期刊
BRITISH JOURNAL OF OPHTHALMOLOGY
卷 86, 期 1, 页码 97-101出版社
BRITISH MED JOURNAL PUBL GROUP
DOI: 10.1136/bjo.86.1.97
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资金
- Wellcome Trust Funding Source: Medline
Background: Sorsby's fundus dystrophy (SFD) and age related macular degeneration (ARMD) are retinal diseases associated with a high level of accumulation of mutant and wild type TIMP-3, respectively, in Bruch's membrane. The pathogenic role of TIMP-3 in these diseases is uncertain, but causative mutations have been identified in the TIMP-3 gene of patients with SFD. Recent reports that TIMP-3 causes apoptosis in certain cell types and not in others prompted the authors to investigate whether causes apoptosis in cultured retinal pigment epithelium (RPE) cells. Methods: RPE and MCF-7 cells (as a positive control) were initially infected with replication deficient adenovirus, to overexpress beta-golactosidose (RAdLacZ) or TIMP-3 (RAdTIMP-3). TIMP-3 was detected by blotting and ELISA. Cell viability was defined by cell counts. ISEL was used to investigate the mechanism of cell death. Results: Cultured RPE cells produced small quantities of endogenous TIMP-3 and remained viable. However, overexpression of TIMP-3 caused a dose related death of RPE cells. The mechanism of cell death was apoptosis. Conclusion: The previously unreported finding of TIMP-3 induced apoptosis of RPE cells may account some of the early features seen in SFD and ARMD.
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