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Tenascin-C may aggravate left ventricular remodeling and function after myocardial infarction in mice.
Tenascin-C (TN-C) is an extracellular matrix glycoprotein with high bioactivity. It is expressed at low levels in normal adult heart, but upregulated under pathological conditions, such as myocardialExpand
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Imatinib mesylate prevents cerebral vasospasm after subarachnoid hemorrhage via inhibiting tenascin-C expression in rats
Platelet-derived growth factor (PDGF) has been implicated in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage (SAH), but the mechanism remains unknown. The purpose of this studyExpand
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Myristoyl moiety of HIV Nef is involved in regulation of the interaction with calmodulin in vivo.
Human immunodeficiency virus Nef is a myristoylated protein expressed early in infection by HIV. In addition to the well known down-regulation of the cell surface receptors CD4 and MHCI, Nef is ableExpand
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Tenascin-C May Accelerate Cardiac Fibrosis by Activating Macrophages via the Integrin &agr;V&bgr;3/Nuclear Factor–&kgr;B/Interleukin-6 Axis
Tenascin-C (TN-C) is an extracellular matrix protein not detected in normal adult heart, but expressed in several heart diseases closely associated with inflammation. Accumulating data suggest thatExpand
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Role of platelet-derived growth factor in cerebral vasospasm after subarachnoid hemorrhage in rats.
BACKGROUND AND PURPOSE The role of platelet-derived growth factor (PDGF) remains unknown in cerebral vasospasm after subarachnoid hemorrhage (SAH). In this study, we examined the effects of PDGFExpand
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Cytological features of adenocarcinoma admixed with small cell neuroendocrine carcinoma of the uterine cervix
Adenocarcinoma admixed with neuroendocrine carcinoma of the uterine cervix is a rare malignancy with a poor prognosis, and few reports have described the cytological features of this carcinoma. ToExpand
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Deficiency of tenascin-C and attenuation of blood-brain barrier disruption following experimental subarachnoid hemorrhage in mice.
OBJECT Tenascin-C (TNC), a matricellular protein, is induced in the brain following subarachnoid hemorrhage (SAH). The authors investigated if TNC causes brain edema and blood-brain barrier (BBB)Expand
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Tenascin‐C enhances crosstalk signaling of integrin αvβ3/PDGFR‐β complex by SRC recruitment promoting PDGF‐induced proliferation and migration in smooth muscle cells
Migration and proliferation of smooth muscle cells (SMCs) are key events during neointimal formation in pathological conditions of vessels. Tenascin‐C (TNC) is upregulated in the developing neointimaExpand
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Effects of Tenascin-C Knockout on Cerebral Vasospasm After Experimental Subarachnoid Hemorrhage in Mice
A matricellular protein tenascin-C (TNC) has been suggested to play a role in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage (SAH), but the direct evidence remains lacking. InExpand
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Atrial natriuretic peptide exerts protective action against angiotensin II-induced cardiac remodeling by attenuating inflammation via endothelin-1/endothelin receptor A cascade
We aimed to investigate whether atrial natriuretic peptide (ANP) attenuates angiotensin II (Ang II)-induced myocardial remodeling and to clarify the possible molecular mechanisms involved.Expand
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