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Hyaluronic acid promotes angiogenesis by inducing RHAMM-TGFβ receptor interaction via CD44-PKCδ

Title
Hyaluronic acid promotes angiogenesis by inducing RHAMM-TGFβ receptor interaction via CD44-PKCδ
Authors
Park D.Kim Y.Kim H.Kim K.Lee Y.-S.Choe J.Hahn J.-H.Lee H.Jeon J.Choi C.Kim Y.-M.Jeoung D.
Ewha Authors
이윤실
SCOPUS Author ID
이윤실scopus
Issue Date
2012
Journal Title
Molecules and Cells
ISSN
1016-8478JCR Link
Citation
vol. 33, no. 6, pp. 563 - 574
Indexed
SCI; SCIE; SCOPUS; KCI WOS scopus
Abstract
Hyaluronic acid (HA) has been shown to promote angio-genesis. However, the mechanism behind this effect remains largely unknown. Therefore, in this study, the mechanism of HA-induced angiogenesis was examined. CD44 and PKCδ were shown to be necessary for induction of the receptor for HA-mediated cell motility (RHAMM), a HA-binding protein. RHAMM was necessary for HA-pro-moted cellular invasion and endothelial cell tube formation. Cytokine arrays showed that HA induced the expression of plasminogen activator-inhibitor-1 (PAI), a downstream target of TGFβ receptor signaling. The induction of PAI-1 was dependent on CD44 and PKCδ. HA also induced an interaction between RHAMM and TGFβ receptor I, and induction of PAI-1 was dependent on RHAMM and TGFβ receptor I. Histone deacetylase 3 (HDAC3), which is decreased by HA via rac1, reduced induction of plasminogen activator inhibitor-1 (PAI-1) by HA. ERK, which interacts with RHAMM, was necessary for induction of PAI-1 by HA. Snail, a downstream target of TGFβ signaling, was also necessary for induction of PAI-1. The down regulation of PAI-1 prevented HA from enhancing endothelial cell tube formation and from inducing expression of angiogenic factors, such as ICAM-1, VCAM-1 and MMP-2. HDAC3 also exerted reduced expression of MMP-2. In this study, we provide a novel mechanism of HA-promoted angiogenesis, which involved RHAMM-TGFβRI signaling necessary for induction of PAI-1. © 2012 KSMCB.
DOI
10.1007/s10059-012-2294-1
Appears in Collections:
약학대학 > 약학과 > Journal papers
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