Gene/Protein Disease Symptom Drug Enzyme Compound
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Subarachnoid hemorrhage (SAH) resulting from the rupture of a cerebral aneurysm represents one major cause of stroke. SAH may be followed by a spontaneous severe contraction of major cerebral arteries, a condition referred to as cerebral vasospasm. Vasospasm may result in brain ischemia or actual tissue death. This constrictive vascular state is devastating, remains largely untreatable, and is a major cause of morbidity and mortality in SAH patients. Approximately 30,000 Americans are affected by this condition each year. The overall death rates are 25%, and significant neurological complications occur in 50% of individuals who survive the initial bleed. This report highlights some of the important aspects of this vascular disease.
Anat Rec 1998 04
PMID:Stroke: anatomy of a catastrophic event. 960 61

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 (Hoboken) 2014 Sep
PMID:Tenascin-C in development and disease of blood vessels. 2512 86