Expression of CCN1 (CYR61) in developing, normal, and diseased human kidney

Sawai, Kenji; Mukoyama, Masashi; Mori, Kiyoshi; Kasahara, Masato; Koshikawa, Masao; Yokoi, Hideki; Yoshioka, Takakazu; Ogawa, Yoshihisa; Sugawara, Akira; Nishiyama, Hiroyuki; Yamada, Shigehito; Kubo, Takashi; Saleem, Moin A.; Shiota, Kohei; Ogawa, Osamu; Miyazato, Minoru; Kangawa, Kenji; Nakao, Kazuwa

doi:10.1152/ajprenal.00205.2007

Cited by 27 publications

(26 citation statements)

References 38 publications

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“…Moreover, contrary to rats, in mouse kidney we did not observe CCN1-positive staining in afferent and efferent arterioles, but in medium size arteries, while similarly as in rats we did not observe any reaction in large arteries. In addition, we detected CCN1-positive staining in mouse glomeruli, probably in podocytes, which supports earlier findings of Sawai et al [15,27] who detected CCN1 expression in cultured mouse podocytes.…”

Section: Discussionsupporting

confidence: 92%

“…Some differences in the pattern of CCN1 distribution in normal human kidney as compared to rodents were described by Sawai et al [27]. CCN1 protein was expressed in podocytes, the thick ascending www.fhc.viamedica.pl limb of Henle's loop, distal and proximal tubules, and collecting ducts in human kidney.…”

Section: Discussionmentioning

confidence: 89%

“…CCN1 protein was expressed in podocytes, the thick ascending www.fhc.viamedica.pl limb of Henle's loop, distal and proximal tubules, and collecting ducts in human kidney. Decreased CCN1 expression in human podocytes was observed in diseases affecting glomeruli, while the intensity of CCN1 staining in the tubular system was not altered [27]. CCN1 was reported to inhibit mesangial cell adhesion and migration and to promote podocyte differentiation and suppress podocyte migration in vitro [27].…”

Section: Discussionmentioning

confidence: 99%

“…Decreased CCN1 expression in human podocytes was observed in diseases affecting glomeruli, while the intensity of CCN1 staining in the tubular system was not altered [27]. CCN1 was reported to inhibit mesangial cell adhesion and migration and to promote podocyte differentiation and suppress podocyte migration in vitro [27]. Authors proposed that reduced CCN1 may affect glomerular structure and function by promoting mesangial migration leading to glomerulosclerosis and allowing for podocyte migration, that would cause glomerular crescent formation [27].…”

Section: Discussionmentioning

confidence: 99%

“…CCN1 was reported to inhibit mesangial cell adhesion and migration and to promote podocyte differentiation and suppress podocyte migration in vitro [27]. Authors proposed that reduced CCN1 may affect glomerular structure and function by promoting mesangial migration leading to glomerulosclerosis and allowing for podocyte migration, that would cause glomerular crescent formation [27]. Biological effects of CCN1 depend on the specific membrane receptor and cell type.…”

Section: Discussionmentioning

confidence: 99%

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CCN1 expression in interleukin-6 deficient mouse kidney in experimental model of heart failure

Bonda

Taranta

Kamiński

et al. 2013

Folia Histochem Cytobiol.

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Chronic heart failure often leads to worsening of the renal function. Mediators of this process include inflammatory and neuroendocrine factors. CCN1 (Cyr 61), a member of growth factor-inducible immediate early genes, which modulates inflammation and fibrogenesis, is excreted with urine in the early phase of acute renal injury and may be involved in the pathogenesis of the cardiorenal syndrome. The aim of the study was to evaluate CCN1 protein abundance and localization in the kidney of IL-6-deficient C57BL/6J (IL-6 KO) mice and respective wild-type (WT) animals in basal conditions and in animals with chronic heart failure twelve weeks after myocardial infarction. Age-and sex-matched mice from both strains subjected to sham operation served as controls. One group of WT animals subjected to myocardial infarction was treated with antagonist of AT1 receptor telmisartan over 12 weeks. Abundance and localization of CCN1 protein in kidney were assessed with Western blotting and immunohistochemistry, respectively. In all groups the strongest immunohistochemical reaction for CCN1 was observed in distal convoluted tubules and in smaller arteries, however, the total expression of CCN1 protein was lower in IL-6 KO mice in comparison to WT animals. The main difference in CCN1 distribution between the examined genotypes was lack of reaction in internal renal medulla and very weak reaction in proximal convoluted tubules in IL-6 KO mice. Experimental heart failure only slightly attenuated the expression of CCN1 protein in the kidney of WT mice and had no effect in IL-6 KO mice. Although, blockade of AT1 receptor did not alter CCN1 protein expression in kidneys of WT mice after myocardial infarction, it significantly changed its CCN1 distribution in the renal tubular system. (Folia Histochemica et Cytobiologica 2013, Vol. 51, No. 1, 84-91)

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 89%