BMP2 rescues deficient cell migration in Tgfbr3−/− epicardial cells and requires Src kinase

Patrick Allison, Daniella Espiritu, Todd D Camenisch

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

During embryogenesis, the epicardium undergoes proliferation, migration, and differentiation into several cardiac cell types which contribute to the coronary vessels. The type III transforming growth factor-β receptor (TGFβR3) is required for epicardial cell invasion and development of coronary vasculature in vivo. Bone Morphogenic Protein-2 (BMP2) is a driver of epicardial cell migration. Utilizing a primary epicardial cell line derived from Tgfbr3+/+ and Tgfbr3−/− mouse embryos, we show that Tgfbr3−/− epicardial cells are deficient in BMP2 mRNA expression. Tgfbr3−/− epicardial cells are deficient in 2-dimensional migration relative to Tgfbr3+/+ cells; BMP2 induces cellular migration to Tgfbr3+/+ levels without affecting proliferation. We further demonstrate that Src kinase activity is required for BMP2 driven Tgfbr3−/− migration. BMP2 also requires Src for filamentous actin polymerization in Tgfbr3−/− epicardial cells. Taken together, our data identifies a novel pathway in epicardial cell migration required for development of the coronary vessels.

Original languageEnglish (US)
Pages (from-to)1-10
Number of pages10
JournalCell Adhesion and Migration
DOIs
StateAccepted/In press - May 3 2016

Fingerprint

src-Family Kinases
Cell Movement
Bone and Bones
Proteins
Coronary Vessels
Growth Factor Receptors
Pericardium
Transforming Growth Factors
Polymerization
Embryonic Development
Actins
Embryonic Structures
Cell Line
Messenger RNA

Keywords

  • BMP2
  • epicardium
  • migration
  • Src
  • TGFβR3

ASJC Scopus subject areas

  • Cell Biology
  • Cellular and Molecular Neuroscience

Cite this

BMP2 rescues deficient cell migration in Tgfbr3−/− epicardial cells and requires Src kinase. / Allison, Patrick; Espiritu, Daniella; Camenisch, Todd D.

In: Cell Adhesion and Migration, 03.05.2016, p. 1-10.

Research output: Contribution to journalArticle

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