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Tuncay 2018 MiP2018
Has abstract [[Image:MITOEAGLE-logo.jpg|left|100px|link
[[Image:MITOEAGLE-logo.jpg|left|100px|link=|COST Action MitoEAGLE]] Zinc is an essential element in human body regulating many physiological processes. It is involved in DNA and protein synthesis, apoptosis and cardiac contractility. We hypothesized that Zn<sup>2+</sup> transporter ZIP7 Zip7 localize not only into SER but also mitochondria affect the sarco(endo)plasmic reticulum S(E)R-mitochondria coupling, and thereby contribute to cellular Zn<sup>2+</sup>-muffling between S(E)R-mitochondria in hyperglycemic H9c2 cells. We found that ZIP7 is highly expressing in cardiomyocytes and H9c2 cells. We first observed subcellular localization of ZIP7 in mitochondria by using fluorescence technique or biochemical analysis in H9c2 cells. We incubated the H9c2 cells with 25mM glucose for 24h (HG). By using recombinant-targeted Förster resonance energy transfer sensors, we showed that HG induced a marked redistribution of cellular free Zn<sup>2+</sup>, increasing cytosolic and mitochondrial free Zn<sup>2+</sup> and lowering free Zn<sup>2+</sup> in the S(E)R. On the other hand, HG caused significant increase of ZIP7 protein level both in S(E)R and mitochondria. Deletion of ZIP7 prevented changes of S(E)R and mitochondrial and intracellular free Zn<sup>2+</sup> in HG group. Determine the role of ZIP7 on sarco(endo)plasmic reticulum-mitochondria coupling and apoptosis, we measured mitofusin-protein Mfn-1/2, a mitochondrial fission protein, Fis-1, which is also a bridge proteins between mitochondria-S(E)R interface, and another bridge proteins between mitochondria-S(E)R interface, Bap31 and apoptosis markers BCL2 and Bax in H9c2 cells. We found the expression levels of Mfn-1/2 and Fis-1 in ZIP7 included cells were markedly high while the Bap31 expression level was dramatically decreased in HG-H9c2 cells. ZIP7 silenced cells slightly prevented these changes. Overall, this study provides an important description about the role of ZIP7, localized to both mitochondria and S(E)R and contribute to cellular Zn<sup>2+</sup>-muffling between cellular-compartments in HG or hypertrophic cardiomyocytes via affecting S(E)R-mitochondria coupling. Any alteration in this axis and/or cellular [Zn<sup>2+</sup>] may provide new insight for prevention/therapy of HF in diabetes and/or hypertrophy.
rapy of HF in diabetes and/or hypertrophy.  +
Has editor [[Plangger M]]  + , [[Kandolf G]]  +
Has title [[File:ErkanTuncay.jpg|left|90px|Mitochondrial Physiology Society|MiPsociety]] Regulation of mitochondrial Zn<sup>2+</sup> transporter ZIP7 effects sarco(endo)plasmic reticulum S(E)R-mitochondria coupling in hyperglycemia.  +
Mammal and model Rat  +
Respiration and regulation Ion;substrate transport  +
Tissue and cell Heart  +
Was submitted in year 2018  +
Was submitted to event MiP2018/MitoEAGLE Jurmala LV +
Was written by Tuncay E + , Bitirim CV + , Olgar Y + , Durak A + , Turan B +
Categories Abstracts
Modification date
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13:43:53, 9 October 2018  +
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