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The TAM-family receptor Mer mediates production of HGF through the RhoA-dependent pathway in response to apoptotic cells

Title
The TAM-family receptor Mer mediates production of HGF through the RhoA-dependent pathway in response to apoptotic cells
Authors
Park, Hyun-JungBaen, Ji-YeonLee, Ye-JiChoi, Youn-HeeKang, Jihee Lee
Ewha Authors
이지희최윤희
SCOPUS Author ID
이지희scopus; 최윤희scopus
Issue Date
2012
Journal Title
MOLECULAR BIOLOGY OF THE CELL
ISSN
1059-1524JCR Link
Citation
vol. 23, no. 16, pp. 3254 - 3265
Publisher
AMER SOC CELL BIOLOGY
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
The TAM receptor protein tyrosine kinases Tyro3, Axl, and Mer play important roles in macrophage function. We investigated the roles of the TAM receptors in mediating the induction of hepatocyte growth factor (HGF) during the interaction of macrophages with apoptotic cells. Mer-specific neutralizing antibody, small interfering RNA (siRNA), and a recombinant Mer protein (Mer/Fc) inhibited HGF mRNA and protein expression, as well as activation of RhoA, Akt, and specific mitogen-activated protein (MAP) kinases in response to apoptotic cells. Inhibition of Axl or Tyro3 with specific antibodies, siRNA, or Fc-fusion proteins did not prevent apoptotic cell-induced HGF mRNA and protein expression and did not inhibit activation of the postreceptor signaling molecules RhoA and certain MAP kinases, including extracellular signal-regulated protein kinase and c-Jun NH2-terminal kinase. However, Axl-and Tyro3-specific blockers did inhibit the activation of Akt and p38 MAP kinase in response to apoptotic cells. In addition, none of the TAM receptors mediated the effects of apoptotic cells on transforming growth factor-beta or epidermal growth factor mRNA expression. However, they were involved in the induction of vascular endothelial growth factor mRNA expression. Our data provide evidence that when macrophages interact with apoptotic cells, only Mer of the TAM-family receptors is responsible for mediating transcriptional HGF production through a RhoA-dependent pathway.
DOI
10.1091/mbc.E12-01-0029
Appears in Collections:
의과대학 > 의학과 > Journal papers
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