Unknown

Dataset Information

0

The permeability transition pore controls cardiac mitochondrial maturation and myocyte differentiation.

ABSTRACT: Although mature myocytes rely on mitochondria as the primary source of energy, the role of mitochondria in the developing heart is not well known. Here, we find that closure of the mitochondrial permeability transition pore (mPTP) drives maturation of mitochondrial structure and function and myocyte differentiation. Cardiomyocytes at embryonic day (E) 9.5, when compared to E13.5, displayed fragmented mitochondria with few cristae, a less-polarized mitochondrial membrane potential, higher reactive oxygen species (ROS) levels, and an open mPTP. Pharmacologic and genetic closing of the mPTP yielded maturation of mitochondrial structure and function, lowered ROS, and increased myocyte differentiation (measured by counting Z bands). Furthermore, myocyte differentiation was inhibited and enhanced with oxidant and antioxidant treatment, respectively, suggesting that redox-signaling pathways lie downstream of mitochondria to regulate cardiac myocyte differentiation.

SUBMITTER: Hom JR 

PROVIDER: S-EPMC3175092 | biostudies-literature | 2011 Sep

REPOSITORIES: biostudies-literature

Json Xml
altmetric image

Publications

The permeability transition pore controls cardiac mitochondrial maturation and myocyte differentiation.

Hom Jennifer R JR   Quintanilla Rodrigo A RA   Hoffman David L DL   de Mesy Bentley Karen L KL   Molkentin Jeffery D JD   Sheu Shey-Shing SS   Porter George A GA  

Developmental cell 20110901 3

Although mature myocytes rely on mitochondria as the primary source of energy, the role of mitochondria in the developing heart is not well known. Here, we find that closure of the mitochondrial permeability transition pore (mPTP) drives maturation of mitochondrial structure and function and myocyte differentiation. Cardiomyocytes at embryonic day (E) 9.5, when compared to E13.5, displayed fragmented mitochondria with few cristae, a less-polarized mitochondrial membrane potential, higher reactiv  ...[more]

Similar Datasets

Unknown Permeability transition pore-mediated mitochondrial superoxide flashes regulate cortical neural progenitor differentiation.
| S-EPMC3792897 | biostudies-literature
Unknown Non-canonical glycosyltransferase modulates post-hypoxic cardiac myocyte death and mitochondrial permeability transition.
| S-EPMC2610867 | biostudies-other
Unknown Ultrafine Particulate Matter Increases Cardiac Ischemia/Reperfusion Injury via Mitochondrial Permeability Transition Pore.
| S-EPMC5617757 | biostudies-literature
Transcriptomics Closing the mitochondrial permeability transition pore in hiPSC-derived endothelial cells induces glycocalyx formation and functional maturation.
2019-12-14 | E-MTAB-8392 | biostudies-arrayexpress
Unknown Dual dynamics of mitochondrial permeability transition pore opening.
| S-EPMC7054270 | biostudies-literature
Unknown Closing the Mitochondrial Permeability Transition Pore in hiPSC-Derived Endothelial Cells Induces Glycocalyx Formation and Functional Maturation.
| S-EPMC6895683 | biostudies-literature
Unknown Involvement of mitochondrial permeability transition pore (mPTP) in cardiac arrhythmias: Evidence from cyclophilin D knockout mice.
| S-EPMC5127715 | biostudies-literature
Unknown Individual Cardiac Mitochondria Undergo Rare Transient Permeability Transition Pore Openings.
| S-EPMC4779382 | biostudies-literature
Unknown Cardiac myocyte-specific expression of inducible nitric oxide synthase protects against ischemia/reperfusion injury by preventing mitochondrial permeability transition.
| S-EPMC2763350 | biostudies-literature
Unknown Characterization of the respiration-induced yeast mitochondrial permeability transition pore.
| S-EPMC3920737 | biostudies-literature