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Robert P. Mecham
Researcher at Washington University in St. Louis
Publications - 328
Citations - 23408
Robert P. Mecham is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Elastin & Tropoelastin. The author has an hindex of 79, co-authored 313 publications receiving 21786 citations. Previous affiliations of Robert P. Mecham include Jewish Hospital & Boston University.
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Journal ArticleDOI
Vascular Extracellular Matrix and Arterial Mechanics
TL;DR: By correlating vessel mechanics with physiological blood pressure across animal species and in mice with altered vessel compliance, it is shown that cardiac and vascular development are physiologically coupled, and there is evidence for a universal elastic modulus that controls the parameters of ECM deposition in vessel wall development.
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Elastin is an essential determinant of arterial morphogenesis
Dean Y. Li,Benjamin S. Brooke,Elaine C. Davis,Robert P. Mecham,Lise K. Sorensen,Beth B. Boak,Ernst J. Eichwald,Mark T. Keating +7 more
TL;DR: Elastin has an unanticipated regulatory function during arterial development, controlling proliferation of smooth muscle and stabilizing arterial structure.
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Extracellular matrix 4: the elastic fiber.
TL;DR: Analysis of the elastin gene has demonstrated that hydrophobic and cross‐linking domains are encoded in separate exons and that there is significant alternative splicing, resulting in multiple isoforms of tropoelastin.
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TGF-β–dependent pathogenesis of mitral valve prolapse in a mouse model of Marfan syndrome
Connie M. Ng,Alan Cheng,Loretha Myers,Francisco Martinez-Murillo,Chunfa Jie,Djahida Bedja,Kathleen L. Gabrielson,Jennifer M.W. Hausladen,Robert P. Mecham,Daniel P. Judge,Harry C. Dietz,Harry C. Dietz +11 more
TL;DR: In this article, the authors showed that increased TGF-beta signaling may contribute to the multisystem pathogenesis of Marfan syndrome, including the development of myxomatous changes of the atrioventricular valves.
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Chemotactic activity of elastin-derived peptides.
TL;DR: Elastin-degradation products enriched in cross-linking regions recruit inflammatory cells in vivo and that elastin proteolysis, characteristic of emphysema, may be a signal for recruitment of mononuclear phagocytes into the lungs.