@article {1549019,
	title = {TNFα activates MAPK and Jak-Stat pathways to promote mouse M{\"u}ller cell proliferation},
	journal = {Exp Eye Res},
	volume = {202},
	year = {2021},
	month = {2021 Jan},
	pages = {108353},
	abstract = {Mouse M{\"u}ller cells, considered as dormant retinal progenitors, often respond to retinal injury by undergoing reactive gliosis rather than displaying neural regenerative responses. Tumor necrosis factor alpha (TNFα) is a key cytokines induced after injury and implicated in mediating inflammatory and neural regenerative responses in zebrafish. To investigate the involvement of TNFα in mouse retinal injury, adult C57BL/6J mice were subjected to light damage for 14 consecutive days. TNFα was elevated in the retina of mice exposed to light damage, which induced M{\"u}ller cell proliferation in vitro. Affymetrix microarray showed that, in M{\"u}ller cells, TNFα induces up-regulation of inflammatory and proliferation-related genes, including NFKB2, leukemia inhibitory factor, interleukin-6, janus kinase (Jak) 1, Jak2, signal transducer and activator of transcription (Stat) 1, Stat2, mitogen-activated protein kinase (MAPK) 7, and MAP4K4 but down-regulation of neuroprogenitor genes, including Sox9, Ascl1, Wnt2 and Hes1. Blocking the Jak/Stat and MAPK pathways attenuated TNFα-induced M{\"u}ller cell proliferation. These results suggest that TNFα may drive the proliferation and inflammatory response, rather than the neural regenerative potential, of mouse M{\"u}ller cells.},
	issn = {1096-0007},
	doi = {10.1016/j.exer.2020.108353},
	author = {Niu, Liangliang and Fang, Yuan and Yao, Xiaoqian and Zhang, Yi and Wu, Jihong and Chen, Dong Feng and Sun, Xinghuai}
}
