Low-Denisty Lipoprotein and Glomerulosclerosis
作者： Hyun Soon Lee
关键词: Chemistry 、 Protein kinase C 、 Activator (genetics) 、 Apolipoprotein B 、 Internal medicine 、 Mesangial cell 、 Endocrinology 、 Glomerulosclerosis 、 Plasminogen activator 、 Lipoprotein 、 Glomerular Mesangial Cell
摘要: Hypercholesterolemia is a common feature of nephrosis or uremia. Dietary hypercholesterolemia aggravates the renal injury in experimental focal segmental glomerulosclerosis (FSGS). mainly due to increased level low-density lipoprotein (LDL). Accumulation apolipoprotein B-containing lipoproteins LDL frequently shown diseased human glomeruli. Furthermore, oxidized (Ox-LDL) has been demonstrated lesions FSGS mesangial areas. Ox-LDL glomeruli could recruit circulating monocytes leading accumulation macrophages and subsequent foam cell formation. Increased release macrophage-derived products produce an altered matrix biosynthesis. In cultured cells, susceptible oxidative modification, stimulates mRNA and/or protein expression α1(I), α1(III) α1(IV) collagen, laminin, fibronectin transforming growth factor-β1 (TGF-β1). also upregulates plasminogen activator inhibitor-1 (PAI-1), urokinase-type plasaminogen (uPA) tissue-type (tPA) after prolonged incubation times cells. LDL-induced inhibitory activity was greater than activity. kinase C (PKC) mitogen-activated (MAPK) as well bioactive TGF-β secretion PAI-1 overexpression cells abrogated by inhibition downregulation PKC administration anti-TGF-β suggesting that through induction TGF-β. Altogether, these effects on regulation synthesis/degradation might have pathophysiological function pathogenesis glomerulosclerosis.
springer.com
sci-hub.st 参考文章(158)
Valentina M. Factor, Erwin P. Böttinger, Snorri S. Thorgeirsson, Jeffrey B. Kopp, Nancy Sanderson, Paul E. Klotman, Peter Nagy, Miklos Mozes, Transgenic mice with increased plasma levels of TGF-beta 1 develop progressive renal disease. Laboratory Investigation. ,vol. 74, pp. 991- 1003 ,(1996)
E.R. Unanue, G.F. Schreiner, Origin of the rat mesangial phagocyte and its expression of the leukocyte common antigen Laboratory Investigation. ,vol. 51, pp. 515- 523 ,(1984)
J. Hagège, E. Rondeau, R. Medcalf, C. Adida, F. Delarue, M. N. Peraldi, J. D. Sraer, W. D. Schleuning, Plasminogen activator inhibitor-1 deposition in the extracellular matrix of cultured human mesangial cells. American Journal of Pathology. ,vol. 141, pp. 117- 128 ,(1992)
John F. Moorhead, Lipids and the Pathogenesis of Kidney Disease Nephrology. ,vol. 17, pp. 165- 177 ,(1991) , 10.1007/978-3-662-35158-1_11
Howard S. Kruth, Cholesterol Deposition in Atherosclerotic Lesions Sub-cellular biochemistry. ,vol. 28, pp. 319- 362 ,(1997) , 10.1007/978-1-4615-5901-6_12
ED Sprengers, C Kluft, Plasminogen activator inhibitors. Blood. ,vol. 69, pp. 381- 387 ,(1987) , 10.1182/BLOOD.V69.2.381.BLOODJOURNAL692381
H G Rennke, D J Sandstrom, J W Fries, T W Meyer, Glomerular hypertrophy and epithelial cell injury modulate progressive glomerulosclerosis in the rat. Laboratory Investigation. ,vol. 60, pp. 205- 218 ,(1989)
M.R. Keeton, S.A. Curriden, A.J. van Zonneveld, D.J. Loskutoff, Identification of regulatory sequences in the type 1 plasminogen activator inhibitor gene responsive to transforming growth factor beta. Journal of Biological Chemistry. ,vol. 266, pp. 23048- 23052 ,(1991) , 10.1016/S0021-9258(18)54461-6
Jeffrey L Wrana, Liliana Attisano, Rotraud Wieser, Francesc Ventura, Joan Massagué, None, Mechanism of activation of the TGF-β receptor Nature. ,vol. 370, pp. 341- 347 ,(1994) , 10.1038/370341A0
T E Carew, R C Pittman, D Steinberg, Tissue sites of degradation of native and reductively methylated [14C]sucrose-labeled low density lipoprotein in rats. Contribution of receptor-dependent and receptor-independent pathways. Journal of Biological Chemistry. ,vol. 257, pp. 8001- 8008 ,(1982) , 10.1016/S0021-9258(18)34288-1