Structural and Functional Features of Ca2+ Transport Systems in Liver Mitochondria of Rats with Experimental Hyperthyroidism

We analyzed structural and functional features of the main mitochondrial Ca 2+ -transporting systems, mitochondrial Ca 2+ uniporter complex (MCUC) and Ca 2+ -dependent cyclosporin A-sensitive mitochondrial permeability transition pore (MPT pore), in rats with hyperthyroid state. It was found that, t...

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Bibliographic Details
Published in:Bulletin of experimental biology and medicine 2020-06, Vol.169 (2), p.224-228
Main Authors: Belosludtseva, N. V., Talanov, E. Yu, Venediktova, N. I., Sharapov, M. G., Mironova, G. D., Belosludtsev, K. N.
Format: Article
Language:English
Subjects:
Biomedical and Life Sciences
Biomedicine
Cell Biology
Internal Medicine
Laboratory Medicine
Pathology
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Summary:We analyzed structural and functional features of the main mitochondrial Ca 2+ -transporting systems, mitochondrial Ca 2+ uniporter complex (MCUC) and Ca 2+ -dependent cyclosporin A-sensitive mitochondrial permeability transition pore (MPT pore), in rats with hyperthyroid state. It was found that, the rate of Ca 2+ accumulation by rat liver mitochondria in this pathology increases by 1.3 times, which can be associated with higher level of the channel-forming subunit of the uniporter MCU and lower content of dominant-negative subunit of this complex MCUb. At the same time, the level of the regulatory subunit MICU1 remained unchanged. It was shown that calcium retention capacity of liver mitochondria in rats with experimental hyperthyroidism decreased by 2 times in comparison with the control, which attested to reduced resistance of liver mitochondria of hyperthyroid rats to induction of the MPT pore. The observed changes are consistent with the data on increased amount of cyclophilin D, a mitochondrial matrix peptidyl-prolyl isomerase that is known to modulate the MPT pore opening and expression of the Ppif gene that encodes mitochondrial cyclophilin D in rats with experimental hyperthyroidism.
ISSN:0007-4888
1573-8221
DOI:10.1007/s10517-020-04855-0