Beta-catenin signaling increases in proliferating NG2+ progenitors and astrocytes during post-traumatic gliogenesis in the adult brain.
Beta-catenin signaling increases in proliferating NG2+ progenitors and astrocytes during post-traumatic gliogenesis in the adult brain.
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DOI：
10.1002/stem.268
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发表时间：
2010-02
期刊：
影响因子：
5.2
通讯作者：
Horner, Philip J.
中科院分区：
文献类型：
--
作者：
White, Bryan D.;Nathe, Ryan J.;Maris, Don O.;Nguyen, Nghi K.;Goodson, Jamie M.;Moon, Randall T.;Horner, Philip J.
Wnt/β-catenin signaling can influence the proliferation and differentiation of progenitor populations in the hippocampus and subventricular zone, known germinal centers in the adult mouse brain. It is not known whether β-catenin signaling occurs in quiescent glial progenitors in cortex or spinal cord, nor is it known whether β-catenin is involved in the activation of glial progenitor populations after injury. Using a β-catenin reporter mouse (BATGAL mouse), we show that β-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 β-catenin signaling increased in the cortex and SCZ following traumatic brain injury (TBI) but did not following spinal cord injury. Initially after TBI, β-catenin signaling was predominantly increased in a subset of NG2+ progenitors in the cortex. One week following injury, the majority of β-catenin signaling appeared in reactive astrocytes but not oligodendrocytes. Bromodeoxyuridine (BrdU) paradigms and Ki-67 staining showed that the increase in β-catenin signaling occurred in newly born cells and was sustained after cell division. Dividing cells with β-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 β-catenin signaling in the cortex, confirming that the majority of β-catenin signaling after TBI occurs in newly born cells. These data argue for manipulating the Wnt/β-catenin pathway after TBI as a way to modify post-traumatic gliogenesis.
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DOI：
10.1023/a:1025751900356
发表时间：
2002-07-01
期刊：
JOURNAL OF NEUROCYTOLOGY
影响因子：
--
作者：
Butt, AM;Kiff, J;Berry, M
通讯作者：
Berry, M
影响因子：
2.7
作者：
Hao, J;Li, TG;Zhao, GQ
通讯作者：
Zhao, GQ
影响因子：
6.2
作者：
Burns, Kevin A.;Murphy, Brian;Kuan, Chia-Yi
通讯作者：
Kuan, Chia-Yi
影响因子：
3.3
作者：
Mothe, AJ;Tator, CH
通讯作者：
Tator, CH
Wnt/β-catenin信号传导控制血脑屏障的发展。
影响因子：
7.8
作者：
Liebner, Stefan;Corada, Monica;Bangsow, Thorsten;Babbage, Jane;Taddei, Andrea;Czupalla, Cathrin J.;Reis, Marco;Felici, Angelina;Wolburg, Hartwig;Fruttiger, Marcus;Taketo, Makoto M.;von Melchner, Harald;Plate, Karl Heinz;Gerhardt, Holger;Dejana, Elisabetta
通讯作者：
Dejana, Elisabetta