Long-term cultivation of human corneal endothelial cells by telomerase expression

Experimental Eye Research
Zhiping LiuZhichong Wang

Abstract

The objective of this study was to explore the potential role of human telomerase reverse transcriptase (TERT) in extending the proliferative lifespan of human corneal endothelial cells (HCECs) under long-term cultivation. A primary culture was initiated with a pure population of HCECs in DMEM/F12 media containing 10% fetal bovine serum and other various supplements. TERT gene was successfully transfected into normal HCECs. A stable HCECs cell line (TERT-HCECs) that expressed TERT was established. The cells could be subcultured for 36 passages. Within this line of cells, TERT not only extended proliferative lifespan and inhibited apoptosis but also enhanced the cell line remaining the normal characteristics similar to HCECs. There were no significantly differences in the expression of the pump function related proteins voltage dependent anion channel 3 (VDAC3), sodium bicarbonate cotransporter member 4 (SLC4A4), chloride channel protein 3 (CLCN3), Na(+)/K(+)-ATPase α1, and ZO-1 in the cell line TERT-HCECs and primary HCECs. TERT-HCECs formed a monolayer cell sheet, maintained similar cell junction formation and pump function with primary HCECs. Karyotype analysis exhibited normal chromosomal numbers. The soft agar colony assay ...Continue Reading

References

Jul 1, 1992·Experimental Gerontology·C B HarleyR C Allsopp
Jan 1, 1992·Graefe's Archive for Clinical and Experimental Ophthalmology = Albrecht Von Graefes Archiv Für Klinische Und Experimentelle Ophthalmologie·B FoetsL Missotten
Jan 1, 1988·Archives of Ophthalmology·M MatsudaS M MacRae
Feb 1, 1972·The Journal of Physiology·S Dikstein, D M Maurice
Feb 1, 1972·The Journal of Physiology·D M Maurice
Jun 1, 1994·Ophthalmology·W M BourneD O Hodge
Dec 1, 1993·The Journal of Cell Biology·M FuruseS Tsukita
Mar 1, 1996·The British Journal of Ophthalmology·E W JohnstoneK A Williams
May 30, 1997·The Journal of Biological Chemistry·M Mandal, R Kumar
Apr 1, 1997·European Journal of Cancer : Official Journal for European Organization for Research and Treatment of Cancer (EORTC) [and] European Association for Cancer Research (EACR)·A M BurgerD R Newell
Mar 6, 1999·The Journal of Biological Chemistry·W FuM P Mattson
Jul 4, 2001·International Journal of Cancer. Journal International Du Cancer·L S GuanZ Y Wang
Nov 16, 2001·Archives of Ophthalmology·Q J LiT P O'Brien
Jul 9, 2002·The Journal of Biological Chemistry·Lynne W ElmoreShawn E Holt
Jun 11, 2003·Archives of Ophthalmology·Bo HuangJay S Pepose
Aug 25, 2004·Experimental Eye Research·Tatsuya MimuraSatoru Yamagami
Aug 25, 2004·Investigative Ophthalmology & Visual Science·Tatsuya MimuraShiro Amano
Jan 27, 2005·Investigative Ophthalmology & Visual Science·Danielle M RobertsonJames V Jester
Jun 28, 2005·Investigative Ophthalmology & Visual Science·Xiao-Qin HuangDavid Wan-Cheng Li
Mar 28, 2006·Investigative Ophthalmology & Visual Science·Tatsuya Mimura, Nancy C Joyce
Sep 28, 2006·Investigative Ophthalmology & Visual Science·Kikuko EnomotoNancy C Joyce
Apr 4, 2008·Investigative Ophthalmology & Visual Science·Efdal YoeruekPeter Szurman
Oct 11, 2008·Tissue Engineering. Part C, Methods·Tongkui CuiXiaohong Wang
Nov 18, 2008·Cell·Antonia Tomás-LobaMaria A Blasco
Oct 10, 2009·Ophthalmology·Adam H RossUNKNOWN National Health Service Blood and Transplant Ocular Tissue Advisory Group and Contributing Ophthalmologists
Oct 27, 2009·Tissue Engineering. Part C, Methods·Tatsuya MimuraShiro Amano
Jan 26, 2010·Cornea·Rahamim Avisar, Dov Weinberger
Sep 13, 2011·Experimental Eye Research·Nancy C Joyce

❮ Previous
Next ❯

Related Concepts

Related Feeds

Apoptosis in Cancer

Apoptosis is an important mechanism in cancer. By evading apoptosis, tumors can continue to grow without regulation and metastasize systemically. Many therapies are evaluating the use of pro-apoptotic activation to eliminate cancer growth. Here is the latest research on apoptosis in cancer.

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis