EndothelialCdkn1a(p21) Overexpression and Accelerated Senescence in a Mouse Model of Fuchs Endothelial Corneal Dystrophy | Zendy

Mario Matthaei | Zendy; Huan Meng | Zendy; Alan K. Meeker | Zendy; Charles G. Eberhart | Zendy; Albert S. Jun | Zendy

Open Access

EndothelialCdkn1a(p21) Overexpression and Accelerated Senescence in a Mouse Model of Fuchs Endothelial Corneal Dystrophy

Author(s) -

Mario Matthaei,

Huan Meng,

Alan K. Meeker,

Charles G. Eberhart,

Albert S. Jun

Publication year - 2012

Publication title -

investigative ophthalmology and visual science

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.935

H-Index - 218

eISSN - 1552-5783

pISSN - 0146-0404

DOI - 10.1167/iovs.12-9669

Subject(s) - senescence , biology , downregulation and upregulation , endothelium , genetically modified mouse , microbiology and biotechnology , mutant , endoplasmic reticulum , transgene , endocrinology , gene , genetics

Stress of the endoplasmic reticulum and oxidative stress play critical roles in the pathogenesis of Fuchs Endothelial Corneal Dystrophy (FECD). In the normal aging cornea, cellular stress has been associated with a loss in proliferative capacity (premature senescence) of corneal endothelial cells (CECs). The present study used a transgenic Col8a2(Q455K/Q455K) knock-in mouse model of early-onset FECD to identify the endothelial expression profile of specific cellular stress response-related targets, which may be relevant to late-onset FECD.

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