P58(IPK) inhibition of endoplasmic reticulum stress in human retinal capillary endothelial cells in vitro

CORC > 计算技术研究所 > 中国科学院计算技术研究所 > 中国科学院计算技术研究所期刊论文 > 英文

	P58(IPK) inhibition of endoplasmic reticulum stress in human retinal capillary endothelial cells in vitro
	Li, Bin 1,2; Li, Dong 3; Li, Gui-gang 1; Wang, Hao-wen 4; Yu, Ai-xia 4
刊名	MOLECULAR VISION
	2008-06-13
卷号	14 期号:133-34 页码:1122-1128
ISSN号	1090-0535
英文摘要	Purpose: The goal of this research was to determine if P58(IPK), a member of the Hsp40 family that inhibits eukaryotic initiation factor 2 alpha (eIF2 alpha), inhibits endoplasmic reticulum (ER) stress and leads to downregulated expression of vascular endothelial growth factor (VEGF) and decreased apoptosis in human retinal capillary endothelial cells (HRCECs). Methods: Recombinant vectors were constructed using P58 in adeno-associated virus type 2 (rAAV2-P58(IPK)) and P58 RNA in the plasmid pGIPZ (pGIPZ-P58(IPK)). The four experimental groups were: (1) non-transfected/non ER stressed control; (2) non-transfected/ER stressed; (3) rAAV2-P58(IPK)-transfected/ER stressed; and (4) pGIPZ-P58(IPK) RNAi transfected/ER stressed. ER stress was induced by treating cells with tunicamycin. Expression of P58(IPK) was determined in transfected cells. Expressions of the following factors were assessed: vascular endothelial growth factor (VEGF), C/EBP homologous protein (CHOP), activating transcription factor 4 (ATF4), and glucose-regulated protein 78 (GRP78). Apoptosis levels were also determined. Results: Significantly increased expression of P58(IPK) was detected in cells transfected with rAAV2-P58(IPK) (0.63 +/- 0.02) as compared to those transfected with pGIPZ-P58(IPK) RNAi (0.23 +/- 0.01). P58(IPK) expression was not different between the control transfected cells (rAAV2-GFP and pGIPZ-GFP). Following ER stress, expression levels of ATF-4, GRP78, CHOP, and VEGF in cells overexpressing P58(IPK) were not different from those in unstressed control cells. This inhibitory effect of P58(IPK) on the expression of ER stress-related factors was suppressed in cells transfected with pGIPZ-P58(IPK) RNAi. Apoptosis was significantly increased in cells transfected with pGIPZ-P58(IPK) RNAi but not with rAAV2-P58(IPK). Conclusions: The study demonstrates that P58(IPK) inhibits ER stress and plays an important role in maintaining balance and stability of the ER in HRCECs.
WOS研究方向	Biochemistry & Molecular Biology ; Ophthalmology
语种	英语
出版者	MOLECULAR VISION
WOS记录号	WOS:000257890600001
内容类型	期刊论文
源URL	[http://119.78.100.204/handle/2XEOYT63/11382]
专题	中国科学院计算技术研究所期刊论文_英文
通讯作者	Li, Bin
作者单位	1.Huazhong Univ Sci & Technol, Tongji Med Coll, Tongji Hosp, Dept Ophthalmol, Wuhan 430030, Hubei, Peoples R China 2.Sun Yat Sen Univ, Zhongshan Ophthalm Ctr, State Key Lab Ophthalmol, Guangzhou 510275, Guangdong, Peoples R China 3.Chinese Acad Sci, Inst Comp Technol, Network Res Div, Beijing, Peoples R China 4.Cent Hosp, E Zhuo City, Hubei, Peoples R China
推荐引用方式 GB/T 7714	Li, Bin,Li, Dong,Li, Gui-gang,et al. P58(IPK) inhibition of endoplasmic reticulum stress in human retinal capillary endothelial cells in vitro[J]. MOLECULAR VISION,2008,14(133-34):1122-1128.
APA	Li, Bin,Li, Dong,Li, Gui-gang,Wang, Hao-wen,&Yu, Ai-xia.(2008).P58(IPK) inhibition of endoplasmic reticulum stress in human retinal capillary endothelial cells in vitro.MOLECULAR VISION,14(133-34),1122-1128.
MLA	Li, Bin,et al."P58(IPK) inhibition of endoplasmic reticulum stress in human retinal capillary endothelial cells in vitro".MOLECULAR VISION 14.133-34(2008):1122-1128.