Casein kinase-2 inhibition promotes retinal ganglion cell survival after acute intraocular pressure elevation
作者机构:Joint Shantou International Eye Center of Shantou University and The Chinese University of Hong KongShantouGuangdong ProvinceChina Shantou University Medical CollegeShantouGuangdong ProvinceChina Beijing Tongren Eye CenterBeijing Tongren HospitalCapital Medical UniversityBeijingChina Department of Ophthalmology and Visual SciencesThe Chinese University of Hong KongHong Kong Special Administrative RegionChina
出 版 物:《Neural Regeneration Research》 (中国神经再生研究(英文版))
年 卷 期:2024年第19卷第5期
页 面:1112-1118页
核心收录:
学科分类:1002[医学-临床医学] 100212[医学-眼科学] 10[医学]
基 金:supported by the National Natural Science Foundation of China,Nos.81570849,81100931 the Natural Science Foundation of Guangdong Province of China,Nos.2015A030313446,2020A1515011413(all to LPC)
主 题:casein kinase-2 glaucoma intraocular pressure elevation macrophages retinal ganglion cells
摘 要:Intraocular pressure elevation can induce retinal ganglion cell death and is a clinically reversible risk factor for glaucoma,the leading cause of irreversible *** previously demonstrated that casein kinase-2 inhibition can promote retinal ganglion cell survival and axonal regeneration in rats after optic nerve *** investigate the underlying mechanism,in the current study we increased the intraocular pressure of adult rats to 75 mmHg for 2 hours and then administered a casein kinase-2 inhibitor(4,5,6,7-tetrabromo-2-azabenzimidazole or 2-dimethylamino-4,5,6,7-tetrabromo-1H-benzimidazole)by intravitreal *** found that intravitreal injection of 4,5,6,7-tetrabromo-2-azabenzimidazole or 2-dimethylamino-4,5,6,7-tetrabromo-1H-benzimidazole promoted retinal ganglion cell survival and reduced the number of infiltrating *** analysis showed that the mitogen activated protein kinase signaling pathway was involved in the response to intraocular pressure elevation but was not modulated by the casein kinase-2 ***,casein kinase-2 inhibition downregulated the expression of genes(Cck,Htrsa,Nef1,Htrlb,Prph,Chat,Slc18a3,Slc5a7,Scn1b,Crybb2,Tsga10ip,and Vstm21)involved in intraocular pressure *** data indicate that inhibition of casein kinase-2 can enhance retinal ganglion cell survival in rats after acute intraocular pressure elevation via macrophage inactivation.