T-cadherin promotes vascular smooth muscle cell dedifferentiation via a GSK3β-inactivation dependent mechanism

Cellular Signalling
Agne FrismantieneMaria Philippova

Abstract

Participation of the cadherin superfamily of adhesion molecules in smooth muscle cell (SMC) phenotype modulation is poorly understood. Immunohistochemical analyses of arterial lesions indirectly suggest upregulated expression of atypical glycosylphosphatidylinositol-anchored T-cadherin on vascular SMCs as a molecular indicator of the dedifferentiated/proliferative phenotype. This study investigated the role of T-cadherin in SMC phenotypic modulation. Morphological, molecular and functional SMC-signature characteristics of rat, porcine and human arterial SMCs stably transduced with respect to T-cadherin upregulation (Tcad+) or T-cadherin-deficiency (shTcad) were compared with their respective control transductants (E-SMCs or shC-SMCs). Tcad+-SMCs displayed several characteristics of the dedifferentiated phenotype including loss of spindle morphology, reduced/disorganized stress fiber formation, decay of SMC-differentiation markers (smooth muscle α-actin, smooth muscle myosin heavy chain, h-caldesmon), gain of SMC-dedifferentiation marker calmodulin, reduced levels of myocardin, nuclear-to-cytoplasmic redistribution of the myocardin related transcription factors MRTFA/B and increased proliferative and migratory capacities. T-cadh...Continue Reading

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Citations

Oct 13, 2019·Developmental Biology·Samir A BelloJosé E García-Arrarás
Feb 8, 2018·Cellular Signalling·Agne FrismantieneTherese J Resink

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