Exosomal microRNAs and long noncoding RNAs: as novel biomarkers for endometriosis

Soltani-Fard, Elahe; Asadi, Mohammad; Taghvimi, Sina; Vafadar, Asma; Vosough, Parisa; Tajbakhsh, Amir; Savardashtaki, Amir

doi:10.1007/s00441-023-03802-5

Cited by 3 publications

(1 citation statement)

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“…Although exosomes derived from endometrial cells have been identified in both uterine and peritoneal fluids [41,42], it is difficult to accurately trace their origin; the vesicles can be derived from eutopic endometrium, stranded endometrium fragments or endometrioid heterotopias, and even from macrophages scavenging the endometrial debris. In any event, the endometrial exosomes may exert a conditioning effect on peritoneal microenvironments, enhancing their receptivity to stranded endometrium fragments, suppressing immunological reactivity and ultimately facilitating engraftment [43]. Exosomal fractions are increasingly considered as a basis for diagnostics and monitoring in various focal disorders as they often provide a proteomic and regulomic footprint of poorly accessible lesions.…”

Section: Discussionmentioning

confidence: 99%

Altered Glycolysis, Mitochondrial Biogenesis, Autophagy and Apoptosis in Peritoneal Endometriosis in Adolescents

Khashchenko,

Vysokikh,

Marey

et al. 2024

IJMS

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Energy metabolism plays a pivotal role in the pathogenesis of endometriosis. For the initial stages of the disease in adolescents, this aspect remains unexplored. The objective of this paper was to analyze the association of cellular and endosomal profiles of markers of glycolysis, mitochondrial biogenesis, apoptosis, autophagy and estrogen signaling in peritoneal endometriosis (PE) in adolescents. We included 60 girls aged 13–17 years in a case–control study: 45 with laparoscopically confirmed PE (main group) and 15 with paramesonephric cysts (comparison group). Samples of plasma and peritoneal fluid exosomes, endometrioid foci and non-affected peritoneum were tested for estrogen receptor (Erα/β), hexokinase (Hex2), pyruvate dehydrogenase kinase (PDK1), glucose transporter (Glut1), monocarboxylate transporters (MCT1 and MCT2), optic atrophy 1 (OPA1, mitochondrial fusion protein), dynamin-related protein 1 (DRP1, mitochondrial fission protein), Bax, Bcl2, Beclin1, Bnip3, P38 mitogen-activated protein kinase (MAPK), hypoxia-inducible factor 1 (Hif-1α), mitochondrial voltage-dependent anion channel (VDAC) and transforming growth factor (TGFβ) proteins as markers of estrogen signaling, glycolysis rates, mitochondrial biogenesis and damage, apoptosis and autophagy (Western-Blot and PCR). The analysis identified higher levels of molecules associated with proliferation (ERβ), glycolysis (MCT2, PDK1, Glut1, Hex2, TGFβ and Hif-1α), mitochondrial biogenesis (OPA1, DRP1) and autophagy (P38, Beclin1 and Bnip3) and decreased levels of apoptosis markers (Bcl2/Bax) in endometrioid foci compared to non-affected peritoneum and that in the comparison group (p < 0.05). Patients with PE had altered profiles of ERβ in plasma and peritoneal fluid exosomes and higher levels of Glut1, MCT2 and Bnip3 in plasma exosomes (p < 0.05). The results of the differential expression profiles indicate microenvironment modification, mitochondrial biogenesis, estrogen reception activation and glycolytic switch along with apoptosis suppression in peritoneal endometrioid foci already in adolescents.

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Section: Discussionmentioning

confidence: 99%