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Human genomic microarrays reveal novel processes that may initiate skeletal muscle regeneration in older adults
Author(s) -
ThalackerMercer Anna Elizabeth,
Dell'Italia Louis J.,
Mayhew David L.,
Cui Xiangqin,
Bamman Marcas M.
Publication year - 2009
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.23.1_supplement.954.7
Subject(s) - skeletal muscle , myogenesis , transcriptome , regeneration (biology) , biology , inflammation , sarcopenia , gene expression , microarray , bioinformatics , medicine , gene , microbiology and biotechnology , genetics , endocrinology , immunology
Aging skeletal muscle demonstrates an impaired and poorly understood capacity for regeneration and growth when provided the same stimuli as young. To better understand the impact of aging and to identify novel responses for targeted studies, we assessed changes in gene expression (GE) of 8 old vs. 8 young humans pre and 24‐h post unaccustomed high‐intensity resistance loading (RL). Within each age group, RL‐mediated changes in GE were determined using a paired t‐test (significance determined at P<0.001). Ingenuity Pathways Analysis (IPA) was used to identify functional networks. Among old, translated protein products of transcripts in the highest scoring network play a role in skeletal and muscular development (DYRK1B, MAP2K3, MYBPH, NRP1, SMARCA4, JUP, PLXNA1); cell growth and proliferation (TCP1, CCT5, FADS3, COL4A3); and inflammation (Heatshock proteins, NFkB, p38MAPK, ERK, MAP3K5, ZFG36). Two transcripts on this network (NFkB and HSP70) were differentially expressed in young post RL. Although acute inflammation is thought to play an important role in initiating early steps of RL‐mediated myogenesis, a heightened inflammatory response (mRNA level) in old may blunt transcriptional changes which support muscle development and growth. Targeted studies in our lab will determine whether these novel transcriptome changes, unique among old, are responsible for age‐related muscle regeneration impairment. Supported by: NIA 5R01 AG017896, 5T32 DK062710‐01A1, GCRC M01 RR00032