scholarly journals The molecular role of Sigmar1 in regulating mitochondrial function through mitochondrial localization in cardiomyocytes

Mitochondrion ◽  
2021 ◽  
Author(s):  
Chowdhury S. Abdullah ◽  
Richa Aishwarya ◽  
Shafiul Alam ◽  
Naznin Sultana Remex ◽  
Mahboob Morshed ◽  
...  
Keyword(s):  
Mitochondrial Function ◽  
Mitochondrial Localization

scholarly journals TOM20-mediated transfer of Bcl2 from ER to MAM and mitochondria upon induction of apoptosis

2021 ◽  
Vol 12 (2) ◽  
Author(s):  
Lisenn Lalier ◽  
Vincent Mignard ◽  
Marie-Pierre Joalland ◽  
Didier Lanoé ◽  
Pierre-François Cartron ◽  
...  
Keyword(s):  
Protein Import ◽  
Glioma Cells ◽  
Mitochondrial Outer Membrane ◽  
Mitochondrial Localization ◽  
Antiapoptotic Protein ◽  
Mitochondrial Transfer ◽  
Small Domain ◽  
Induction Of Apoptosis ◽  
And Function

AbstractIn this work, we have explored the subcellular localization of Bcl2, a major antiapoptotic protein. In U251 glioma cells, we found that Bcl2 is localized mainly in the ER and is translocated to MAM and mitochondria upon induction of apoptosis; this mitochondrial transfer was not restricted to the demonstrator cell line, even if cell-specific modulations exist. We found that the Bcl2/mitochondria interaction is controlled by TOM20, a protein that belongs to the protein import machinery of the mitochondrial outer membrane. The expression of a small domain of interaction of TOM20 with Bcl2 potentiates its anti-apoptotic properties, which suggests that the Bcl2–TOM20 interaction is proapoptotic. The role of MAM and TOM20 in Bcl2 apoptotic mitochondrial localization and function has been confirmed in a yeast model in which the ER–mitochondria encounter structure (ERMES) complex (required for MAM stability in yeast) has been disrupted. Bcl2–TOM20 interaction is thus an additional player in the control of apoptosis.

scholarly journals Role of Renal Oxygenation and Mitochondrial Function in the Pathophysiology of Acute Kidney Injury

2014 ◽  
Vol 127 (1-4) ◽  
pp. 149-152 ◽  
Author(s):  
Noureddin Nourbakhsh ◽  
Prabhleen Singh
Keyword(s):  
Acute Kidney Injury ◽  
Mitochondrial Function ◽  
Kidney Injury

scholarly journals Novel Role of miR-33 in Regulating of Mitochondrial Function

2015 ◽  
Vol 117 (3) ◽  
pp. 225-228 ◽  
Author(s):  
Nathan L. Price ◽  
Carlos Fernández-Hernando
Keyword(s):  
Mitochondrial Function

scholarly journals Using chemical biology to assess and modulate mitochondria: progress and challenges

2017 ◽  
Vol 7 (2) ◽  
pp. 20160151 ◽  
Author(s):  
Angela Logan ◽  
Michael P. Murphy
Keyword(s):  
Mitochondrial Function ◽  
Chemical Biology ◽  
Biomedical Sciences ◽  
Interdisciplinary Approaches ◽  
Wide Range ◽  
Challenges And Opportunities ◽  
Future Challenges ◽  
The Many ◽  
Opening Up

Our understanding of the role of mitochondria in biomedical sciences has expanded considerably over the past decade. In addition to their well-known metabolic roles, mitochondrial are also central to signalling for various processes through the generation of signals such as ROS and metabolites that affect cellular homeostasis, as well as other processes such as cell death and inflammation. Thus, mitochondrial function and dysfunction are central to the health and fate of the cell. Consequently, there is considerable interest in better understanding and assessing the many roles of mitochondria. Furthermore, there is also a growing realization that mitochondrial are a promising drug target in a wide range of pathologies. The application of interdisciplinary approaches at the interface between chemistry and biology are opening up new opportunities to understand mitochondrial function and in assessing the role of the organelle in biology. This work and the experience thus gained are leading to the development of new classes of therapies. Here, we overview the progress that has been made to date on exploring the chemical biology of the organelle and then focus on future challenges and opportunities that face this rapidly developing field.

Dexamethasone provoked mitochondrial perturbations in thymus: Possible role of N-acetylglucosamine in restoration of mitochondrial function

2016 ◽  
Vol 83 ◽  
pp. 1485-1492 ◽  
Author(s):  
Santhosh Kumar Venugopalan ◽  
Shanmugarajan T.S. ◽  
Navaratnam V. ◽  
Mansor S.M. ◽  
Ramanathan S.
Keyword(s):  
Mitochondrial Function

Abstract 431: Mitochondrial Fission in the Heart is an Adaptation to Increased Energetic Demands: The Role of Physiologic Fragmentation

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Michael Coronado ◽  
Giovanni Fajardo ◽  
Kim Nguyen ◽  
Mingming Zhao ◽  
Kristina Bezold Kooiker ◽  
...  
Keyword(s):  
Cell Death ◽  
Exercise Capacity ◽  
Mitochondrial Function ◽  
Adrenergic Receptor ◽  
Mitochondrial Fission ◽  
Physiological Adaptation ◽  
Mitochondrial Fragmentation ◽  
Energetic Demand ◽  
Adaptation To Exercise

Mitochondria play a dual role in the heart, responsible for meeting energetic demands and regulating cell death. Current paradigms hold that mitochondrial fission and fragmentation are the result of pathologic stresses such as ischemia, are an indicator of poor mitochondrial health, and lead to mitophagy and cell death. However, recent studies demonstrate that inhibiting fission also results in cardiac impairment, suggesting that fission is important for maintaining normal mitochondrial function. In this study, we identify a novel role for mitochondrial fragmentation as a normal physiological adaptation to increased energetic demand. Using two models of exercise, we demonstrate that “physiologic” mitochondrial fragmentation occurs, results in enhanced mitochondrial function, and is mediated through beta 1-adrenergic receptor signaling. Similar to pathologic fragmentation, physiologic fragmentation is induced by activation of Drp1; however, unlike pathologic fragmentation, membrane potential is maintained and regulators of mitophagy are downregulated. To confirm the role of fragmentation as a physiological adaptation to exercise, we inhibited the pro-fission mediator Drp1 in mice using the peptide inhibitor P110 and had mice undergo exercise. Mice treated with P110 had significantly decreased exercise capacity, decreased fragmentation and inactive Drp1 vs controls. To further confirm these findings, we generated cardiac-specific Drp1 KO mice and had them undergo exercise. Mice with cardiac specific Drp1 KO had significantly decreased exercise capacity and abnormally large mitochondria compared to controls. These findings indicate the requirement for physiological mitochondrial fragmentation to meet the energetic demands of exercise and support the still evolving conceptual framework, where fragmentation plays a role in the balance between mitochondrial maintenance of normal physiology and response to disease.

Ischemic preconditioning in rats: role of mitochondrial KATP channel in preservation of mitochondrial function

2000 ◽  
Vol 278 (1) ◽  
pp. H305-H312 ◽  
Author(s):  
Ryan M. Fryer ◽  
Janis T. Eells ◽  
Anna K. Hsu ◽  
Michele M. Henry ◽  
Garrett J. Gross
Keyword(s):  
Infarct Size ◽  
Ischemic Preconditioning ◽  
Mitochondrial Function ◽  
Ischemia Reperfusion ◽  
Mitochondrial Protein ◽  
Atp Synthesis ◽  
Area At Risk ◽  
Selective Antagonist ◽  
Mitochondrial Katp Channel

We examined the role of the sarcolemmal and mitochondrial KATPchannels in a rat model of ischemic preconditioning (IPC). Infarct size was expressed as a percentage of the area at risk (IS/AAR). IPC significantly reduced infarct size (7 ± 1%) versus control (56 ± 1%). The sarcolemmal KATP channel-selective antagonist HMR-1098 administered before IPC did not significantly attenuate cardioprotection. However, pretreatment with the mitochondrial KATP channel-selective antagonist 5-hydroxydecanoic acid (5-HD) 5 min before IPC partially abolished cardioprotection (40 ± 1%). Diazoxide (10 mg/kg iv) also reduced IS/AAR (36.2 ± 4.8%), but this effect was abolished by 5-HD. As an index of mitochondrial bioenergetic function, the rate of ATP synthesis in the AAR was examined. Untreated animals synthesized ATP at 2.12 ± 0.30 μmol ⋅ min−1 ⋅ mg mitochondrial protein−1. Rats subjected to ischemia-reperfusion synthesized ATP at 0.67 ± 0.06 μmol ⋅ min−1 ⋅ mg mitochondrial protein−1. IPC significantly increased ATP synthesis to 1.86 ± 0.23 μmol ⋅ min−1 ⋅ mg mitochondrial protein−1. However, when 5-HD was administered before IPC, the preservation of ATP synthesis was attenuated (1.18 ± 0.15 μmol ⋅ min−1 ⋅ mg mitochondrial protein−1). These data are consistent with the notion that inhibition of mitochondrial KATPchannels attenuates IPC by reducing IPC-induced protection of mitochondrial function.

scholarly journals Mitochondrial Localization of the Yeast Forkhead Factor Hcm1

2020 ◽  
Vol 21 (24) ◽  
pp. 9574
Author(s):  
María José Rodríguez Colman ◽  
Joaquim Ros ◽  
Elisa Cabiscol
Keyword(s):  
Transcription Factor ◽  
Transcriptional Activity ◽  
Spindle Pole ◽  
Respiratory Metabolism ◽  
Mitochondrial Localization ◽  
Transcription Factor Family ◽  
Forkhead Transcription Factor ◽  
Mitochondrial Transcription Factor ◽  
Gradient Density

Hcm1 is a member of the forkhead transcription factor family involved in segregation, spindle pole dynamics, and budding in Saccharomyces cerevisiae. Our group described the role of Hcm1 in mitochondrial biogenesis and stress resistance, and in the cellular adaptation to mitochondrial respiratory metabolism when nutrients decrease. Regulation of Hcm1 activity occurs at the protein level, subcellular localization, and transcriptional activity. Here we report that the amount of protein increased in the G1/S transition phase when the factor accumulated in the nucleus. In the G2/M phases, the Hcm1 amount decreased, and it was translocated outside the nucleus with a network-like localization. Preparation of highly purified mitochondria by a sucrose gradient density demonstrated that Hcm1 colocalized with mitochondrial markers, inducing expression of COX1, a mitochondrial encoded subunit of cytochrome oxidase, in the G2/M phases. Taken together, these results show a new localization of Hcm1 and suggest that it acts as a mitochondrial transcription factor regulating the metabolism of this organelle.

scholarly journals Mitochondrial Function, Biology, and Role in Disease

2016 ◽  
Vol 118 (12) ◽  
pp. 1960-1991 ◽  
Author(s):  
Elizabeth Murphy ◽  
Hossein Ardehali ◽  
Robert S. Balaban ◽  
Fabio DiLisa ◽  
Gerald W. Dorn ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Mitochondrial Function ◽  
The United States ◽  
Therapeutic Interventions ◽  
Therapeutic Approaches ◽  
Mitochondrial Defects ◽  
Exciting Time ◽  
Insight Into ◽  
Novel Therapeutic

Cardiovascular disease is a major leading cause of morbidity and mortality in the United States and elsewhere. Alterations in mitochondrial function are increasingly being recognized as a contributing factor in myocardial infarction and in patients presenting with cardiomyopathy. Recent understanding of the complex interaction of the mitochondria in regulating metabolism and cell death can provide novel insight and therapeutic targets. The purpose of this statement is to better define the potential role of mitochondria in the genesis of cardiovascular disease such as ischemia and heart failure. To accomplish this, we will define the key mitochondrial processes that play a role in cardiovascular disease that are potential targets for novel therapeutic interventions. This is an exciting time in mitochondrial research. The past decade has provided novel insight into the role of mitochondria function and their importance in complex diseases. This statement will define the key roles that mitochondria play in cardiovascular physiology and disease and provide insight into how mitochondrial defects can contribute to cardiovascular disease; it will also discuss potential biomarkers of mitochondrial disease and suggest potential novel therapeutic approaches.

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