Matrilin-2, an extracellular adaptor protein, is needed for the regeneration of muscle, nerve and other tissues

• Main Authors: Éva Korpos, Ferenc Deák, Ibolya Kiss
• Format: Article
• Language: English
• Published: Wolters Kluwer Medknow Publications 2015-01-01
• Series: Neural Regeneration Research
• Subjects: microtubule; axon; kinesin-5; Eg5; regeneration; monastrol; molecular motor protein; aging; neurodegenerative disorders; telomere shortening; MSCs; cellular therapy; traumatic brain injury; spinal cord injuries; dual diagnosis; diagnosis; complications; rehabilitation; post-concussion syndrome; brain concussion; blood brain barrier; phage display; peptide library; nanocarrier; targeting; Schwann cells; neurite outgrowth; neuromuscular junction (NMJ); multiple sclerosis; TGF-β/BMP-7/Smad signaling; myogenic differentiation; Trf3; tumor suppression
• Online Access: http://www.nrronline.org/article.asp?issn=1673-5374;year=2015;volume=10;issue=6;spage=866;epage=869;aulast=

The extracellular matrix (ECM) performs essential functions in the differentiation, maintenance and remodeling of tissues during development and regeneration, and it undergoes dynamic changes during remodeling concomitant to alterations in the cell-ECM interactions. Here we discuss recent data addressing the critical role of the widely expressed ECM protein, matrilin-2 (Matn2) in the timely onset of differentiation and regeneration processes in myogenic, neural and other tissues and in tumorigenesis. As a multiadhesion adaptor protein, it interacts with other ECM proteins and integrins. Matn2 promotes neurite outgrowth, Schwann cell migration, neuromuscular junction formation, skeletal muscle and liver regeneration and skin wound healing. Matn2 deposition by myoblasts is crucial for the timely induction of the global switch toward terminal myogenic differentiation during muscle regeneration by affecting transforming growth factor beta/bone morphogenetic protein 7/Smad and other signal transduction pathways. Depending on the type of tissue and the pathomechanism, Matn2 can also promote or suppress tumor growth.