Abstract
Stroke is still one of the most common causes for mortality and morbidity worldwide. Following acute stroke onset, biochemical and cellular changes induce further brain injury such as neuroinflammation, cell death, and blood-brain barrier disruption. Matricellular proteins are non-structural proteins induced by many stimuli and tissue damage including stroke induction, while its levels are generally low in a normal physiological condition in adult tissues. Currently, a matricellular protein tenascin-C (TNC) is considered to be an important inducer to promote neuroinflammatory cascades and the resultant pathology in stroke. TNC is upregulated in cerebral arteries and brain tissues including astrocytes, neurons, and brain capillary endothelial cells following subarachnoid hemorrhage (SAH). TNC may be involved in blood-brain barrier disruption, neuronal apoptosis, and cerebral vasospasm via the activation of mitogen-activated protein kinases and nuclear factor-kappa B following SAH. In addition, post-SAH TNC levels in cerebrospinal fluid predicted the development of delayed cerebral ischemia and angiographic vasospasm in clinical settings. On the other hand, TNC is reported to promote fibrosis and exert repair effects for an experimental aneurysm via macrophages-induced migration and proliferation of smooth muscle cells. The authors review TNC-induced inflammatory signal cascades and the relationships with other matricellular proteins in stroke-related pathology.
Highlights
Stroke is a large public concern in terms of both human and financial resources [1, 2]
We focus on a Matricellular proteins (MCPs) tenascin-C (TNC) involved in neuroinflammation following stroke, and highlight current evidence for its use as a clinical biomarker and a therapeutic target
Its N-terminal contains highly conserved heptad repeats, followed by epidermal growth factor (EGF)-like repeats and up to fibronectin type III (FN III) repeats comprised of universal repeats and alternatively spliced repeats; and a fibrinogen repeat domain is located at the C-terminal [25, 27,28,29,30]
Summary
Stroke is a large public concern in terms of both human and financial resources [1, 2]. Neuroinflammation is a key pathologic change arising from stroke Findings from both clinical and animal studies have indicated that inflammatory reactions may contribute to the development of brain injury following stroke [3,4,5]. Post-stroke tissue damage releases secondary breakdown products of brain tissue and blood components. The TLR4 signaling pathway is involved in the initial steps of neuroinflammation cascades, which result in brain injury such as vasogenic and cytotoxic edema and blood-brain barrier (BBB) disruption [11]. Neuroinflammation is currently considered to be a critical factor contributing to morbidity and mortality in stroke patients who survive the initial brain damage and needs to be addressed in order to improve clinical outcomes [11,12,13]. We focus on a MCP tenascin-C (TNC) involved in neuroinflammation following stroke, and highlight current evidence for its use as a clinical biomarker and a therapeutic target
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
