Background: The objective of this study was to evaluate the levels of Vascular Peroxidase 1 (VPO1), humanin, and MOTS-c in relation to miR-200c expression in untreated preeclamptic pregnancies, and to compare these findings with endoglin levels.
Methods And Results: In this study, blood samples were collected from preeclamptic patients presenting to the clinic prior to the initiation of treatment. The levels of endoglin, VPO1, humanin, and MOTS-c were measured using enzyme-linked immunosorbent assay (ELISA), while miR-200c expression was quantified using reverse transcription polymerase chain reaction (RT-PCR). Receiver operating characteristic (ROC) analysis was performed to assess diagnostic accuracy. Statistical significance was determined at p < 0.05. The levels of endoglin, VPO1, and miR-200c were found to be significantly elevated in the preeclampsia group compared to the control group (p < 0.05), whereas MOTS-c levels were significantly reduced (p < 0.05). No significant difference was observed in humanin levels between the two groups. A positive correlation was identified between endoglin levels and VPO1 (r = 0.943, p < 0.001), humanin (r = 0.421, p < 0.01), and uric acid (r = 0.314, p = 0.02) in the preeclamptic group.
Conclusions: Our findings suggest that the elevation of VPO1 and miR-200c levels, along with the reduction of humanin and MOTS-c levels, may contribute to the increased endoglin levels and subsequent endothelial dysfunction observed in preeclampsia. These changes may be associated with the pathogenesis and severity of the disease.
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http://dx.doi.org/10.1007/s11033-024-10148-w | DOI Listing |
Mol Biol Rep
December 2024
Department of Medical Biochemistry, Cerrahpasa Faculty of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey.
Front Physiol
August 2024
Department of Exercise Science, University of Puget Sound, Tacoma, WA, United States.
Skeletal muscle hypertrophy is generally associated with a fast-to-slow phenotypic adaptation in both human and rodent models. Paradoxically, this phenotypic shift is not paralleled by a concomitant increase in mitochondrial content and aerobic markers that would be expected to accompany a slow muscle phenotype. To understand the temporal response of the mitochondrial life cycle (i.
View Article and Find Full Text PDFEur J Pharmacol
November 2024
Department of Physiology, Faculty of Medicine, Gaziantep University, Gaziantep, Turkey.
Sodium-glucose cotransporter 2 (SGLT2) inhibitors produce cardioprotective effects on heart failure (HF), even in the absence of diabetes. However, the underlying mechanisms of this cardioprotective effect remain unexplored. The purpose of this study was to examine the effects of SGLT2 inhibitors on serum MOTS-c, humanin levels, nitrosative stress, and ferroptosis parameters in diabetic patients with HF with reduced ejection fraction (HFrEF).
View Article and Find Full Text PDFReprod Toxicol
October 2024
Department of Reproduction and Genetics, The First Affiliated Hospital of Kunming Medical University, Kunming 650032, China. Electronic address:
Male patients who undergo prepubertal chemotherapy face the dual problems of fertility preservation in adulthood, including low testosterone, hypersexual function, and infertility. Humanin, as a small polypeptide coded within the mitochondrial DNA, with the mitochondrial short open reading frame named MOTS-c, both was believed to regulate mitochondrial homeostasis, be anti-inflammatory, improve metabolism, anti-apoptosis, and multiple pharmacological effects. However, there exists little evidence that reported Humanin and MOTS-c 's effects on moderating male spermatogenic function of patients after prepubertal chemotherapy.
View Article and Find Full Text PDFSleep Med
July 2024
Department of Neurology, Weihai Municipal Hospital, Cheeloo College of Medicine, Shandong University, Weihai, Shandong, China. Electronic address:
Study Objectives: Increased reactive oxygen species associated with loss of mitochondrial function affect synaptic activity, which is an important mechanism underlying cognitive decline. This study assesses the role of mitochondrial proteins in neuron-derived exosomes (NDEs) on cognitive impairment in patients with obstructive sleep apnea (OSA) without dementia.
Methods: Analyses were conducted in 268 study participants with complete polysomnography data, cognitive tests, and important clinical data available.
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