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Please add updates@feedmyinbox.com to your address book to make sure you receive these messages in the future. RegenMD Beta-catenin signaling increases in proliferating NG2+ progenitors and astrocytes during post-traumatic gliogenesis in the adult brain. May 15, 2010 at 8:36 AM Related Articles Beta-catenin signaling increases in proliferating NG2+ progenitors and astrocytes during post-traumatic gliogenesis in the adult brain. Stem Cells. 2010 Feb;28(2):297-307 Authors: White BD, Nathe RJ, Maris DO, Nguyen NK, Goodson JM, Moon RT, Horner PJ Wnt/beta-catenin signaling can influence the proliferation and differentiation of progenitor populations in the hippocampus and subventricular zone, kno! wn germinal centers in the adult mouse brain. It is not known whether beta-catenin signaling occurs in quiescent glial progenitors in cortex or spinal cord, nor is it known whether beta-catenin is involved in the activation of glial progenitor populations after injury. Using a beta-catenin reporter mouse (BATGAL mouse), we show that beta-catenin signaling occurs in NG2 chondroitin sulfate proteoglycan+ (NG2) progenitors in the cortex, in subcallosal zone (SCZ) progenitors, and in subependymal cells surrounding the central canal. Interestingly, cells with beta-catenin signaling increased in the cortex and SCZ following traumatic brain injury (TBI) but did not following spinal cord injury. Initially after TBI, beta-catenin signaling was predominantly increased in a subset of NG2+ progenitors in the cortex. One week following injury, the majority of beta-catenin signaling appeared in reactive astrocytes but not oligodendrocytes. Bromodeoxyuridine (BrdU) paradigms and Ki-67 sta! ining showed that the increase in beta-catenin signaling occur! red in n ewly born cells and was sustained after cell division. Dividing cells with beta-catenin signaling were initially NG2+; however, by four days after a single injection of BrdU, they were predominantly astrocytes. Infusing animals with the mitotic inhibitor cytosine arabinoside prevented the increase of beta-catenin signaling in the cortex, confirming that the majority of beta-catenin signaling after TBI occurs in newly born cells. These data argue for manipulating the Wnt/beta-catenin pathway after TBI as a way to modify post-traumatic gliogenesis. PMID: 19960516 [PubMed - indexed for MEDLINE]   This email was sent to regenmd@gmail.com.  Account Login Don't want to receive this feed any longer? Unsubscribe here This email was carefully delivered by Feed My Inbox. 230 Franklin Road Suite 814 Franklin, TN 37064