LOX-1, an Oxidized Low-Density Lipoprotein Receptor, Was Upregulated in the Kidneys of Chronic Renal Failure Rats

LOX-1 is a novel receptor for oxidized low-density lipoprotein (LDL) isolated from vascular endothelial cells and has been suggested to be involved in the formation of atherosclerotic and hypertensive vascular lesions. We previously reported that salt loading caused glomerulosclerosis and upregulati...

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Veröffentlicht in:Hypertension Research 2003, Vol.26(1), pp.117-122
Hauptverfasser: UENO, Tomoko, KANAME, Shinya, TAKAICHI, Kenmei, NAGASE, Miki, TOJO, Akihiro, ONOZATO, Maristela Lika, FUJITA, Toshiro
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container_end_page 122
container_issue 1
container_start_page 117
container_title Hypertension Research
container_volume 26
creator UENO, Tomoko
KANAME, Shinya
TAKAICHI, Kenmei
NAGASE, Miki
TOJO, Akihiro
ONOZATO, Maristela Lika
FUJITA, Toshiro
description LOX-1 is a novel receptor for oxidized low-density lipoprotein (LDL) isolated from vascular endothelial cells and has been suggested to be involved in the formation of atherosclerotic and hypertensive vascular lesions. We previously reported that salt loading caused glomerulosclerosis and upregulation of LOX-1 in the kidney of Dahl salt-sensitive hypertensive rats. In the present study, we investigated LOX-1 expression in the remnant kidney, an established rat model for chronic renal failure. Six weeks after 5/6 nephrectomy, the rats showed elevated blood pressure, impaired renal function and increased renal expression of type I collagen. The LOX-1 gene expression in the remnant kidney was markedly increased compared with that in control rats, and immunohistochemical analysis showed that LOX-1 was widely expressed in the interstitial cells, whereas there was almost no staining in the glomeruli or tubules. Moreover, reduction of blood pressure by the angiotensin II type 1 (AT1) receptor antagonist candesartan significantly suppressed the renal LOX-1 expression, and this suppression was accompanied by amelioration of renal injury. These results suggest that enhanced renal expression of LOX-1 might play some roles in the progression of chronic renal failure in rats. (Hypertens Res 2003; 26: 117-122)
doi_str_mv 10.1291/hypres.26.117
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We previously reported that salt loading caused glomerulosclerosis and upregulation of LOX-1 in the kidney of Dahl salt-sensitive hypertensive rats. In the present study, we investigated LOX-1 expression in the remnant kidney, an established rat model for chronic renal failure. Six weeks after 5/6 nephrectomy, the rats showed elevated blood pressure, impaired renal function and increased renal expression of type I collagen. The LOX-1 gene expression in the remnant kidney was markedly increased compared with that in control rats, and immunohistochemical analysis showed that LOX-1 was widely expressed in the interstitial cells, whereas there was almost no staining in the glomeruli or tubules. Moreover, reduction of blood pressure by the angiotensin II type 1 (AT1) receptor antagonist candesartan significantly suppressed the renal LOX-1 expression, and this suppression was accompanied by amelioration of renal injury. These results suggest that enhanced renal expression of LOX-1 might play some roles in the progression of chronic renal failure in rats. 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We previously reported that salt loading caused glomerulosclerosis and upregulation of LOX-1 in the kidney of Dahl salt-sensitive hypertensive rats. In the present study, we investigated LOX-1 expression in the remnant kidney, an established rat model for chronic renal failure. Six weeks after 5/6 nephrectomy, the rats showed elevated blood pressure, impaired renal function and increased renal expression of type I collagen. The LOX-1 gene expression in the remnant kidney was markedly increased compared with that in control rats, and immunohistochemical analysis showed that LOX-1 was widely expressed in the interstitial cells, whereas there was almost no staining in the glomeruli or tubules. Moreover, reduction of blood pressure by the angiotensin II type 1 (AT1) receptor antagonist candesartan significantly suppressed the renal LOX-1 expression, and this suppression was accompanied by amelioration of renal injury. These results suggest that enhanced renal expression of LOX-1 might play some roles in the progression of chronic renal failure in rats. 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We previously reported that salt loading caused glomerulosclerosis and upregulation of LOX-1 in the kidney of Dahl salt-sensitive hypertensive rats. In the present study, we investigated LOX-1 expression in the remnant kidney, an established rat model for chronic renal failure. Six weeks after 5/6 nephrectomy, the rats showed elevated blood pressure, impaired renal function and increased renal expression of type I collagen. The LOX-1 gene expression in the remnant kidney was markedly increased compared with that in control rats, and immunohistochemical analysis showed that LOX-1 was widely expressed in the interstitial cells, whereas there was almost no staining in the glomeruli or tubules. Moreover, reduction of blood pressure by the angiotensin II type 1 (AT1) receptor antagonist candesartan significantly suppressed the renal LOX-1 expression, and this suppression was accompanied by amelioration of renal injury. 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ispartof Hypertension Research, 2003, Vol.26(1), pp.117-122
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subjects angiotensin II type 1 receptor antagonist
Angiotensin Receptor Antagonists
Animals
Antihypertensive Agents - pharmacology
Benzimidazoles - pharmacology
chronic renal failure
Collagen Type I - genetics
Disease Models, Animal
Gene Expression
Hypertension, Renal - drug therapy
Hypertension, Renal - metabolism
Hypertension, Renal - pathology
Kidney - metabolism
Kidney - pathology
Kidney - surgery
Kidney Failure, Chronic - metabolism
Kidney Failure, Chronic - pathology
LOX-1
Male
Nephrectomy
oxidized low-density lipoprotein
Rats
Rats, Sprague-Dawley
Receptor, Angiotensin, Type 1
Receptors, LDL - genetics
Receptors, LDL - metabolism
Receptors, Oxidized LDL
remnant kidney
Scavenger Receptors, Class E
Tetrazoles - pharmacology
Up-Regulation
title LOX-1, an Oxidized Low-Density Lipoprotein Receptor, Was Upregulated in the Kidneys of Chronic Renal Failure Rats
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