Influence of standard and stimulated growth of B16/F10 melanoma on AIF levels in mitochondria in cells of the heart and other somatic organs in female mice

Influence of standard and stimulated growth of B16/F10 melanoma on AIF levels in mitochondria in cells of the heart and other somatic organs in female mice

Автор: Kit O.I., Frantsiyants E.M., Neskubina I.V., Cheryarina N.D., Shikhlyarova A.I., Przhedetskiy Y.V., Pozdnyakova V., Surikova E.I., Kaplieva I.V., Bandovkina V.A.

Журнал: Cardiometry @cardiometry

Статья в выпуске: 18, 2021 года.

Бесплатный доступ

studying AIF levels in mitochondria in cells of the heart and various organs in female mice with the growth of experimental melanoma B16 / F10 and comorbid pathology

Keywords mitochondria of cells, aif, chronic neurogenic pain, experimental в16/f10 melanoma, female mice

Короткий адрес: https://sciup.org/148321603

IDR: 148321603   |   DOI: 10.18137/cardiometry.2021.18.113120

Список литературы Influence of standard and stimulated growth of B16/F10 melanoma on AIF levels in mitochondria in cells of the heart and other somatic organs in female mice

  • Reinhardt С., et al. AIF meets the CHCHD4/Mia40- dependent mitochondrial import pathway. Biochim Biophys Acta Mol Basis Dis. 2020; 1866(6): 165746. DOI:10.1016/j.bbadis.2020.165746.
  • Otera H, et al. Export of mitochondrial AIF in response to proapoptotic stimuli depends on processing at the intermembrane space. EMBO J. 2014; 24: 1375–1386. DOI:10.1038/sj.emboj.7600614.
  • Bano D., Prehn J. Apoptosis-Inducing Factor (AIF) in Physiology and Disease: The Tale of a Repented Natural Born Killer. EBioMedicine. 2018; 30: 29–37. DOI:10.1016/j.ebiom.2018.03.016.
  • Hangen E, Blomgren K, Benit P, Kroemer G, Modjtahedi N. Life with or without AIF. Trends Biochem. Sci. 2010; 35: 278-287. DOI:10.1016 / j.tibs.2009.12.008.
  • Meyer K., et al. Loss of apoptosis-inducing factor critically affects MIA40 function. Cell Death Dis. 2015; 6(7): 1814. DOI:10.1038 / cddis.2015.170.
  • Chatzi A, Manganas P, Tokatlidis K. Oxidative folding in the mitochondrial intermembrane space: a regulated process important for cell physiology and disease. Biochim Biophys Acta. 2016; 1863(6): 1298-306. DOI:10.1016/j.bbamcr.2016.03.023.
  • Modjtahedi N, Tokatlidis K, Dessen P, Kroemer G. Mitochondrial proteins containing Coiled-Coil-Helix-Coiled-Coil-Helix (CHCH) domains in health and disease. Trends Biochem. Sci. 2016; 41(3): 245-260. DOI:10.1016 / j.tibs.2015.12.004.
  • Habich M, Salscheider SL, Riemer J. Cysteine residues in mitochondrial intermembrane space proteins: more than just import. Br. J. Pharmacol. 2019; 176(4): 514-531. DOI:10.1111 / bph.14480.
  • Kit OI, et al. A method for producing liver metastases in the experiment. Byulleten' eksperimental'noj biologii i mediciny. 2014;157(6):745-7. [in Russian]
  • Kit OI, et al. Neoangiogenesis and fibrinolityc system biomarkers expression in the dinamics of experimental kidney ischemia in rats/ Eksperimental'naya i klinicheskaya urologiya. 2015;1:20-3. [in Russian]
  • Zhukova GI, et al. Effekty kombinir. vozdejstviya nizkointensivnogo elektromag. izluch. millimetr. diap. i kompleksov nezamen. aminokislot u krys-opuholenositelej starcheskogo vozrasta. Yuzhno-rossijskij onkologicheskij zhurnal. 2020;1(4):38-46 [in Russian]
  • Kit OI, Kotieva IM, Frantsiyants EM, et al. Influence of chronic neuropathic pain on the course of malignant в16/f10 melanoma in male mice. Severo-Kavkazskij region. Seriya: Estestvennye nauki - Bulletin of higher educational institutions. North Caucasus region. Natural sciences. 2019;1(201):106-111. [in Russian]
  • Egorova MV, Afanasiev SA. Isolation of mitochondria from cells and tissues of animals and human: Modern methodical approaches. Sibirskiy meditsinskiy zhurnal – Sibirian Medical Journal. 2011; 26(1-1): 22-28 [in Russian]
  • Bano D, Prehn JHM. Apoptosis-inducing factor (AIF) in physiology and disease: the tale of a repented natural born killer. EBioMedicine. 2018; 30: 29-37. DOI: 10.1016/j.ebiom.2018.03.016.
  • Zong L., et al. AIF knockdown induce apoptosis and mitochondrial dysfunction in cochlear spiral ganglion neurons in vitro. Molecular medicine reports. 2020; 21(4): 1910–1920. DOI:10.3892/mmr.2020.10970.
  • Calvo SE, Clauser KR, Mootha VK. MitoCarta2.0: an updated inventory of mammalian mitochondrial proteins. Nucleic Acids Res. 2016; 44(1): 1251–1257. DOI: 10.1093/nar/gkv1003.
  • Vahsen N, et al. AIF deficiency compromises oxidative phosphorylation. EMBO J. 2004; 23(23): 4679–4689. DOI: 10.1038/sj.emboj.7600461.
  • Elguindy MM, Nakamaru-Ogiso E. Apoptosis-inducing factor (AIF) and its family member protein, AMID, are rotenone-sensitive NADH:ubiquinone oxidoreductases (NDH-2). J. Biol. Chem. 2015; 290(34): 20815–20826. DOI: 10.1074/jbc.M115.641498.
  • Kim JT, et al. Apoptosis-inducing factor (AIF) inhibits protein synthesis by interacting with the eukaryotic translation initiation factor 3 subunit p44 (eIF3g). FEBS Lett. 2006; 580(27): 6375–6383. DOI:10.1016/j.febslet.2006.10.049.
  • Pospisilik JA, et al. Targeted Deletion of AIF Decreases Mitochondrial Oxidative Phosphorylation and Protects from Obesity and Diabetes. Cell. 2007; 131: 476–491. DOI:10.1016/j.cell.2007.08.047.
  • Timper K, et al. Mild Impairment of Mitochondrial OXPHOS Promotes Fatty Acid Utilization in POMC Neurons and Improves Glucose Homeostasis in Obesity. Cell reports. 2018; 25(2): 383–397. DOI:10.1016/j.celrep.2018.09.034.
  • Milasta S, et al. Apoptosis-Inducing-Factor-Dependent Mitochondrial Function Is Required for T Cell but Not B Cell Function. Immunity. 2016; 44(1): 88–102. DOI:10.1016/j.immuni.2015.12.002.
  • Franciyanc EM, et al. Vliyanie nokauta po genu urokinazy na rost melanomy v eksperimente. Sibirskij nauchnyj medicinskij zhurnal. 2019;39(4):62-70. [in Russian]
  • Siu PM, et al. Response of caspase-independent apoptotic factors to high salt diet-induced heart failure. J. Mol. Cell. Cardiol. 2007; 42(3): 678–686. DOI:10.1016/j.yjmcc.2007.01.001.
  • Van Empel VP, et al. Downregulation of apoptosis-inducing factor in harlequin mutant mice sensitizes the myocardium to oxidative stress-related cell death and pressure overload-induced decompensation. Circ. Res. 2005; 96:92–e101. DOI: 10.1161/01.RES.0000172081.30327.28.
  • Kit OI, et al. Processy samoorganizacii mitohondrij pri roste eksperimental'nyh opuholej v usloviyah hronicheskoj nejrogennoj boli. Izvestiya vysshih uchebnyh zavedenij. Severo-Kavkazskij region. Seriya: Estestvennye nauki. 2019;2 (202):97-105. [in Russian]
Еще
Статья научная
QR-код для установки приложения SciUp Наведите камеру и скачайте бесплатное приложение SciUp