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PGC1‐α transcript and protein levels are increased in copper deficient rat hearts
Author(s) -
Klaahsen Darcey,
Medeiros Denis M
Publication year - 2007
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.21.5.a722-b
Subject(s) - mitochondrial biogenesis , copper deficiency , western blot , blot , regulator , messenger rna , medicine , endocrinology , northern blot , biology , microbiology and biotechnology , mitochondrion , copper , biogenesis , superoxide dismutase , gene expression , sod1 , dismutase , chemistry , gene , oxidative stress , biochemistry , organic chemistry
PGC‐1α is known to be the major regulator of mitochondrial biogenesis. The main objective of this study was to determine if PGC‐1α is involved in mitochondrial biogenesis during copper deficiency. We investigated PGC‐1α transcript levels by real‐time qPCR (i.e., Taqman Gene Expression Assays) and protein levels by Western blotting in rat hearts after five weeks on a copper deficient diet (n=4 in each group). Results: Copper deficient status was shown by decreased liver Cu‐Zn superoxide dismutase (SOD), decreased hematocrit levels, and increased heart:body weight ratios. A 2.8‐fold increase in PGC‐1α mRNA expression was detected in copper deficient rat hearts, using 18S rRNA (1:6) as an endogenous control for relative quantitation by the comparative method (ΔΔCt). In addition, Western blot analysis showed a 2‐fold increase in PGC‐1α protein expression, using β‐actin as a loading control This data reveals that PGC‐1α could be a sensitive regulator of mitochondrial biogenesis during copper deficiency and cardiac hypertrophy.