WNT1 inducible signaling pathway protein 1 (WISP1): A novel mediator linking development and disease

Berschneider, Barbara; Königshoff, Mélanie

doi:10.1016/j.biocel.2010.11.013

Cited by 92 publications

(86 citation statements)

References 28 publications

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“…Wisp1, GDNF, and IFRD1 are RA target genes that mediate cell proliferation and differentiation. 14,16,23 These data suggest that induction of RDH9 expression in podocytes activates these RA target genes to improve podocyte differentiation and attenuate kidney injury. Many studies have shown that exogenous RA is able to improve kidney diseases in various experimental models, including the HIV-1 transgenic mouse (Tg26), 3 anti-Thy-1 nephritis, 24 puromycin aminonucleoside-induced nephrosis, 25 lupus nephritis, 26 diabetic nephropathy, 27 and anti-glomerular basement membrane nephritis.…”

Section: Discussionmentioning

confidence: 86%

Induction of Retinol Dehydrogenase 9 Expression in Podocytes Attenuates Kidney Injury

Dai

Chuang

et al. 2014

Journal of the American Society of Nephrology

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The intracellular concentration of retinoic acid is determined by two sequential oxidation reactions that convert retinol to retinoic acid. We recently demonstrated that retinoic acid synthesis is significantly impaired in glomeruli of HIV-1 transgenic mice (Tg26), a murine model of HIV-associated nephropathy. This impaired retinoic acid synthesis correlates with reduced renal expression of retinol dehydrogenase 9, which catalyzes the rate-limiting step of retinoic acid synthesis by converting retinol to retinal. Because retinoic acid has renal protective effects and can induce podocyte differentiation, we hypothesized that restoration of retinoic acid synthesis could slow the progression of renal disease. Herein, we demonstrate that overexpression of retinol dehydrogenase 9 in cultured podocytes induces the expression of podocyte differentiation markers. Furthermore, we confirm that podocyte-specific overexpression of retinol dehydrogenase 9 in mice with established kidney disease due to either HIV-associated nephropathy or adriamycin-induced nephropathy decreases proteinuria, attenuates kidney injury, and restores podocyte differentiation markers. Our data suggest that restoration of retinoic acid synthesis could be a new approach to treat kidney disease.

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Section: Discussionmentioning

confidence: 86%

Induction of Retinol Dehydrogenase 9 Expression in Podocytes Attenuates Kidney Injury

Dai

Chuang

et al. 2014

Journal of the American Society of Nephrology

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“…We show that IL-10 promotes intestinal epithelial wound healing through the activation of CREB signaling, with subsequent synthesis and secretion of the WNT1-inducible signaling protein 1 (WISP-1). WISP-1 is a member of the connective tissue growth factor (CTGF) family and has been increasingly recognized for its roles in facilitating repair (6). Our study identifies a link between the antiinflammatory cytokine IL-10 and WISP-1, which serve to promote epithelial wound repair and restore mucosal homeostasis.…”

Section: Introductionmentioning

confidence: 84%

“…Our study demonstrates a STAT3-dependent link between IL-10 and epithelial CREB signaling that serves to promote epithelial cell proliferation and repair. IT has been previously reported that CREB activation promotes the expression of a pro-proliferative WISP-1 protein that belongs to the CCN family of extracellular matrix-associated proteins (6,12). Our study supports the idea that IL-10-induced epithelial WISP-1 secretion in epithelial cells is mediated by CREB activation.…”

Section: Discussionmentioning

confidence: 99%

Macrophage-derived IL-10 mediates mucosal repair by epithelial WISP-1 signaling

Quirós¹,

Nishio²,

Neumann³

et al. 2017

Journal of Clinical Investigation

155

132

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“…CCN4 is a member of the CCN family that is defined by the first three members of the family, cysteine-rich protein 61, connective tissue growth factor, and Nephroblastoma overexpressed gene (Berschneider and Königshoff, 2011). CCN4 was initially identified as a gene in a mouse mammary epithelial cell line (Pennica et al, 1998), was later determined to modulate gastric tumor growth (Davies et al, 2007), and was regulated by Wnt1, a cysteine-rich glycosylated protein that controls cell development and survival in multiple systems of the body (Chong et al, 2011;He et al, 2005;Maiese et al, 2008).…”

Section: Introductionmentioning

confidence: 99%