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Claudin-3 and claudin-19 partially restore native phenotype to ARPE-19 cells via effects on tight junctions and gene expression

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WOS被引频次:7
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成果类型:
期刊论文
作者:
Peng, Shaomin;Wang, Shao-Bin;Singh, Deepti;Zhao, Peter Y. C.;Davis, Katherine;Chen, Bo;Adelman, Ron A.;Rizzolo, Lawrence J.*
通讯作者:
Rizzolo, Lawrence J.
作者机构:
[Peng, Shaomin] Cent S Univ, Aier Sch Ophthalmol, Changsha, Hunan, Peoples R China.
[Davis, Katherine; Peng, Shaomin; Singh, Deepti; Wang, Shao-Bin; Zhao, Peter Y. C.; Rizzolo, Lawrence J.] Yale Univ, Sch Med, Dept Surg, POB 208062, New Haven, CT 06520 USA.
[Davis, Katherine; Peng, Shaomin; Singh, Deepti; Wang, Shao-Bin; Zhao, Peter Y. C.; Rizzolo, Lawrence J.; Chen, Bo; Adelman, Ron A.] Yale Univ, Sch Med, Dept Ophthalmol, 333 Cedar St, New Haven, CT 06520 USA.
通讯机构:
[Rizzolo, Lawrence J.] Yale Univ, Sch Med, Dept Surg, POB 208062, New Haven, CT 06520 USA.
语种:
英文
关键词:
Claudin;Tight junction;AKT;Retinal pigment epithelium;Outer blood-retinal barrier;Wound-healing
期刊:
Experimental Eye Research
ISSN:
0014-4835
年:
2016
卷:
151
页码:
179-189
文献类别:
WOS:Article
所属学科:
ESI学科类别:临床医学;WOS学科类别:Ophthalmology
入藏号:
WOS:000385607300023;PMID:27593915
基金类别:
Connecticut Regenerative Medicine Research Fund [14-SCB-YALE-18]; Department of Defense [W81XWH-15-1-0029]; Alonzo Family Fund; National Natural Science Foundation of China [81570867]; Science Research Foundation of Aier Eye Hospital Group [AF151D06]; Newman's Own Foundation; Leir Foundation; Research to Prevent Blindness (Yale University)
机构署名:
本校为第一机构
院系归属:
爱尔眼科学院
摘要:
Mutations of claudin-19 cause severe ocular deficits that are not easily reconciled with its role in regulating the outer blood retinal barrier. ARPE-19 is a widely used culture model of the retinal pigment epithelium (RPE). ARPE-19 is unique among epithelial cell lines, because it expresses all tight junction proteins except claudin family members. ARPE-19 also loses aspects of the RPE phenotype with cell passage. This study asks whether exogenous expression of the main RPE claudins, claudin-3 and claudin-19, would restore RPE phenotype, and whether these claudins have distinct roles in RPE. An Ussing chamber was used to measure the transepithelial electrical resistance and transepithelial electrical potential. These measurements were used to estimate the permeability co-efficients of ions. The trans epithelial diffusion of polyethylene glycols were used to examine the leak pathway of tight junctions. Wound-healing, quantitative RT-PCR and immunoblotting examined diverse aspects of the RPE phenotype. Over-expression of either claudin decreased the permeability of small ions and polyethylene glycol. Both claudins were slightly cation-specific, but claudin-3 was less permeable to large solutes. Claudin expression widely affected gene expression to partially restore RPE phenotype. Claudins redistributed filamentous actin from stress fibers to circumferential bands associated with tight junctions, and made wound-healing more epithelial-like. Both claudins increased the expression of genes related to RPE core functions and increased steady-state levels of phosphorylated-AKT. In conclusion, claudin-3 and claudin-19 formed general permeability barriers and affected cell morphology, proliferation, migration, AKT signaling, and gene expression. When claudins are exogenously expressed, ARPE-19 more closely model native RPE. (C) 2016 Elsevier Ltd. All rights reserved.
参考文献:
Ablonczy Z, 2011, INVEST OPHTH VIS SCI, V52, P8614, DOI 10.1167/iovs.11-8021
Ahmado A, 2011, INVEST OPHTH VIS SCI, V52, P7148, DOI 10.1167/iovs.10-6374
Balda MS, 1996, J CELL BIOL, V134, P1031, DOI 10.1083/jcb.134.4.1031
Ban Y, 2000, AM J PHYSIOL-CELL PH, V279, pC744
Cai H, 2006, MOL VIS, V12, P1

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