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

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.

Mitofusin 2 ameliorates hypoxia-induced apoptosis via mitochondrial function and signaling pathways

2015 ◽  
Vol 69 ◽  
pp. 29-40 ◽  
Author(s):  
Cheng Peng ◽  
Wei Rao ◽  
Lei Zhang ◽  
Kai Wang ◽  
Hao Hui ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Mitochondrial Function ◽  
Mitofusin 2 ◽  
Induced Apoptosis

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.

Cryopreservation-induced alterations in boar spermatozoa mitochondrial function are related to changes in the expression and location of midpiece mitofusin-2 and actin network

2010 ◽  
Vol 74 (3) ◽  
pp. 354-363 ◽  
Author(s):  
E. Flores ◽  
J.M. Fernández-Novell ◽  
A. Peña ◽  
T. Rigau ◽  
J.E. Rodríguez-Gil
Keyword(s):  
Mitochondrial Function ◽  
Actin Network ◽  
Mitofusin 2 ◽  
Boar Spermatozoa

scholarly journals Mitofusin-2 Enhances Mitochondrial Contact With the Endoplasmic Reticulum and Promotes Diabetic Cardiomyopathy

2021 ◽  
Vol 12 ◽  
Author(s):  
Jing Zhang ◽  
Feng Zhang ◽  
Yanou Wang
Keyword(s):  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Diabetic Cardiomyopathy ◽  
Mitochondrial Function ◽  
Important Determinant ◽  
Mitofusin 2 ◽  
And Function ◽  
Species Production ◽  
Er Homeostasis ◽  
Cardiomyocyte Survival

Diabetic cardiomyopathy has been associated with mitochondrial damage. Mitochondria–endoplasmic reticulum (ER) contact is an important determinant of mitochondrial function and ER homeostasis. We therefore investigated whether hyperglycemia can damage the mitochondria by increasing their contact with the ER in cardiomyocytes. We found that hyperglycemia induced mitochondria–ER contact in cardiomyocytes, as evidenced by the increased MMM1, MDM34, and BAP31 expressions. Interestingly, the silencing of Mfn2 reduced the cooperation between the mitochondria and the ER in cardiomyocytes. Mfn2 silencing improved cardiomyocyte viability and function under hyperglycemic conditions. Additionally, the silencing of Mfn2 markedly attenuated the release of calcium from the ER to the mitochondria, thereby preserving mitochondrial metabolism in cardiomyocytes under hyperglycemic conditions. Mfn2 silencing reduced mitochondrial reactive oxygen species production, which reduced mitochondria-dependent apoptosis in hyperglycemia-treated cardiomyocytes. Finally, Mfn2 silencing attenuated ER stress in cardiomyocytes subjected to high-glucose stress. These results demonstrate that Mfn2 promotes mitochondria–ER contact in hyperglycemia-treated cardiomyocytes. The silencing of Mfn2 sustained mitochondrial function, suppressed mitochondrial calcium overload, prevented mitochondrial apoptosis, and reduced ER stress, thereby enhancing cardiomyocyte survival under hyperglycemic conditions.

scholarly journals Quercetin Affects Erythropoiesis and Heart Mitochondrial Function in Mice

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Lina M. Ruiz ◽  
Celia Salazar ◽  
Erik Jensen ◽  
Paula A. Ruiz ◽  
William Tiznado ◽  
...  
Keyword(s):  
Mitochondrial Function ◽  
Serum Insulin ◽  
Food Supplement ◽  
Prooxidant Effect ◽  
Mitofusin 2 ◽  
Cellular Models ◽  
Voltage Dependent ◽  
Dietary Flavonoid

Quercetin, a dietary flavonoid used as a food supplement, showed powerful antioxidant effects in different cellular models. However, recentin vitroandin vivostudies in mammals have suggested a prooxidant effect of quercetin and described an interaction with mitochondria causing an increase inO2∙-production, a decrease in ATP levels, and impairment of respiratory chain in liver tissue. Therefore, because of its dual actions, we studied the effect of quercetinin vivoto analyze heart mitochondrial function and erythropoiesis. Mice were injected with 50 mg/kg of quercetin for 15 days. Treatment with quercetin decreased body weight, serum insulin, and ceruloplasmin levels as compared with untreated mice. Along with an impaired antioxidant capacity in plasma, quercetin-treated mice showed a significant delay on erythropoiesis progression. Heart mitochondrial function was also impaired displaying more protein oxidation and less activity for IV, respectively, than no-treated mice. In addition, a significant reduction in the protein expression levels of Mitofusin 2 and Voltage-Dependent Anion Carrier was observed. All these results suggest that quercetin affects erythropoiesis and mitochondrial function and then its potential use as a dietary supplement should be reexamined.

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