Academic Journal

The Effect of Tissue Inhibitor of Metalloproteinases on Scar Formation after Spinal Cord Injury

التفاصيل البيبلوغرافية
العنوان: The Effect of Tissue Inhibitor of Metalloproteinases on Scar Formation after Spinal Cord Injury
المؤلفون: Raveena R. Mishra, Brooke E. Nielsen, Melissa A. Trudrung, Samuel Lee, Luke J. Bolstad, Daniel J. Hellenbrand, Amgad S. Hanna
المصدر: Cells, Vol 13, Iss 18, p 1547 (2024)
بيانات النشر: MDPI AG, 2024.
سنة النشر: 2024
المجموعة: LCC:Cytology
مصطلحات موضوعية: TIMP-1, spinal cord injury, astrocytes, activation, blood–brain barrier, blood–spinal cord barrier, Cytology, QH573-671
الوصف: Spinal cord injury (SCI) often results in permanent loss of motor and sensory function. After SCI, the blood–spinal cord barrier (BSCB) is disrupted, causing the infiltration of neutrophils and macrophages, which secrete several kinds of cytokines, as well as matrix metalloproteinases (MMPs). MMPs are proteases capable of degrading various extracellular matrix (ECM) proteins, as well as many non-matrix substrates. The tissue inhibitor of MMPs (TIMP)-1 is significantly upregulated post-SCI and operates via MMP-dependent and MMP-independent pathways. Through the MMP-dependent pathway, TIMP-1 directly reduces inflammation and destruction of the ECM by binding and blocking the catalytic domains of MMPs. Thus, TIMP-1 helps preserve the BSCB and reduces immune cell infiltration. The MMP-independent pathway involves TIMP-1’s cytokine-like functions, in which it binds specific TIMP surface receptors. Through receptor binding, TIMP-1 can stimulate the proliferation of several types of cells, including keratinocytes, aortic smooth muscle cells, skin epithelial cells, corneal epithelial cells, and astrocytes. TIMP-1 induces astrocyte proliferation, modulates microglia activation, and increases myelination and neurite extension in the central nervous system (CNS). In addition, TIMP-1 also regulates apoptosis and promotes cell survival through direct signaling. This review provides a comprehensive assessment of TIMP-1, specifically regarding its contribution to inflammation, ECM remodeling, and scar formation after SCI.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 2073-4409
Relation: https://www.mdpi.com/2073-4409/13/18/1547; https://doaj.org/toc/2073-4409
DOI: 10.3390/cells13181547
URL الوصول: https://doaj.org/article/32455382a36f4d979a687d92a529f470
رقم الانضمام: edsdoj.32455382a36f4d979a687d92a529f470
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:20734409
DOI:10.3390/cells13181547