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Alzheimer's and Parkinson's brain tissues have reduced expression of genes for mtDNA OXPHOS Proteins, mitobiogenesis regulator PGC-1α protein and mtRNA stabilizing protein LRPPRC (LRP130).
Mitochondrion
July 2020
Neurodegeneration Therapeutics, Inc., Charlottesville, VA 22901, United States.
We used RNA sequencing (RNA-seq) to quantitate gene expression in total RNA extracts of vulnerable brain tissues from Alzheimer's disease (AD, frontal cortical ribbon) and Parkinson's disease (PD, ventral midbrain) subjects and phenotypically negative control subjects. Paired-end sequencing files were processed with HISAT2 aligner/Cufflinks quantitation against the hg38 human genome. We observed a significant decrease in gene expression of all mtDNA OXPHOS genes in AD and PD tissues.
View Article and Find Full Text PDFLncRNA GUARDIN suppresses cellular senescence through a LRP130-PGC1α-FOXO4-p21-dependent signaling axis.
EMBO Rep
April 2020
CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS Centre for Excellence in Molecular Cell Science, School of Life Sciences, University of Science and Technology of China and The First Affiliated Hospital of University of Science and Technology of China, Hefei, China.
The long noncoding RNA GUARDIN functions to protect genome stability. Inhibiting GUARDIN expression can alter cell fate decisions toward senescence or apoptosis, but the underlying molecular signals are unknown. Here, we show that GUARDIN is an essential component of a transcriptional repressor complex involving LRP130 and PGC1α.
View Article and Find Full Text PDFFiber-specific and whole-muscle LRP130 expression in rested, exercised, and fasted human skeletal muscle.
Pflugers Arch
March 2020
School of Kinesiology and Health Studies, Queen's University, Kingston, Ontario, Canada.
Leucine-rich pentatricopeptide repeat motif-containing protein (LRP130) is implicated in the control of mitochondrial gene expression and oxidative phosphorylation in the liver, partly due to its interaction with peroxisome proliferator-activated receptor gamma co-activator 1-alpha (PGC-1α). To investigate LRP130's role in healthy human skeletal muscle, we examined LRP130's fiber-type distribution and subcellular localization (n = 6), as well as LRP130's relationship with PGC-1α protein and citrate synthase (CS) maximal activity (n = 33) in vastus lateralis samples obtained from young males. The impact of an acute bout of exercise (endurance [END] and sprint interval training [SIT]) and fasting (8 h) on LRP130 and PGC-1α expression was also determined (n = 10).
View Article and Find Full Text PDFMitochondrial retrograde signaling connects respiratory capacity to thermogenic gene expression.
Sci Rep
May 2017
Division of Cardiovascular Medicine, Department of Medicine, University of Massachusetts Medical School, Worcester, MA, 01605, USA.
Mitochondrial respiration plays a crucial role in determining the metabolic state of brown adipose tissue (BAT), due to its direct roles in thermogenesis, as well as through additional mechanisms. Here, we show that respiration-dependent retrograde signaling from mitochondria to nucleus contributes to genetic and metabolic reprogramming of BAT. In mouse BAT, ablation of LRPPRC (LRP130), a potent regulator of mitochondrial transcription and respiratory capacity, triggers down-regulation of thermogenic genes, promoting a storage phenotype in BAT.
View Article and Find Full Text PDFAn unexpected role for the transcriptional coactivator isoform NT-PGC-1α in the regulation of mitochondrial respiration in brown adipocytes.
J Biol Chem
June 2017
From the Laboratory of Gene Regulation and Metabolism, Pennington Biomedical Research Center, Baton Rouge, Louisiana 70808.
Brown adipose tissue dissipates energy as heat, a process that relies on a high abundance of mitochondria and high levels of electron transport chain (ETC) complexes within these mitochondria. Two regulators of mitochondrial respiration and heat production in brown adipocytes are the transcriptional coactivator PGC-1α and its splicing isoform NT-PGC-1α, which control mitochondrial gene expression in the nucleus. Surprisingly, we found that, in brown adipocytes, some NT-PGC-1α localizes to mitochondria, whereas PGC-1α resides in the nucleus.
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