scholarly journals The Effects of NAD+ on Apoptotic Neuronal Death and Mitochondrial Biogenesis and Function after Glutamate Excitotoxicity

2014 ◽  
Vol 15 (11) ◽  
pp. 20449-20468 ◽  
Author(s):  
Xiaowan Wang ◽  
Hailong Li ◽  
Shinghua Ding
Keyword(s):  
Mitochondrial Biogenesis ◽  
Neuronal Death ◽  
Glutamate Excitotoxicity ◽  
And Function ◽  
Apoptotic Neuronal Death

scholarly journals PPAR-gamma induced AKT3 expression increases levels of mitochondrial biogenesis driving prostate cancer

Oncogene ◽  
2021 ◽  
Vol 40 (13) ◽  
pp. 2355-2366
Author(s):  
Laura C. A. Galbraith ◽  
Ernest Mui ◽  
Colin Nixon ◽  
Ann Hedley ◽  
David Strachan ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Mitochondrial Biogenesis ◽  
Nuclear Export ◽  
Epithelial To Mesenchymal Transition ◽  
Ppar Gamma ◽  
Peroxisome Proliferator ◽  
Serine Threonine Kinase ◽  
Peroxisome Proliferator Activated Receptor ◽  
Mesenchymal Transition ◽  
And Function

AbstractPeroxisome Proliferator-Activated Receptor Gamma (PPARG) is one of the three members of the PPAR family of transcription factors. Besides its roles in adipocyte differentiation and lipid metabolism, we recently demonstrated an association between PPARG and metastasis in prostate cancer. In this study a functional effect of PPARG on AKT serine/threonine kinase 3 (AKT3), which ultimately results in a more aggressive disease phenotype was identified. AKT3 has previously been shown to regulate PPARG co-activator 1 alpha (PGC1α) localisation and function through its action on chromosome maintenance region 1 (CRM1). AKT3 promotes PGC1α localisation to the nucleus through its inhibitory effects on CRM1, a known nuclear export protein. Collectively our results demonstrate how PPARG over-expression drives an increase in AKT3 levels, which in turn has the downstream effect of increasing PGC1α localisation within the nucleus, driving mitochondrial biogenesis. Furthermore, this increase in mitochondrial mass provides higher energetic output in the form of elevated ATP levels which may fuel the progression of the tumour cell through epithelial to mesenchymal transition (EMT) and ultimately metastasis.

scholarly journals GATA3 induces mitochondrial biogenesis in primary human CD4+ T cells during DNA damage

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Lauren A. Callender ◽  
Johannes Schroth ◽  
Elizabeth C. Carroll ◽  
Conor Garrod-Ketchley ◽  
Lisa E. L. Romano ◽  
...  
Keyword(s):  
Dna Damage ◽  
T Cells ◽  
T Cell ◽  
Mitochondrial Biogenesis ◽  
Cell Manipulation ◽  
Th2 Cells ◽  
Related Factor ◽  
Mitochondrial Mass ◽  
T Helper 2 ◽  
And Function

AbstractGATA3 is as a lineage-specific transcription factor that drives the differentiation of CD4+ T helper 2 (Th2) cells, but is also involved in a variety of processes such as immune regulation, proliferation and maintenance in other T cell and non-T cell lineages. Here we show a mechanism utilised by CD4+ T cells to increase mitochondrial mass in response to DNA damage through the actions of GATA3 and AMPK. Activated AMPK increases expression of PPARG coactivator 1 alpha (PPARGC1A or PGC1α protein) at the level of transcription and GATA3 at the level of translation, while DNA damage enhances expression of nuclear factor erythroid 2-related factor 2 (NFE2L2 or NRF2). PGC1α, GATA3 and NRF2 complex together with the ATR to promote mitochondrial biogenesis. These findings extend the pleotropic interactions of GATA3 and highlight the potential for GATA3-targeted cell manipulation for intervention in CD4+ T cell viability and function after DNA damage.

MicroRNA-128 inhibits mitochondrial biogenesis and function via targeting PGC1α and NDUFS4

Mitochondrion ◽  
2021 ◽  
Author(s):  
Kritika Sharma ◽  
Amit Chandra ◽  
Yasha Hasija ◽  
Neeru Saini
Keyword(s):  
Mitochondrial Biogenesis ◽  
And Function

Increased Mitochondrial Biogenesis and Function Is Necessary for Muscle Cell Differentiation

2015 ◽  
Vol 87 ◽  
pp. S131
Author(s):  
Neelu E Varghese ◽  
Gobinath Shanmugam ◽  
Daniel J Bolus ◽  
Balu K Chacko ◽  
Victor M Darley-Usmar ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Muscle Cell ◽  
Mitochondrial Biogenesis ◽  
Muscle Cell Differentiation ◽  
And Function

scholarly journals Involvement of mitochondrial K+ release and cellular efflux in ischemic and apoptotic neuronal death

2003 ◽  
Vol 86 (4) ◽  
pp. 966-979 ◽  
Author(s):  
Dong Liu ◽  
John R. Slevin ◽  
Chengbiao Lu ◽  
Sic L. Chan ◽  
Magnus Hansson ◽  
...  
Keyword(s):  
Neuronal Death ◽  
Apoptotic Neuronal Death ◽  
K Release

scholarly journals Spermidine alleviates cardiac aging by improving mitochondrial biogenesis and function

Aging ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 650-671 ◽  
Author(s):  
Junying Wang ◽  
Shaoqi Li ◽  
Ju Wang ◽  
Feixiang Wu ◽  
Yuhan Chen ◽  
...  
Keyword(s):  
Mitochondrial Biogenesis ◽  
Cardiac Aging ◽  
And Function

scholarly journals MiR 208a Regulates Mitochondrial Biogenesis in Metabolically Challenged Cardiomyocytes

Cells ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 3152
Author(s):  
Naveen Mekala ◽  
Jacob Kurdys ◽  
Alexis Paige Vicenze ◽  
Leana Rose Weiler ◽  
Carmen Avramut ◽  
...  
Keyword(s):  
Mitochondrial Biogenesis ◽  
Protein Trafficking ◽  
Cardiac Contractility ◽  
Metabolic Stress ◽  
Mitochondrial Translation ◽  
Human Cardiomyocytes ◽  
Bioenergetic Metabolism ◽  
Mitochondrial Defects ◽  
And Function ◽  
High Albumin

Metabolic syndrome increases the risk for cardiovascular disease including metabolic cardiomyopathy that may progress to heart failure. The decline in mitochondrial metabolism is considered a critical pathogenic mechanism that drives this progression. Considering its cardiac specificity, we hypothesized that miR 208a regulates the bioenergetic metabolism in human cardiomyocytes exposed to metabolic challenges. We screened in silico for potential miR 208a targets focusing on mitochondrial outcomes, and we found that mRNA species for mediator complex subunit 7, mitochondrial ribosomal protein 28, stanniocalcin 1, and Sortin nexin 10 are rescued by the CRISPR deletion of miR 208a in human SV40 cardiomyocytes exposed to metabolic challenges (high glucose and high albumin-bound palmitate). These mRNAs translate into proteins that are involved in nuclear transcription, mitochondrial translation, mitochondrial integrity, and protein trafficking. MiR 208a suppression prevented the decrease in myosin heavy chain α isoform induced by the metabolic stress suggesting protection against a decrease in cardiac contractility. MiR 208a deficiency opposed the decrease in the mitochondrial biogenesis signaling pathway, mtDNA, mitochondrial markers, and respiratory properties induced by metabolic challenges. The benefit of miR 208a suppression on mitochondrial function was canceled by the reinsertion of miR 208a. In summary, miR 208a regulates mitochondrial biogenesis and function in cardiomyocytes exposed to diabetic conditions. MiR 208a may be a therapeutic target to promote mitochondrial biogenesis in chronic diseases associated with mitochondrial defects.

scholarly journals Thyroid hormone effect on activity levels and tissue mitochondrial biogenesis and function in young and old rats

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Katherine A Klaus ◽  
Stephane Walrand ◽  
Dawn Morse ◽  
Jill M Schimke ◽  
Kevin R Short ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Mitochondrial Biogenesis ◽  
Activity Levels ◽  
Hormone Effect ◽  
Old Rats ◽  
And Function
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