Distribution of type I collagen in human kidney diseases in comparison with type III collagen

Yoshioka, Kazuo; Tohda, Machi; Takemura, Tamiko; Akano, Norihisa; Matsubara, K; Ooshima, Akira; Maki, Sunao

doi:10.1002/path.1711620207

Cited by 71 publications

(58 citation statements)

References 19 publications

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“…Because collagen I is a major component in the development of vascular fibrosis, 8 we examined the ability of renal vessels to produce collagen I during chronic NO synthase inhibition. Synthesis of PICP was higher in renal resistance vessels of L-NAME-treated rats than in control rats (4.24Ϯ0.27 versus 2.38Ϯ0.17 ng/mg, nϭ7, PϽ0.05; Figure 6).…”

Section: Collagen I Productionmentioning

confidence: 99%

“…7 Because collagen I is almost absent in renal vessels and glomeruli, it is considered to be a marker of pathophysiological process in abnormal vascular remodeling. 8 Therefore, we hypothesized that longterm blockade of vascular NO production would be associated with enhanced renal vascular production of both ET-1 and collagen I. To this end, we measured ET-1 and collagen I mRNA expression and synthesis.…”

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confidence: 99%

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Vascular Endothelin-1 Gene Expression and Synthesis and Effect on Renal Type I Collagen Synthesis and Nephroangiosclerosis During Nitric Oxide Synthase Inhibition in Rats

et al. 1999

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Background-The progression of hypertension during NO deficiency is associated with renal vascular fibrosis due to increased extracellular matrix (mainly collagen I) formation. The purpose of the present study was to investigate whether endothelin-1 (ET-1) is involved in this pathophysiological process. Methods and Results-Treatment of rats for 4 weeks with the NO synthase inhibitor N -nitro-L-arginine methyl ester (L-NAME) 50 mg ⅐ kg Ϫ1 ⅐ d Ϫ1 increased systolic blood pressure to 159Ϯ12 mm Hg. In animals treated with L-NAME, histological evaluation of renal sections revealed an increased formation of extracellular matrix (Masson's trichrome), and specifically of collagens (Sirius red). A part of this fibrosis was attributed to abnormal collagen I presence, because mRNA expression of the collagen I ␣1 chain (reverse transcription-polymerase chain reaction) and procollagen I formation (radioimmunoassay) were increased 3-and 2.5-fold, respectively, in the renal resistance vessels of hypertensive animals. In subsequent experiments, we examined whether ET-1 was involved in activation of collagen I formation. mRNA expression (RNase protection assay) of preproET-1 and ET-1 content (radioimmunoassay) were 10-fold and 3-fold increased, respectively, in renal microvessels of rats treated with L-NAME. Interestingly, in these vessels, ET-1 (immunostaining) was colocalized with sudanophilic lesions. Bosentan, an ET receptor antagonist (20 mg, coadministered with L-NAME canceled the increased mRNA expression and synthesis of collagen I and attenuated the severity of renal vascular lesions without affecting L-NAME-induced high blood pressure. Conclusions-These data demonstrate that ET-1 synthesis is increased in renal microvessels when NO production is suppressed. In this model of hypertension, ET-1 is a major activator of collagen I formation in renal resistance vessels and participates in the development of renal fibrosis without affecting systolic blood pressure. (Circulation. 1999;99:2185-2191.)

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Section: Collagen I Productionmentioning

confidence: 99%

mentioning

confidence: 99%

Vascular Endothelin-1 Gene Expression and Synthesis and Effect on Renal Type I Collagen Synthesis and Nephroangiosclerosis During Nitric Oxide Synthase Inhibition in Rats

et al. 1999

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“…1 This pathophysiological process is associated with changes in the structure of renal vasculature caused by abnormal accumulation of extracellular matrix (mainly collagen type I) in renal resistance vessels, glomeruli, and interstitium. 2 Several recent studies indicated that endothelial vasoactive agents such as nitric oxide (NO) and endothelin could be involved in the development of renal fibrosis. NO is an important inhibitor of vascular smooth muscle cell growth and extracellular matrix synthesis in vitro and in vivo, 3,4 whereas chronic inhibition of NO synthesis is accompanied by renal vascular fibrosis.…”

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confidence: 99%

Regression of Renal Vascular Fibrosis by Endothelin Receptor Antagonism

et al. 2001

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Abstract-In previous studies, we have observed that endothelin participates in the progression of renal vascular and glomerular fibrosis during hypertension by activating collagen I gene synthesis. The present study investigated whether administration of endothelin receptor antagonists leads to the regression of renal sclerotic lesions. Experiments were performed in transgenic mice harboring the luciferase gene under the control of the collagen I-␣2 chain promoter. Hypertension was induced by long-term inhibition of nitric oxide synthesis by N G -nitro-L-arginine methyl ester (L-NAME); systolic pressure gradually increased, reaching a plateau of 165 mm Hg after 10 weeks of hypertensive treatment. At the same time, collagen I gene expression was increased 2-and 5-fold compared with control animals in afferent arterioles and glomeruli, respectively (PϽ0.01). This increase was accompanied by the appearance of sclerotic lesions within the renal vasculature. When renal vascular lesions had been established (20 weeks of L-NAME), animals were divided into 2 subgroups: the one continued to receive L-NAME, whereas in the other, bosentan, a dual endothelin antagonist, was coadministered with L-NAME for an additional period of 10 weeks. Bosentan coadministration did not alter the increased systolic pressure at 30 weeks; in contrast, collagen I gene activity returned almost to control levels in renal vessels and glomeruli. In this subgroup of animals, renal vascular lesions (collagen and/or extracellular matrix deposition) and mortality rates were substantially reduced compared with untreated mice. These data indicate that endothelin participates in the mechanism(s) of renal vascular fibrosis by activating collagen I gene. Treatment with an endothelin antagonist normalizes expression of collagen I gene and leads to the regression of renal vascular fibrosis and to the improvement of survival, thus providing a complementary curative approach against renal fibrotic complications associated with hypertension.

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“…Hypertension is usually associated with the development of vascular and renal fibrosis [3]. This pathophysiological process is characterized by structural changes in vasculature caused by increased synthesis and rearrangement of extracellular matrix proteins, such as the collagen type I [4]. Several studies support a major role for the renin-angiotensin system in the development of fibrosis [5,6].…”

Section: Introductionmentioning

confidence: 99%

Molecular Mechanisms of Nephro-Protective Action of HE-86 Liquid Extract in Experimental Chronic Renal Failure

He¹,

Fang²,

Fu³

et al. 2012

Chronic Kidney Disease

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Distribution of type I collagen in human kidney diseases in comparison with type III collagen

Cited by 71 publications

References 19 publications

Vascular Endothelin-1 Gene Expression and Synthesis and Effect on Renal Type I Collagen Synthesis and Nephroangiosclerosis During Nitric Oxide Synthase Inhibition in Rats

Vascular Endothelin-1 Gene Expression and Synthesis and Effect on Renal Type I Collagen Synthesis and Nephroangiosclerosis During Nitric Oxide Synthase Inhibition in Rats

Regression of Renal Vascular Fibrosis by Endothelin Receptor Antagonism

Molecular Mechanisms of Nephro-Protective Action of HE-86 Liquid Extract in Experimental Chronic Renal Failure

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