In vivo high-resolution magic angle spinning magnetic and electron paramagnetic resonance spectroscopic analysis of mitochondria-targeted peptide in Drosophila melanogaster with trauma-induced thoracic injury
| Autor: | Constantinou, Constantina, Apidianakis, Yiorgos, Psychogios, N., Righi, V., Mindrinos, M. N., Khan, N., Swartz, H. M., Szeto, H. H., Tompkins, R. G., Rahme, L. G., Aria Tzika, A. |
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| Přispěvatelé: | Apidianakis, Yiorgos [0000-0002-7465-3560], Constantinou, C, Apidianakis, Y, Psychogios, N, Righi, V, Mindrinos, MN, Khan, N, Swartz, HM, Szeto, HH, Tompkins, RG, Rahme, LG, Tzika, AA. |
| Rok vydání: | 2015 |
| Předmět: |
Aging
Pathology Magnetic Resonance Spectroscopy medicine.medical_treatment mitochondrial protein Apoptosis Adenosine Triphosphate oligopeptide mitochondrion genetics insulin receptor Uncoupling Protein 1 genome analysis mitochondrial uncoupling protein 4 General Medicine Thermogenin Cell biology aged Drosophila melanogaster priority journal enzyme synthesis Oligopeptides signal transduction medicine.medical_specialty Thoracic Injuries complication Article in vivo study 03 medical and health sciences In vivo Genetics Humans human apoptosis inducing factor animal model Electron Spin Resonance Spectroscopy biomarkers medicine.disease nuclear magnetic resonance Insulin receptor 030104 developmental biology chemistry ion channel biosynthesis Electron paramagnetic resonance Adenosine triphosphate upregulation Biomarkers 0301 basic medicine Mitochondrion Ion Channels Nuclear magnetic resonance chemistry.chemical_compound insulin resistance animal Drosophila forkhead box O protein biology apoptosis Articles biological marker unclassified drug Mitochondria oxidative phosphorylation uncoupling Insulin signaling electron paramagnetic resonance thorax injury High-resolution magic angle spinning biomarker Drosophila phosphatase and tensin homolog protein injury uncoupling protein 1 animal experiment adenosine triphosphate arginyl-2 '6'-dimethyltyrosyl-lysyl-phenylalaninamide medical school high-resolution magic angle spinning Mitochondrial Proteins Insulin resistance male image analysis medicine Animals controlled study insulin signaling nuclear magnetic resonance spectroscopy nonhuman disease model Insulin electron spin resonance biology.organism_classification Disease Models Animal gene expression biology.protein Wounds and Injuries pathology Insulin Resistance metabolism |
| Zdroj: | International journal of molecular medicine Int.J.Mol.Med. International Journal of Molecular Medicine |
| ISSN: | 1791-244X 1107-3756 |
| DOI: | 10.3892/ijmm.2015.2426 |
| Popis: | Trauma is the most common cause of mortality among individuals aged between 1 and 44 years and the third leading cause of mortality overall in the US. In this study, we examined the effects of trauma on the expression of genes in Drosophila melanogaster, a useful model for investigating genetics and physiology. After trauma was induced by a non-lethal needle puncture of the thorax, we observed the differential expression of genes encoding for mitochondrial uncoupling proteins, as well as those encoding for apoptosis-related and insulin signaling-related proteins, thus indicating muscle functional dysregulation. These results prompted us to examine the link between insulin signaling and mitochondrial dysfunction using in vivo nuclear magnetic resonance (NMR) with complementary electron paramagnetic resonance (EPR) spectroscopy. Trauma significantly increased insulin resistance biomarkers, and the NMR spectral profile of the aged flies with trauma-induced thoracic injury resembled that of insulin-resistant chico mutant flies. In addition, the mitochondrial redox status, as measured by EPR, was significantly altered following trauma, indicating mitochondrial uncoupling. A mitochondria-targeted compound, Szeto-Schiller (SS)-31 that promotes adenosine triphosphate (ATP) synthesis normalized the NMR spectral profile, as well as the mitochondrial redox status of the flies with trauma-induced thoracic injury, as assessed by EPR. Based on these findings, we propose a molecular mechanism responsible for trauma-related mortality and also propose that trauma sequelae in aging are linked to insulin signaling and mitochondrial dysfunction. Our findings further suggest that SS-31 attenuates trauma-associated pathological changes. 37 299 308 |
| Databáze: | OpenAIRE |
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