Wnt2 accelerates cardiac myocyte differentiation from ES-cell derived mesodermal cells via non-canonical pathway

Onizuka, Takeshi; Yuasa, Shinsuke; Kusumoto, Dai; Shimoji, Koki; Egashira, Toru; Ohno, Yohei; Kageyama, Takahiro; Tanaka, Tomofumi; Hattori, Fumiyuki; Fujita, Jun; Ieda, Masaki; Kimura, Kensuke; Makino, Shinji; Sano, Motoaki; Kudo, Akira; Fukuda, Keiichi

doi:10.1016/j.yjmcc.2011.11.010

Cited by 42 publications

(33 citation statements)

References 48 publications

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“…WNT2 plays a role in SM and cardiac muscle differentiation: it is strongly up-regulated during cardiomyocyte differentiation and plays a strong positive stage-specific role in cardiogenesis through the non-canonical WNT pathway in murine embryonic stem (ES) cells (46). Mice deficient for WNT2 displayed vascular abnormalities, including defective placental vasculature (47), and it was shown that WNT2 signaling was necessary and sufficient for activation of a transcriptional and signaling network critical for smooth muscle specification and differentiation, including myocardin/ MRTF-B and the signaling factor FGF10 (48).…”

Section: Journal Of Biological Chemistry 7081mentioning

confidence: 99%

MicroRNA MiR-199a-5p Regulates Smooth Muscle Cell Proliferation and Morphology by Targeting WNT2 Signaling Pathway

Gheinani

Burkhard

Rehrauer³

et al. 2015

Journal of Biological Chemistry

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Background: MicroRNA miR-199a-5p, implicated in cell motility and proliferation, is highly expressed in bladder smooth muscle. Results: MiR-199a-5p regulates WNT, cytoskeleton, and cell cycle pathways in urothelial and smooth muscle cells and promotes myocardin-driven gene expression. Conclusion: MiR-199a-5p acts via its target WNT2 to control smooth muscle proliferation and morphology. Significance: MiR-199a-5p is a key modulator of smooth muscle hypertrophy, relevant for bladder organ remodeling.

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Section: Journal Of Biological Chemistry 7081mentioning

confidence: 99%

MicroRNA MiR-199a-5p Regulates Smooth Muscle Cell Proliferation and Morphology by Targeting WNT2 Signaling Pathway

Gheinani

Burkhard

Rehrauer³

et al. 2015

Journal of Biological Chemistry

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“…β-catenin-independent) Wnt signalling mechanisms also regulate heart development (e.g. Eisenberg and Eisenberg, 1999;Pandur et al, 2002;Afouda et al, 2008;Cohen et al, 2012;Onizuka et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

sfrp1 promotes cardiomyocyte differentiation in Xenopus via negative-feedback regulation of Wnt signalling

2013

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SUMMARYWnt signalling is a key regulator of vertebrate heart development, yet it is unclear which specific Wnt signalling components are required to regulate which aspect of cardiogenesis. Previously, we identified Wnt6 as an endogenous Wnt ligand required for controlling heart muscle differentiation via canonical Wnt/β-catenin signalling. Here we show for the first time a requirement for an endogenous Wnt signalling inhibitor for normal heart muscle differentiation. Expression of sfrp1 is strongly induced in differentiating heart muscle. We show that sfrp1 is not only able to promote heart muscle differentiation but is also required for the formation of normal size heart muscle in the embryo. sfrp1 is functionally able to inhibit Wnt6 signalling and its requirement during heart development relates to relieving the cardiogenesis-restricting function of endogenous wnt6. In turn, we discover that sfrp1 expression in the heart is regulated by Wnt6 signalling, which for the first time indicates that sfrp genes can function as part of a Wnt negativefeedback regulatory loop. Our experiments indicate that sfrp1 controls the size of the differentiating heart muscle primarily by regulating cell fate within the cardiac mesoderm between muscular and non-muscular cell lineages. The cardiac mesoderm is therefore not passively patterned by signals from the surrounding tissue, but regulates its differentiation into muscular and non-muscular tissue using positional information from the surrounding tissue. This regulatory network might ensure that Wnt activation enables expansion and migration of cardiac progenitors, followed by Wnt inhibition permitting cardiomyocyte differentiation.

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“…Recently, a number of studies have emerged that provide hope in overcoming these problems. Previous studies reported BMP, Wnts, FGFs, hedgehog, and notch as cardiomyogenic regulators [22][23][24][25][26]. In addition, the purification of ES cell-derived cardiomyocytes decreased the risk of teratoma formation after transplantation to NOD/ SCID mouse [27,28].…”

Section: Testosterone Is a 'New' Inducer For Cardiomyocyte Differentimentioning

confidence: 94%

Testosterone induces cardiomyocyte differentiation from embryonic stem cells

Hashimoto

Yuasa

2013

Journal of Molecular and Cellular Cardiology

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Wnt2 accelerates cardiac myocyte differentiation from ES-cell derived mesodermal cells via non-canonical pathway

Cited by 42 publications

References 48 publications

MicroRNA MiR-199a-5p Regulates Smooth Muscle Cell Proliferation and Morphology by Targeting WNT2 Signaling Pathway

MicroRNA MiR-199a-5p Regulates Smooth Muscle Cell Proliferation and Morphology by Targeting WNT2 Signaling Pathway

sfrp1 promotes cardiomyocyte differentiation in Xenopus via negative-feedback regulation of Wnt signalling

Testosterone induces cardiomyocyte differentiation from embryonic stem cells

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