Mitochondrial Ca overload is proposed to regulate cell death via opening of the mitochondrial permeability transition pore. It is hypothesized that inhibition of the mitochondrial Ca uniporter (MCU) will prevent Ca accumulation during ischemia/reperfusion and thereby reduce cell death. To address this, we evaluate mitochondrial Ca in ex-vivo-perfused hearts from germline MCU-knockout (KO) and wild-type (WT) mice using transmural spectroscopy. Matrix Ca levels are measured with a genetically encoded, red fluorescent Ca indicator (R-GECO1) using an adeno-associated viral vector (AAV9) for delivery. Due to the pH sensitivity of R-GECO1 and the known fall in pH during ischemia, hearts are glycogen depleted to decrease the ischemic fall in pH. At 20 min of ischemia, there is significantly less mitochondrial Ca in MCU-KO hearts compared with MCU-WT controls. However, an increase in mitochondrial Ca is present in MCU-KO hearts, suggesting that mitochondrial Ca overload during ischemia is not solely dependent on MCU.
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http://dx.doi.org/10.1016/j.celrep.2023.112735 | DOI Listing |
Ying Yong Sheng Tai Xue Bao
October 2024
Liaoning Ocean and Fisheries Science Research Institute/Key Laboratory of Protection and Utilization of Aquatic Germplasm Resource, Ministry of Agriculture and Rural Affairs/Key Laboratory of Molecular Biology for Marine Fishery, Dalian 116023, Liaoning, China.
We investigated food composition and feeding selectivity of jellyfish () from the coastal aquaculture ponds in Liaodong Bay by DNA metabarcoding technology. The DNA from environmental water samples and stomach contents of were extracted and sequenced by high-throughput sequencing with 18S rDNA V4 region and mitochondrial cytochrome c oxidase subunit I (COI) as metabarcoding markers. Based on 18S rDNA metabarcoding, we detected 27 phyla in the stomach contents of , in which Mollusc was the dominant phylum followed by Arthropod, and 34 phyla in the environmental water samples, in which Pyrrophyta was the dominant phylum followed by Ciliophora and Ascomycota.
View Article and Find Full Text PDFJ Cachexia Sarcopenia Muscle
February 2025
Mitodicure GmbH, Kriftel, Germany.
Background: Recent studies provide strong evidence for a key role of skeletal muscle pathophysiology in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). In a 2021 review article on the pathophysiology of ME/CFS, we postulated that hypoperfusion and ischemia can result in excessive sodium and calcium overload in skeletal muscles of ME/CFS patients to cause mitochondrial damage. Since then, experimental evidence has been provided that supports this concept.
View Article and Find Full Text PDFRedox Biochem Chem
December 2024
Food Chemistry with Focus on Toxicology, Faculty of Mathematics and Natural Sciences, University of Wuppertal, Germany.
While copper (Cu) is an essential trace element for biological systems due to its redox properties, excess levels may lead to adverse effects partly due to overproduction of reactive species. Thus, a tightly regulated Cu homeostasis is crucial for health. Cu dyshomeostasis and elevated labile Cu levels are associated with oxidative stress and neurodegenerative disorders, but the underlying mechanisms have yet to be fully characterized.
View Article and Find Full Text PDFCurr Res Microb Sci
November 2024
Division of Nephrology, Minhang Hospital, Fudan University, Shanghai, China.
The intestinal microbiota comprises approximately 10-10 species of bacteria and plays a crucial role in host metabolism by facilitating various chemical reactions. Secondary bile acids (BAs) are key metabolites produced by gut microbiota.Initially synthesized by the liver, BA undergoes structural modifications through the activity of various intestinal microbiota enzymes, including eukaryotic, bacterial, and archaeal enzymes.
View Article and Find Full Text PDFFront Microbiol
December 2024
Department of Biotechnology, Delft University of Technology, Delft, Netherlands.
Mitochondria from harbor a branched electron-transport chain containing a proton-pumping Complex I NADH dehydrogenase and three Type II NADH dehydrogenases (NDH-2). To investigate the physiological role, localization and substrate specificity of these enzymes, the growth of various NADH dehydrogenase knockout mutants was quantitatively characterized in shake-flask and chemostat cultures, followed by oxygen-uptake experiments with isolated mitochondria. NAD(P)H:quinone oxidoreduction of the three NDH-2 were individually assessed.
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