calreticulin is required for tgf-β-induced epithelial-to-mesenchymal transition during cardiogenesis in mouse embryonic stem cells

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ID: 159090
2017
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Ranked #17 of 101 articles by views in nature reviews gastroenterology & hepatology

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Abstract
Calreticulin, a multifunctional endoplasmic reticulum resident protein, is required for TGF-β-induced epithelial-to-mesenchymal transition (EMT) and subsequent cardiomyogenesis. Using embryoid bodies (EBs) derived from calreticulin-null and wild-type (WT) embryonic stem cells (ESCs), we show that expression of EMT and cardiac differentiation markers is induced during differentiation of WT EBs. This induction is inhibited in the absence of calreticulin and can be mimicked by inhibiting TGF-β signaling in WT cells. The presence of calreticulin in WT cells permits TGF-β-mediated signaling via AKT/GSK3β and promotes repression of E-cadherin by SNAIL2/SLUG. This is paralleled by induction of N-cadherin in a process known as the cadherin switch. We show that regulated Ca2+ signaling between calreticulin and calcineurin is critical for the unabated TGF-β signaling that is necessary for the exit from pluripotency and the cadherin switch during EMT. Calreticulin is thus a key mediator of TGF-β-induced commencement of cardiomyogenesis in mouse ESCs.
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karimzadeh2017stemcalreticulin Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Fereshteh Karimzadeh;Michal Opas
Journal nature reviews gastroenterology & hepatology
Year 2017
DOI
10.1016/j.stemcr.2017.03.018
URL
http://www.sciencedirect.com/science/article/pii/S2213671117301248
Keywords
tgf-β emt cardiac differentiation

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