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Tenascin‐C in Development and Disease of Blood Vessels
Author(s) -
ImanakaYoshida Kyoko,
Yoshida Toshimichi,
MiyagawaTomita Sachiko
Publication year - 2014
Publication title -
the anatomical record
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.678
H-Index - 62
eISSN - 1932-8494
pISSN - 1932-8486
DOI - 10.1002/ar.22985
Subject(s) - tenascin c , biology , paracrine signalling , matricellular protein , extracellular matrix , microbiology and biotechnology , intimal hyperplasia , autocrine signalling , embryonic stem cell , wound healing , vascular smooth muscle , elastin , pathology , immunology , medicine , endocrinology , biochemistry , receptor , smooth muscle , gene
ABSTRACT Tenascin‐C (TNC) is an extracellular glycoprotein categorized as a matricellular protein. It is highly expressed during embryonic development, wound healing, inflammation, and cancer invasion, and has a wide range of effects on cell response in tissue morphogenesis and remodeling including the cardiovascular system. In the heart, TNC is sparsely detected in normal adults but transiently expressed at restricted sites during embryonic development and in response to injury, playing an important role in myocardial remodeling. Although TNC in the vascular system appears more complex than in the heart, the expression of TNC in normal adult blood vessels is generally low. During embryonic development, vascular smooth muscle cells highly express TNC on maturation of the vascular wall, which is controlled in a way that depends on the embryonic site of cell origin. Strong expression of TNC is also linked with several pathological conditions such as cerebral vasospasm, intimal hyperplasia, pulmonary artery hypertension, and aortic aneurysm/ dissection. TNC synthesized by smooth muscle cells in response to developmental and environmental cues regulates cell responses such as proliferation, migration, differentiation, and survival in an autocrine/paracrine fashion and in a context‐dependent manner. Thus, TNC can be a key molecule in controlling cellular activity in adaptation during normal vascular development as well as tissue remodeling in pathological conditions. Anat Rec, 297:1747–1757, 2014. © 2014 Wiley Periodicals, Inc.