کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10739061 | 1046858 | 2005 | 16 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Differences in gene expression profiles in dermal fibroblasts from control and patients with age-related macular degeneration elicited by oxidative injury
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کلمات کلیدی
CNVXTTAREDSRPEAMDRT-PCRROIPBSDMEMChoroidal neovascularization - neovascularization choroidalROS - ROSOxidative injury - آسیب اکسیداتیوretinal pigment epithelial - اپیتلیال رنگدانه شبکیهAge-Related Eye Disease Study - بررسی بیماری های مرتبط با بیماری های مرتبط با سنPerfect Match - بهترین همسانMicroarray - ریزآرایهage-related macular degeneration - سن تخریب ماکولا مربوط به سن استEASE - سهولتdermal fibroblast - فیبروبلاست پوستPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریDulbecco’s modified eagle’s medium - محیط عقاب اصلاح شده DulbeccoReactive oxygen intermediates - واکنش اکسیژن واسطهreal-time polymerase chain reaction - واکنش زنجیره ای پلیمراز واقعی در زمان واقعیC-reactive protein - پروتئین واکنشی سیCRP - پروتئین واکنشی سی یا سی. آر. پی Reactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Differences in gene expression profiles in dermal fibroblasts from control and patients with age-related macular degeneration elicited by oxidative injury Differences in gene expression profiles in dermal fibroblasts from control and patients with age-related macular degeneration elicited by oxidative injury](/preview/png/10739061.png)
چکیده انگلیسی
The pathogenesis of age-related macular degeneration (AMD) is still unknown but there is growing evidence that a combination of both oxidative injury and genetic factors may play a role. One particle hypothesis proposes that dysregulation of multiple genes in response to an oxidative injury could contribute to the development of AMD. While direct examination of ocular cells from AMD patients is difficult, AMD also appears to have a systemic component. Therefore, as is the case with other central nervous diseases, peripheral sites may also manifest any underlying genetic abnormalities. For the present study, biopsy-derived fibroblasts from 4 patients with the early form and 4 patients with the late form of AMD and 3 age-matched control patients were grown in culture and treated with a nonlethal dose of the oxidative stimulus menadione. Gene expression patterns were quantitatively and qualitatively examined using Human Genome U95A GeneChips (Affymetrix) and verified by real-time PCR analysis. In response to the oxidative injury 755 genes were found to be upregulated at least twofold in one of the patients groups. Cluster analysis of expression profiles detected six patterns of dysregulation initiated by oxidative injury specific for the disease groups (98 genes total). Clusters of genes dysregulated by the sublethal oxidative injury in either early and/or late AMD groups were further categorized by overrepresentation of GO “biological process” categories using Expression Analysis Systematic Explorer (EASE) software. This approach demonstrated that four major functional gene groups including inflammatory/innate immune response, transcriptional regulation, cell cycle, and proliferation were significantly overrepresented (Fisher test ranging from 0.0393 to 0.00018) in both AMD patients groups in response to the oxidative injury. Despite the small number of patients in the study, specific biological and statistical differences in gene expression profiles between control and AMD patients were identified but only in the presence of an environmental stimulus.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 39, Issue 6, 15 September 2005, Pages 781-796
Journal: Free Radical Biology and Medicine - Volume 39, Issue 6, 15 September 2005, Pages 781-796
نویسندگان
Nataly Strunnikova, Sara Hilmer, Jessica Flippin, Michael Robinson, Eric Hoffman, Karl G. Csaky,