Nature.
[43] M. Berridge,et al. Capacitative calcium entry. , 1995, The Biochemical journal.
[44] Z. Makita,et al. Human and rat mesangial cell receptors for glucose-modified proteins: potential role in kidney tissue remodelling and diabetic nephropathy , 1991, The Journal of experimental medicine.
[45] M. Brownlee,et al. Effects of Nonenzymatic Glycosylation of Mesangial Matrix on Proliferation of Mesangial Cells , 1991, Diabetes.
[46] M. Dunn,et al. Physiology of the mesangial cell. , 1989, Physiological reviews.
[47] C. Seidel,et al. Insulin-stimulated glucose transport inhibits Ca2+ influx and contraction in vascular smooth muscle. , 1995, Circulation.
[48] L. Fine,et al. Renal hypertrophy, growth factors, and nephropathy in diabetes mellitus. , 1990, Seminars in nephrology.
[49] R. Schrier,et al. Characterization of Glucose-Induced In Situ Protein Kinase C Activity in Cultured Vascular Smooth Muscle Cells , 1992, Diabetes.