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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Amir, Jawaria Morris, Stephan W. Siddiqui, M. A. Q. Lau, Lester F. Liu, Haibo Sun, Yi Chaqour, Brahim Hanna, Mary |
| Description | Author Affiliation: Hanna M ( Department of Cell Biology, State University of New York Downstate Medical Center, Brooklyn, New York 11203, USA.) |
| Abstract | Smooth muscle-rich tissues respond to mechanical overload by an adaptive hypertrophic growth combined with activation of angiogenesis, which potentiates their mechanical overload-bearing capabilities. Neovascularization is associated with mechanical strain-dependent induction of angiogenic factors such as CCN1, an immediate-early gene-encoded matricellular molecule critical for vascular development and repair. Here we have demonstrated that mechanical strain-dependent induction of the CCN1 gene involves signaling cascades through RhoA-mediated actin remodeling and the p38 stress-activated protein kinase (SAPK). Actin signaling controls serum response factor (SRF) activity via SRF interaction with the myocardin-related transcriptional activator (MRTF)-A and tethering to a single CArG box sequence within the CCN1 promoter. Such activity was abolished in mechanically stimulated mouse MRTF-A(-/-) cells or upon inhibition of CREB-binding protein (CBP) histone acetyltransferase (HAT) either pharmacologically or by siRNAs. Mechanical strain induced CBP-mediated acetylation of histones 3 and 4 at the SRF-binding site and within the CCN1 gene coding region. Inhibition of p38 SAPK reduced CBP HAT activity and its recruitment to the SRF.MRTF-A complex, whereas enforced induction of p38 by upstream activators (e.g. MKK3 and MKK6) enhanced both CBP HAT and CCN1 promoter activities. Similarly, mechanical overload-induced CCN1 gene expression in vivo was associated with nuclear localization of MRTF-A and enrichment of the CCN1 promoter with both MRTF-A and acetylated histone H3. Taken together, these data suggest that signal-controlled activation of SRF, MRTF-A, and CBP provides a novel connection between mechanical stimuli and angiogenic gene expression. |
| ISSN | 00219258 |
| e-ISSN | 1083351X |
| Journal | Journal of Biological Chemistry |
| Issue Number | 34 |
| Volume Number | 284 |
| Language | English |
| Publisher | American Society for Biochemistry and Molecular Biology (United States) |
| Publisher Date | 2009-08-21 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | CREB-Binding Protein Physiology Cysteine-Rich Protein 61 Genetics DNA-Binding Proteins Histone Acetyltransferases Metabolism Oncogene Proteins, Fusion Stress, Mechanical Trans-Activators Acetylation Drug Effects Animals Blotting, Western Antagonists & Inhibitors Cells, Cultured Chromatin Immunoprecipitation Enzyme Inhibitors Pharmacology Histones Immunohistochemistry Immunoprecipitation Mice Molecular Sequence Data Promoter Regions, Genetic Protein Binding Protein Transport Serum Response Element P38 Mitogen-Activated Protein Kinases Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Biochemistry Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Biochemistry Molecular Biology |
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