Dataset Information


Aging of Human Fibroblast

ABSTRACT: Human fibroblast of different age were investigated for their gene expression profiles in quiescence. Cultures were established from skin samples derived from young and old donors, obtained from the NIA Aging Cell Repository (Coriell Institute for Medical Research, Camden, NJ). All cell lines originated from 2 mm punch biopsies taken from the medial aspect of the upper arm. The donors were members of the Baltimore Longitudinal Study of Aging (BLSA) where they were characterized as "healthy" indviduals. The cell lines investigated had normal karyotypes. Overall design: RNA was isolated from the cell lysate using Qiagen RNeasy mini kit according to the manufacturer's instructions. Gene expression analysis was performed using the Codelink human bioarray containing single-stranded 30-mer oligonucleotide probes (Applied Microarrays, Tempe, AZ) and chips were run in duplicate. Details of this platform are available on the vendor's homepage website. Slides were scanned at 5 μm resolution with a ScanArray 4000 × l (Perkin Elmer, Waltham, Ma) and analyzed with the CodeLink Analysis Software, providing an integrated optical density (IOD) value for each hybridization spot, which is a measurement of an integrated background intensity value subtracted from the total pixel intensities within the area of the spot.

INSTRUMENT(S): GE Healthcare/Amersham Biosciences CodeLink Human Whole Genome Bioarray

SUBMITTER: Andres Kriete 

PROVIDER: GSE15829 | GEO | 2010-02-26



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Cell autonomous expression of inflammatory genes in biologically aged fibroblasts associated with elevated NF-kappaB activity.

Kriete Andres A   Mayo Kelli L KL   Yalamanchili Nirupama N   Beggs William W   Bender Patrick P   Kari Csaba C   Rodeck Ulrich U  

Immunity & ageing : I & A 20080716

BACKGROUND: Chronic inflammation is a well-known corollary of the aging process and is believed to significantly contribute to morbidity and mortality of many age-associated chronic diseases. However, the mechanisms that cause age-associated inflammatory changes are not well understood. Particularly, the contribution of cell stress responses to age-associated inflammation in 'non-inflammatory' cells remains poorly defined. The present cross-sectional study focused on differences in molecular sig  ...[more]

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