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10.1681/ASN.2013080893 http://scihub22266oqcxt.onion/10.1681/ASN.2013080893 C4178435!4178435 !24744439     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24744439 &cmd=llinks): Failed to open stream: HTTP request failed! 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Sonic hedgehog is a novel tubule-derived growth factor for interstitial fibroblasts after kidney injury |pdf=|usr=}}{{24744439 }} gab.com Text Sonic hedgehog is a novel tubule-derived growth factor for interstitial fibroblasts after kidney injury JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=24744439 #FOAvip Tubular epithelium constitutes the majority of the renal parenchyma and is the primary target of various kidney injuries. However, how the injured tubules drive interstitial fibroblast activation and proliferation remains poorly understood. Here, we investigated the role of sonic hedgehog (Shh), a secreted extracellular signaling protein, in fibroblast proliferation. Shh was induced in renal tubular epithelia in animal models of CKD induced by ischemia/reperfusion injury (IRI), adriamycin, or renal mass ablation, and in renal tubules of kidney biopsy specimens from CKD patients with different etiologies. Using Gli1-CreER(T2) reporter mice, we identified interstitial fibroblasts as the principal targets of renal Shh signaling in vivo. In vitro, incubation with Shh promoted normal rat kidney fibroblast proliferation, which was assessed by cell counting, MTT assay, and BrdU incorporation assay, and stimulated the induction of numerous proliferation-related genes. However, Shh had no effect on the proliferation of renal tubular epithelial cells. In vivo, overexpression of Shh promoted fibroblast expansion and aggravated kidney fibrotic lesions after IRI. Correspondingly, blockade of Shh signaling by cyclopamine, a small molecule inhibitor of Smoothened, inhibited fibroblast proliferation, reduced myofibroblast accumulation, and attenuated renal fibrosis. These studies identify Shh as a novel, specific, and potent tubule-derived growth factor that promotes interstitial fibroblast proliferation and activation. Our data also suggest that blockade of Shh signaling is a plausible strategy for therapeutic intervention of renal fibrosis. Twit Text FOAVip Sonic hedgehog is a novel tubule-derived growth factor for interstitial fibroblasts after kidney injury ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=24744439 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24744439 #FOAvip English Wikipedia <ref>{{Cite pmid|24744439 }}</ref> Sonic hedgehog is a novel tubule-derived growth factor for interstitial fibroblasts after kidney injury #MMPMID24744439 Zhou D ; Li Y ; Zhou L ; Tan RJ ; Xiao L ; Liang M ; Hou FF ; Liu Y J Am Soc Nephrol 2014[Oct]; 25 (10 ): 2187-200 PMID24744439 show ga Tubular epithelium constitutes the majority of the renal parenchyma and is the primary target of various kidney injuries. However, how the injured tubules drive interstitial fibroblast activation and proliferation remains poorly understood. Here, we investigated the role of sonic hedgehog (Shh), a secreted extracellular signaling protein, in fibroblast proliferation. Shh was induced in renal tubular epithelia in animal models of CKD induced by ischemia/reperfusion injury (IRI), adriamycin, or renal mass ablation, and in renal tubules of kidney biopsy specimens from CKD patients with different etiologies. Using Gli1-CreER(T2) reporter mice, we identified interstitial fibroblasts as the principal targets of renal Shh signaling in vivo. In vitro, incubation with Shh promoted normal rat kidney fibroblast proliferation, which was assessed by cell counting, MTT assay, and BrdU incorporation assay, and stimulated the induction of numerous proliferation-related genes. However, Shh had no effect on the proliferation of renal tubular epithelial cells. In vivo, overexpression of Shh promoted fibroblast expansion and aggravated kidney fibrotic lesions after IRI. Correspondingly, blockade of Shh signaling by cyclopamine, a small molecule inhibitor of Smoothened, inhibited fibroblast proliferation, reduced myofibroblast accumulation, and attenuated renal fibrosis. These studies identify Shh as a novel, specific, and potent tubule-derived growth factor that promotes interstitial fibroblast proliferation and activation. Our data also suggest that blockade of Shh signaling is a plausible strategy for therapeutic intervention of renal fibrosis. |Adult [MESH] |Animals [MESH] |Biopsy [MESH] |Cell Proliferation [MESH] |Disease Models, Animal [MESH] |Disease Progression [MESH] |Female [MESH] |Fibroblasts/*physiology [MESH] |Fibrosis [MESH] |Hedgehog Proteins/*metabolism [MESH] |Humans [MESH] |Kidney Tubules/metabolism [MESH] |Kidney/pathology [MESH] |Male [MESH] |Mice, Inbred BALB C [MESH] |Middle Aged [MESH] |Nephrosclerosis/*metabolism [MESH] |Rats, Sprague-Dawley [MESH] |Renal Insufficiency, Chronic/*metabolism [MESH] |Up-Regulation [MESH]Sonic hedgehog is a novel tubule-derived growth factor for interstitia(epmc).pdf DeepDyve Pubget Overpricing