中国神经再生研究(英文版) ›› 2019, Vol. 14 ›› Issue (8): 1380-1382.doi: 10.4103/1673-5374.253521

• 观点:退行性病与再生 • 上一篇    下一篇

半乳糖凝集素3 在脱髓鞘疾病治疗中的前景

  

  • 出版日期:2019-08-15 发布日期:2019-08-15

Galectin-3 prospects as a therapeutic agent for multiple sclerosis

Laura Thomas, Laura Andrea Pasquini   

  1. Polyc Department of Biological Chemistry, School of Pharmacy and Biochemistry, Institute of Chemistry Biological Physicochemistry (IQUIFIB), University of Buenos Aires and National Research Council (CONICET), Buenos Aires, Argentina
  • Online:2019-08-15 Published:2019-08-15
  • Contact: Laura Andrea Pasquini, PhD, laupasq@yahoo.com.
  • Supported by:

    This work was supported by grants from Agencia Nacional de Promoción Científica y Tecnológica (Argentina, PICT 20143116) and Universidad de Buenos Aires (20920160100683BA, to LAP).

摘要:

orcid: 0000-0003-4292-3463 (Laura Andrea Pasquini)

Abstract:

Galectin-3 (Gal-3) in oligodendrocyte (OLG) differentiation: OLGs are the cells in charge of myelination in the central nervous system (CNS), allowing rapid conduction of the neural action potential and giving trophic support to axons. OLGs undergo a series of changes throughout their life cycle: first, upon neural stem cell commitment to the OLG lineage, cells referred to as OLG precur sor cells (OPC) present a bipolar morphology, have proliferative and migratory capacity and express molecular markers like platelet-derived growth factor receptor alpha and neural/glial antigen 2;  next, in an intermediate stage called preOLG, OLGs are more ramified and express CNPase, Olig1 and O4, among others; finally, cells develop into myelin forming cells which express molecular markers like myelin basic protein (MBP), adenomatous polyposis polyposis and proteolipid protein. Worth pointing out, the actin cytoskeleton plays an important role in OLG maturation, as it evolves from pro-polymerization to pro-depolymerization dynamics, which allows axon ensheathing. These mechanisms are controlled in part by the relationship between MBP and actin disassembly proteins such as cofilin-1 and gelsolin. The latter are normally sequestered and inactivated by phosphatidylinositol 4,5-bisphosphate present in the plasma membrane. When MBP is expressed in mature OLG, it competes with gelsolin and cofilin-1 for phosphatidylinositol 4,5-bisphosphate binding, displacing and hence activating them, to trigger the disassembly of actin filaments.