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The involvement of Akt, mTOR, and S6K in the in vivo effect of IGF-1 on the regulation of rat cardiac Na+/K+-ATPase
dc.creator | Banjac, Katarina | |
dc.creator | Obradović, Milan | |
dc.creator | Zafirović, Sonja | |
dc.creator | Essack, Magbubah | |
dc.creator | Gluvić, Zoran | |
dc.creator | Šunderić, Miloš | |
dc.creator | Nedić, Olgica | |
dc.creator | Isenović, Esma R. | |
dc.date.accessioned | 2024-04-23T08:58:36Z | |
dc.date.available | 2024-04-23T08:58:36Z | |
dc.date.issued | 2024 | |
dc.identifier.issn | 0301-4851 | |
dc.identifier.issn | 1573-4978 | |
dc.identifier.uri | https://vinar.vin.bg.ac.rs/handle/123456789/13184 | |
dc.description.abstract | Background We previously demonstrated that insulin-like growth factor-1 (IGF-1) regulates sodium/potassium adenosine triphosphatase (Na+/K+-ATPase) in vascular smooth muscle cells (VSMC) via phosphatidylinositol-3 kinase (PI3K). Taking into account that others’ work show that IGF-1 activates the PI3K/protein kinase B (Akt) signaling pathway in many different cells, we here further questioned if the Akt/mammalian target of rapamycin (mTOR)/ribosomal protein p70 S6 kinase (S6K) pathway stimulates Na+/K+-ATPase, an essential protein for maintaining normal heart function. Methods and results There were 14 adult male Wistar rats, half of whom received bolus injections of IGF-1 (50 μg/kg) for 24 h. We evaluated cardiac Na+/K+-ATPase expression, activity, and serum IGF-1 levels. Additionally, we examined the phosphorylated forms of the following proteins: insulin receptor substrate (IRS), phosphoinositide-dependent kinase-1 (PDK-1), Akt, mTOR, S6K, and α subunit of Na+/K+-ATPase. Additionally, the mRNA expression of the Na+/K+-ATPase α1 subunit was evaluated. Treatment with IGF-1 increases levels of serum IGF-1 and stimulates Na+/K+-ATPase activity, phosphorylation of α subunit of Na+/K+-ATPase on Ser23, and protein expression of α2 subunit. Furthermore, IGF-1 treatment increased phosphorylation of IRS-1 on Tyr1222, Akt on Ser473, PDK-1 on Ser241, mTOR on Ser2481 and Ser2448, and S6K on Thr421/Ser424. The concentration of IGF-1 in serum positively correlates with Na+/K+-ATPase activity and the phosphorylated form of mTOR (Ser2448), while Na+/K+-ATPase activity positively correlates with the phosphorylated form of IRS-1 (Tyr1222) and mTOR (Ser2448). Conclusion These results indicate that the Akt/mTOR/S6K signalling pathway may be involved in the IGF-1 regulating cardiac Na+/K+-ATPase expression and activity | en |
dc.relation | Collaboration between the Department of Radiobiology and Molecular Genetics, “VINČA” Institute of Nuclear Sciences - National Institute of the Republic of Serbia, University of Belgrade, Belgrade, Serbia and Computational Bioscience Research Center (CBRC), King Abdullah University of Science and Technology (KAUST), Thuwal 23955-6900, Kingdom of Saudi Arabia | |
dc.rights | restrictedAccess | |
dc.source | Molecular Biology Reports | en |
dc.subject | IGF-1 | en |
dc.subject | Na+/K+-ATPase | en |
dc.subject | mTOR | en |
dc.subject | S6K | en |
dc.subject | Heart | en |
dc.title | The involvement of Akt, mTOR, and S6K in the in vivo effect of IGF-1 on the regulation of rat cardiac Na+/K+-ATPase | en |
dc.type | article | en |
dc.rights.license | ARR | |
dc.citation.volume | 51 | |
dc.citation.issue | 1 | |
dc.identifier.doi | 10.1007/s11033-024-09451-3 | |
dc.identifier.pmid | 38622478 | |
dc.type.version | publishedVersion | |
dc.identifier.scopus | 2-s2.0-85190451725 |
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