<i>WISP1</i> silencing confers protection against epithelial–mesenchymal transition of renal tubular epithelial cells in rats via inactivation of the wnt/β‐catenin signaling pathway in uremia

Chen, Yuan‐Zhen; Sun, Dan‐Qin; Zheng, Yi; Zheng, Guang‐Kuai; Chen, Rongquan; Mei, Lin; Huang, Liejun; Huang, Cong; Song, Dan; Wu, Benqing

doi:10.1002/jcp.27654

Cited by 15 publications

(16 citation statements)

References 52 publications

(72 reference statements)

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“…Our findings are just one example of how the matricellular protein WISP1 alters cellular fate and differentiation decisions. Past studies have implicated WISP1 in the balance of osteoblast versus adipocyte formation (38,39) and, more broadly, epithelial cells adopting a mesenchymal cell fate (epithelial-mesenchymal transition) (40)(41)(42)(43). As CCN family members, including WISP1, have numerous extracellular binding partners it is understandable that they may have context-dependent effects on cellular differentiation.…”

Section: Discussionmentioning

confidence: 99%

Endogenous CCN family member WISP1 inhibits trauma-induced heterotopic ossification

Hsu¹,

Marini²,

Negri³

et al. 2020

JCI Insight

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Section: Discussionmentioning

confidence: 99%

Endogenous CCN family member WISP1 inhibits trauma-induced heterotopic ossification

Hsu¹,

Marini²,

Negri³

et al. 2020

JCI Insight

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“…9A), indicating that the transition of fibroblasts into myofibroblasts was also the important mechanism of LF fibrosis. It has been reported that CCN protein induces a-SMA expression in the fibrosis of many organs (Chen et al, 2019;Morales et al, 2011). Therefore, we suspected that WISP-1 might also induce a-SMA expression in LF fibroblast during fibrogenesis.…”

Section: Wisp-1 Promotesa-sma Expression Through Hedgehog Signalingmentioning

confidence: 87%

WISP-1 induced by mechanical stress contributes to the fibrosis and hypertrophy of ligamentum flavum via the Hedgehog-Gli1 signaling

Sun

Yin

et al. 2020

Preprint

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Background and Purpose: The ongoing chronic fibrosis and hypertrophy of ligamentum flavum (LF) is an important cause of lumbar spinal canal stenosis (LSCS). Our previous work showed that WNT1 inducible signaling pathway protein 1 (WISP-1) is a critical driver of LF fibrosis. This study was designed to explore the mechanism by which WISP-1 is activated and its underlying mechanisms in LF fibrosis. Experimental Approach: We studied the expression of Hedgehog-related proteins in human LF tissues. Cell viability, cell cycle, apoptosis rate and molecular mechanisms were evaluated in LF cells. Finally, the molecular mechanism was confirmed in vivo studies. Key Results: The results showed that Gli1 was upregulated in hypertrophic LF tissues and required for fibroblast viability and collagen expression in fibroblasts. Moreover, mechanical stretching increased WISP-1 expression in LF fibroblasts. Furthermore, WISP-1 induced fibrogenesis through Hedgehog-Gli1 pathway. This conclusion was supported by the fact that WISP-1 activated Hedgehog-Gli1 pathway in LF fibroblasts and cyclopamine attenuated the effect of WISP-1-induced fibrogenesis. WISP-1 also promoted the transition of fibroblasts into myofibroblasts via Hedgehog pathway. Importantly, hypertrophic LF rabbit model induced by mechanical stress also showed pathological change of fibrosis and more higher expression of WISP-1, Gli1 and a-SMA. Therapeutic administration of cyclopamine reduced collagen expression, fibroblast proliferation, myofibroblast differentiation and ameliorated LF fibrosis in mechanical stress-induced rabbit model. WISP-1 induced by mechanical stress contributes to the fibrosis and hypertrophy of ligamentum flavum via the Hedgehog-Gli1 signaling

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“…CircRNAs are competitive endogenous RNAs (ceRNAs) that regulate gene expression by sponging their target miRNAs [ 30 – 32 ]. For example, circular RNA YAP1 protects against ischemic injury by regulating the miRNA-21-5p/PI3K/AKT/mTOR axis [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

CircRNA_30032 promotes renal fibrosis in UUO model mice via miRNA-96-5p/HBEGF/KRAS axis

Lee

et al. 2021

Aging

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In this study, we investigated the role of circular RNA_30032 (circRNA_30032) in renal fibrosis and the underlying mechanisms. The study was carried out using TGF-β1-induced BUMPT cells and unilateral ureteral obstruction (UUO)-induced mice, respectively, as in vitro and in vivo models. CircRNA_30032 expression was significantly increased by 9.15- and 16.6-fold on days 3 and 7, respectively, in the renal tissues of UUO model mice. In TGF-β1-treated BUMPT cells, circRNA_30032 expression was induced by activation of the p38 mitogen-activated protein kinase signaling pathway. Quantitative real-time PCR, western blotting and dual luciferase reporter assays showed that circRNA_30032 mediated TGF-β1-induced and UUO-induced renal fibrosis by sponging miR-96-5p and increasing the expression of profibrotic proteins, including HBEGF, KRAS, collagen I, collagen III and fibronectin. CircRNA_30032 silencing significantly reduced renal fibrosis in UUO model mice by increasing miR-96-5p levels and decreasing levels of HBEGF and KRAS. These results demonstrate that circRNA_30032 promotes renal fibrosis via the miR-96-5p/HBEGF/KRAS axis and suggest that circRNA_30032 is a potential therapeutic target for treatment of renal fibrosis.

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WISP1 silencing confers protection against epithelial–mesenchymal transition of renal tubular epithelial cells in rats via inactivation of the wnt/β‐catenin signaling pathway in uremia

Cited by 15 publications

References 52 publications

Endogenous CCN family member WISP1 inhibits trauma-induced heterotopic ossification

Endogenous CCN family member WISP1 inhibits trauma-induced heterotopic ossification

WISP-1 induced by mechanical stress contributes to the fibrosis and hypertrophy of ligamentum flavum via the Hedgehog-Gli1 signaling

CircRNA_30032 promotes renal fibrosis in UUO model mice via miRNA-96-5p/HBEGF/KRAS axis

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