RGMa mediates reactive astrogliosis and glial scar formation through TGFβ1/Smad2/3 signaling after stroke

• Published in: Cell death and differentiation Vol. 25; no. 8; pp. 1503 - 1516
• Main Authors: Zhang, Rongrong, Wu, Yanping, Xie, Fei, Zhong, Yiliang, Wang, Yu, Xu, Mengxue, Feng, Jinzhou, Charish, Jason, Monnier, Philippe P., Qin, Xinyue
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 01.08.2018; Nature Publishing Group
• Subjects: 13; 13/1; 13/21; 13/51; 13/89; 13/95; 14/19; 14/63; 42/109; 631/378/2596/1308; 631/45/612; 82/80; Activin; Apoptosis; Astrocytes; Biochemistry; Biomedical and Life Sciences; Cell adhesion & migration; Cell Biology; Cell Cycle Analysis; Cell migration; Cerebral blood flow; Chondroitin sulfate; Glial fibrillary acidic protein; Gliosis; Hypertrophy; Ischemia; Life Sciences; Phosphorylation; Proteoglycans; Recovery of function; Regeneration; Reperfusion; Rodents; Scars; Smad2 protein; Stem Cells; Stroke; Therapeutic applications; Transforming growth factor; Transforming growth factor-b1

In response to stroke, astrocytes become reactive astrogliosis and are a major component of a glial scar. This results in the formation of both a physical and chemical (production of chondroitin sulfate proteoglycans) barrier, which prevent neurite regeneration that, in turn, interferes with functio...