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Paradoxes in cell‐based transcriptomic and systematic research data in aging and obesity studies and the attempt of bridging (1180.1)
Author(s) -
Tan Ningzhi,
Zhou Yanjiao,
Lu Jihong,
Gao Ling,
Yao Yisang,
Dong Yunzi,
Bartlett Mark,
Zhu JiaShi
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1180.1
Subject(s) - adiponectin , medicine , transcriptome , endocrinology , gene expression , biology , microarray , obesity , gene , insulin resistance , biochemistry
Transcriptomic studies unmask important molecular information at cellular levels, which may meet paradoxes in interpretation in whole body settings when hyper‐/atrophy or hyper‐/hypoplasia occurs (FASEB J 2007, 21:A1352). In an obesity study, microarray assay revealed an unaltered expression of adiponectin gene in obese adipocytes, paradoxically to the reduced plasma adiponectin (‐27%, p<0.01). After normalized with total DNA and tissue weight, we observed reduced adiponectin mRNA at the tissue level (‐26%, p<0.01), consistent with the plasma changes under the physiological control. In an aging study, Chuk (NF‐κB activator) was down‐regulated (‐20%, P<0.01), inhibitor Ikbkb gene up‐regulated (+20%, p=0.02) & NF‐κB gene (Rela) unchanged at a hepatocyte level in the enlarged, inflammatory liver, but these genes were all up‐regulated at the tissue level (+40% → +100%; p<0.02). But NF‐κB activity was not changed in the whole liver. Gstk1 & Gstk7 genes were unchanged with aging per cell, but up‐regulated at the level of whole liver (p<0.01). In contrast, GSH‐Px activity was reduced in the aged liver (p<0.01). Our studies indicate that bridging the cell‐based trancriptomic data to systems physiology levels is necessary for understanding the whole body physiological and pathological regulations, including feedback compensatory regulations and decompensation, of different biological pathways.