Abstract

The extracellular matrix is composed of a variety of macromolecular substances secreted by cells, which form a complex network that supports and connects tissue structures, regulates the morphogenesis of tissues, and maintains the physiological activities of cells. Tenascin-C, a secreted extracellular matrix glycoprotein, is abundantly expressed after exposure to pathological stimuli. It plays an important regulatory role in brain tumors, vascular diseases, and neurodegenerative diseases by mediating inflammatory responses, inducing brain damage, and promoting cell proliferation, migration, and angiogenesis through multiple signaling pathways. Therefore, tenascin-C may become a potential therapeutic target for intracranial diseases. Here, we review and discuss the latest literature regarding tenascin-C, and we comprehensively explain the role and clinical significance of tenascin-C in intracranial diseases.

Highlights

  • Tenascin-C (TN-C) was the first and most important member of the oligomeric glycoprotein family to be discovered

  • TN-C induces brain edema and Blood–brain barrier (BBB) destruction after subarachnoid hemorrhage (SAH), which may be related to matrix metalloprotein (MMP)-9 secretion and zonula occludens (ZO)-1 breakdown through the mitogen-activated protein kinase (MAPK) signaling pathway [50]

  • Cilostazol reportedly attenuates post-SAH cerebral vasospasm in rats [74], and its molecular mechanism may be related to the inhibition of TN-C expression through the protein kinase A system and MAPK pathway [75]

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Summary

Introduction

Tenascin-C (TN-C) was the first and most important member of the oligomeric glycoprotein family to be discovered. TN-C-induced tumor angiogenesis could be related to the binding and stimulatory effect of TN-C on endothelial cells [8]. Profound influence, exerting multiple effects, such as increasing cell migration and proliferation [12,13,14], downregulating focal adhesion integrity [15], promoting angiogenesis [16], altering ECM composition, and regulating gene expression [17].

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