scholarly journals Mitofusin 2: A Link Between Mitochondrial Function and Substrate Metabolism?

Mitochondrion ◽  
2021 ◽  
Author(s):  
Janna M. Emery ◽  
Rudy M. Ortiz
Keyword(s):  
Mitochondrial Function ◽  
Mitofusin 2 ◽  
Substrate Metabolism

scholarly journals Protective Effect of Qiliqiangxin Capsule on Energy Metabolism and Myocardial Mitochondria in Pressure Overload Heart Failure Rats

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Junfang Zhang ◽  
Cong Wei ◽  
Hongtao Wang ◽  
Siwen Tang ◽  
Zhenhua Jia ◽  
...  
Keyword(s):  
Heart Failure ◽  
Energy Metabolism ◽  
Mitochondrial Function ◽  
Pressure Overload ◽  
Metabolic Intermediate ◽  
Substrate Metabolism ◽  
Myocardial Mitochondria ◽  
Tcm Theory

Qiliqiangxin capsule (QL) was developed under the guidance of TCM theory of collateral disease and had been shown to be effective and safe for the treatment of heart failure. The present study explored the role of and mechanism by which the herbal compounds QL act on energy metabolism,in vivo, in pressure overload heart failure. SD rats received ascending aorta constriction (TAC) to establish a model of myocardial hypertrophy. The animals were treated orally for a period of six weeks. QL significantly inhibited cardiac hypertrophy due to ascending aortic constriction and improved hemodynamics. This effect was linked to the expression levels of the signaling factors in connection with upregulated energy and the regulation of glucose and lipid substrate metabolism and with a decrease in metabolic intermediate products and the protection of mitochondrial function. It is concluded that QL may regulate the glycolipid substrate metabolism by activating AMPK/PGC-1αaxis and reduce the accumulation of free fatty acids and lactic acid, to protect cardiac myocytes and mitochondrial function.

scholarly journals The Protective Effect of Alpha-Mangostin against Cisplatin-Induced Cell Death in LLC-PK1 Cells is Associated to Mitochondrial Function Preservation

Antioxidants ◽  
2019 ◽  
Vol 8 (5) ◽  
pp. 133 ◽  
Author(s):  
Laura María Reyes-Fermín ◽  
Sabino Hazael Avila-Rojas ◽  
Omar Emiliano Aparicio-Trejo ◽  
Edilia Tapia ◽  
Isabel Rivero ◽  
...  
Keyword(s):  
Cell Death ◽  
Mitochondrial Function ◽  
Anion Channel ◽  
Laboratory Culture ◽  
Mitochondrial Morphology ◽  
Protective Effects ◽  
Mitofusin 2 ◽  
Mitochondrial Mass ◽  
Protein Levels ◽  
Function Preservation

Cis-dichlorodiammineplatinum II (CDDP) is a chemotherapeutic agent that induces nephrotoxicity by different mechanisms, including oxidative stress, mitochondrial dysfunction, autophagy, and endoplasmic reticulum stress. This study aimed to evaluate if the protective effects of the antioxidant alpha-mangostin (αM) in CDDP-induced damage in proximal tubule Lilly laboratory culture porcine kidney (LLC-PK1) cells, are related to mitochondrial function preservation. It was found that αM co-incubation prevented CDDP-induced cell death. Furthermore, αM prevented the CDDP-induced decrease in cell respiratory states, in the maximum capacity of the electron transfer system (E) and in the respiration associated to oxidative phosphorylation (OXPHOS). CDDP also decreased the protein levels of voltage dependence anion channel (VDAC) and mitochondrial complex subunits, which together with the reduction in E, the mitofusin 2 decrease and the mitochondrial network fragmentation observed by MitoTracker Green, suggest the mitochondrial morphology alteration and the decrease in mitochondrial mass induced by CDDP. CDDP also induced the reduction in mitochondrial biogenesis observed by transcription factor A, mitochondria (TFAM) decreased protein-level and the increase in mitophagy. All these changes were prevented by αM. Taken together, our results imply that αM’s protective effects in CDDP-induced toxicity in LLC-PK1 cells are associated to mitochondrial function preservation.

scholarly journals MiR-195 regulates mitochondrial function by targeting mitofusin-2 in breast cancer cells

2018 ◽  
Author(s):  
Paresh Kumar Purohit ◽  
Ruairidh Edwards ◽  
Kostas Tokatlidis ◽  
Neeru Saini
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Mitochondrial Function ◽  
Breast Cancer Cells ◽  
Therapeutic Potential ◽  
Mitochondrial Dynamics ◽  
Mitochondrial Fission ◽  
Mitofusin 2 ◽  
Er Positive ◽  
And Function

AbstractMitochondrial dynamics is a highly dysregulated process in cancer. Apoptosis and mitochondrial fission are two concurrent events wherein increased mitochondrial fragmentation serves as a hallmark of apoptosis. We have shown earlier that miR-195 exerts pro-apoptotic effects in breast cancer cells. Herein, we have demonstrated miR-195 as a modulator of mitochondrial dynamics and function. Imaging experiments upon miR-195 treatment have shown that mitochondria undergo extensive fission. We validated mitofusin2 as a potential target of miR-195. Which may provide a molecular explanation for the respiratory defects induced by miR-195 over-expression in breast cancer cells? Active, but not total, mitochondrial mass, was reduced with increasing levels of miR-195. We have further shown that miR-195 enhances mitochondrial SOD-2 expression but does not affect PINK1 levels in breast cancer cells. Collectively, we have revealed that miR-195 is a modulator of mitochondrial dynamics by targeting MFN2 thereby impairing mitochondrial function. Concomitantly, it enhances the scavenger of reactive oxygen species (SOD-2) to maintain moderate levels of oxidative stress. Our findings suggest a therapeutic potential of miR-195 in both ER-positive as well as ER-negative breast cancer cells.

scholarly journals Loading MiR-210 in Endothelial Progenitor Cells Derived Exosomes Boosts Their Beneficial Effects on Hypoxia/Reoxygeneation-Injured Human Endothelial Cells via Protecting Mitochondrial Function

2018 ◽  
Vol 46 (2) ◽  
pp. 664-675 ◽  
Author(s):  
Xiaotang Ma ◽  
Jinju Wang ◽  
Jiao Li ◽  
Chunlian Ma ◽  
Shuzhen Chen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Mitochondrial Function ◽  
Tube Formation ◽  
Mechanism Analysis ◽  
Protective Effects ◽  
Endothelial Progenitor ◽  
Mitofusin 2 ◽  
Atp Level ◽  
Beneficial Effects ◽  
Angiogenesis Assay

Background/Aims: Stem cell-derived exosomes (EXs) offer protective effects on various cells via their carried microRNAs (miRs). Meanwhile, miR-210 has been shown to reduce mitochondrial reactive oxygen species (ROS) overproduction. In this study, we determined the potential effects of endothelial progenitor cell-derived EXs (EPC-EXs) on hypoxia/ reoxygenation (H/R) injured endothelial cells (ECs) and investigated whether these effects could be boosted by miR-210 loading. Methods: Human EPCs were used to generate EPC-EXs, or transfected with scrambler control or miR-210 mimics to generate EPC-EXssc and EPC-EXsmiR-210. H/R-injured human ECs were used as a model for functional analysis of EXs on apoptosis, viability, ROS production and angiogenic ability (migration and tube formation) by flow cytometry, MTT, dihydroethidium and angiogenesis assay kits, respectively. For mechanism analysis, the mitochondrion morphology, membrane potential (MMP), ATP level and the expression of fission/fusion proteins (dynamin-related protein 1: drp1 and mitofusin-2: mfn2) were assessed by using JC-1 staining, ELISA and western blot, respectively. Results: 1) Transfection of miR-210 mimics into EPCs induced increase of miR-210 in EPC-EXsmiR-210 without change of average size; 2) EPC-EXsmiR-210, but not EPC-EXs or EPC-EXssc, significantly elevated miR-210 level in ECs; 3) EPC-EXsmiR-210 were more effective than EPC-EXs and EPC-EXssc in reducing H/R-induced EC apoptosis, ROS overproduction and angiogenic dysfunction; 4) EPC-EXs decreased mitochondrial fragmentation, elevated MMP and ATP level, as well as improved mitochondrial mfn2 and drp1 dysregulation, which were more effective in EPC-EXsmiR-210. Conclusion: Our results suggest that EPC-EXs protect ECs against H/R injury via improving mitochondrial function and miR-210 enrichment could boost their effects.

scholarly journals Mitofusin 2 regulates the oocytes development and quality by modulating meiosis and mitochondrial function

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Qun Liu ◽  
Lina Kang ◽  
Lingjuan Wang ◽  
Ling Zhang ◽  
Wenpei Xiang
Keyword(s):  
Mitochondrial Function ◽  
Mitofusin 2
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