NDLI: Gα13 regulates MEF2-dependent gene transcription in endothelial cells: role in angiogenesis

Content Provider	Springer Nature Link
Author	Liu, Guoquan Han, Jingyan Profirovic, Jasmina Strekalova, Elena Voy Yasenetskaya, Tatyana A.
Copyright Year	2008
Abstract	The α subunit of heterotrimeric G13 protein is required for the embryonic angiogenesis (Offermanns et al., Science 275:533–536, 1997). However, the molecular mechanism of Gα13-dependent angiogenesis is not understood. Here, we show that myocyte-specific enhancer factor-2 (MEF2) mediates Gα13-dependent angiogenesis. Our data showed that constitutively activated Gα13Q226L stimulated MEF2-dependent gene transcription. In addition, downregulation of endogenous Gα13 inhibited thrombin-stimulated MEF2-dependent gene transcription in endothelial cells. Both Ca2+/calmodulin-dependent kinase IV (CaMKIV) and histone deacetylase 5 (HDAC5) were involved in Gα13-mediated MEF2-dependent gene transcription. Gα13Q226L also increased Ca2+/calmodulin-independent CaMKIV activity, while dominant negative mutant of CaMKIV inhibited MEF2-dependent gene transcription induced by Gα13Q226L. Furthermore, Gα13Q226L was able to derepress HDAC5-mediated repression of gene transcription and induce the translocation of HDAC5 from nucleus to cytoplasm. Finally, downregulation of endogenous Gα13 and MEF2 proteins in endothelial cells reduced cell proliferation and capillary tube formation. Decrease of endothelial cell proliferation that was caused by the Gα13 downregulation was partially restored by the constitutively active MEF2-VP16. Our studies suggest that MEF2 proteins are an important component in Gα13-mediated angiogenesis.
Starting Page	1
Ending Page	15
Page Count	15
File Format	PDF
ISSN	09696970
Journal	Angiogenesis
Volume Number	12
Issue Number	1
e-ISSN	15737209
Language	English
Publisher	Springer Netherlands
Publisher Date	2008-12-18
Publisher Place	Dordrecht
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Heterotrimeric G13 protein MEF2-dependent transcription Endothelium CaMKII HDAC5 Oncology Ophthalmology Cardiology Cell Biology Biomedicine general Cancer Research
Content Type	Text
Resource Type	Article
Subject	Physiology Clinical Biochemistry Cancer Research

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