FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4297009270> ?p ?o ?g. }

• W4297009270 abstract "Myocardial tissue homeostasis is critically important for heart development, growth and function throughout the life course. The loss of cardiomyocytes under pathological conditions ultimately leads to cardiovascular disease due to the limited regenerative capacity of the postnatal mammalian heart. Inhibition of electron transport along the mitochondrial respiratory chain causes cellular stress characterized by ATP depletion as well as excessive generation of reactive oxygen species. Adult cardiomyocytes are highly susceptible to mitochondrial dysfunction whereas embryonic cardiomyocytes in the mouse heart have been shown to be resistant towards mitochondrial complex III inhibition. To functionally characterize the molecular mechanisms mediating this stress tolerance, we used H9c2 cells as an in vitro model for immature cardiomyoblasts and treated them with various inhibitors of mitochondrial respiration. The complex I inhibitor rotenone rapidly induced cell cycle arrest and apoptosis whereas the complex III inhibitor antimycin A (AMA) had no effect on proliferation and only mildly increased cell death. HL-1 cells, a differentiated and contractile cardiomyocyte cell line from mouse atrium, were highly susceptible to AMA treatment evident by cell cycle arrest and death. AMA induced various stress response mechanisms in H9c2 cells, such as the mitochondrial unfolded protein response (UPR mt ), integrated stress response (ISR), heat shock response (HSR) and antioxidative defense. Inhibition of the UPR, ISR and HSR by siRNA mediated knock down of key components does not impair growth of H9c2 cells upon AMA treatment. In contrast, knock down of NRF2, an important transcriptional regulator of genes involved in detoxification of reactive oxygen species, reduces growth of H9c2 cells upon AMA treatment. Various approaches to activate cell protective mechanisms and alleviate oxidative stress in HL-1 cells failed to rescue them from AMA induced growth arrest and death. In summary, these data show that the site of electron transport interruption along the mitochondrial respiratory chain determines cell fate in immature cardiomyoblasts. The study furthermore points to fundamental differences in stress tolerance and cell survival between immature and differentiated cardiomyocytes which may underlie the growth plasticity of embryonic cardiomyocytes during heart development but also highlight the obstacles of cardioprotective therapies in the adult heart." @default.
• W4297009270 created "2022-09-25" @default.
• W4297009270 creator A5008295313 @default.
• W4297009270 creator A5053507144 @default.
• W4297009270 creator A5056507973 @default.
• W4297009270 creator A5062176660 @default.
• W4297009270 creator A5072663096 @default.
• W4297009270 creator A5080611152 @default.
• W4297009270 creator A5081632776 @default.
• W4297009270 date "2022-09-23" @default.
• W4297009270 modified "2023-09-30" @default.
• W4297009270 title "Inhibition of mitochondrial respiration has fundamentally different effects on proliferation, cell survival and stress response in immature versus differentiated cardiomyocyte cell lines" @default.
• W4297009270 cites W1603693553 @default.
• W4297009270 cites W1932780354 @default.
• W4297009270 cites W1953694301 @default.
• W4297009270 cites W1963787838 @default.
• W4297009270 cites W1975027704 @default.
• W4297009270 cites W1978631786 @default.
• W4297009270 cites W1983078193 @default.
• W4297009270 cites W1994446230 @default.
• W4297009270 cites W2007956123 @default.
• W4297009270 cites W2018457456 @default.
• W4297009270 cites W2023374667 @default.
• W4297009270 cites W2024873692 @default.
• W4297009270 cites W2025904708 @default.
• W4297009270 cites W2029621610 @default.
• W4297009270 cites W2032758675 @default.
• W4297009270 cites W2035754217 @default.
• W4297009270 cites W2038031971 @default.
• W4297009270 cites W2038221909 @default.
• W4297009270 cites W2040499888 @default.
• W4297009270 cites W2042473359 @default.
• W4297009270 cites W2052472486 @default.
• W4297009270 cites W2053789606 @default.
• W4297009270 cites W2054599082 @default.
• W4297009270 cites W2056015556 @default.
• W4297009270 cites W2059010449 @default.
• W4297009270 cites W2065756643 @default.
• W4297009270 cites W2070734183 @default.
• W4297009270 cites W2081762851 @default.
• W4297009270 cites W2085927442 @default.
• W4297009270 cites W2094657005 @default.
• W4297009270 cites W2108738634 @default.
• W4297009270 cites W2111753723 @default.
• W4297009270 cites W2125502542 @default.
• W4297009270 cites W2125563383 @default.
• W4297009270 cites W2131632095 @default.
• W4297009270 cites W2137472233 @default.
• W4297009270 cites W2140487984 @default.
• W4297009270 cites W2148525121 @default.
• W4297009270 cites W2149301933 @default.
• W4297009270 cites W2154229994 @default.
• W4297009270 cites W2162482990 @default.
• W4297009270 cites W2165132732 @default.
• W4297009270 cites W2166744427 @default.
• W4297009270 cites W2170706610 @default.
• W4297009270 cites W2281291981 @default.
• W4297009270 cites W2295289052 @default.
• W4297009270 cites W2316348002 @default.
• W4297009270 cites W2341584684 @default.
• W4297009270 cites W2412985586 @default.
• W4297009270 cites W2518959324 @default.
• W4297009270 cites W2525940465 @default.
• W4297009270 cites W2750745925 @default.
• W4297009270 cites W2767261781 @default.
• W4297009270 cites W2769077130 @default.
• W4297009270 cites W2770372563 @default.
• W4297009270 cites W2807803570 @default.
• W4297009270 cites W2885025259 @default.
• W4297009270 cites W2916049297 @default.
• W4297009270 cites W2941824620 @default.
• W4297009270 cites W2946106600 @default.
• W4297009270 cites W2957289901 @default.
• W4297009270 cites W2995162523 @default.
• W4297009270 cites W3004765641 @default.
• W4297009270 cites W3013813924 @default.
• W4297009270 cites W3087415224 @default.
• W4297009270 cites W3099019722 @default.
• W4297009270 cites W3133804825 @default.
• W4297009270 cites W3158001093 @default.
• W4297009270 cites W3163011232 @default.
• W4297009270 cites W3164842107 @default.
• W4297009270 cites W3196942636 @default.
• W4297009270 cites W3205624353 @default.
• W4297009270 cites W4254119740 @default.
• W4297009270 cites W4362172418 @default.
• W4297009270 doi "https://doi.org/10.3389/fcell.2022.1011639" @default.
• W4297009270 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/36211452" @default.
• W4297009270 hasPublicationYear "2022" @default.
• W4297009270 type Work @default.
• W4297009270 citedByCount "1" @default.
• W4297009270 countsByYear W42970092702023 @default.
• W4297009270 crossrefType "journal-article" @default.
• W4297009270 hasAuthorship W4297009270A5008295313 @default.
• W4297009270 hasAuthorship W4297009270A5053507144 @default.
• W4297009270 hasAuthorship W4297009270A5056507973 @default.
• W4297009270 hasAuthorship W4297009270A5062176660 @default.
• W4297009270 hasAuthorship W4297009270A5072663096 @default.
• W4297009270 hasAuthorship W4297009270A5080611152 @default.
• W4297009270 hasAuthorship W4297009270A5081632776 @default.

• next