| Autor: |
Khashchenko EP; FSBI 'National Medical Research Center for Obstetrics, Gynecology and Perinatology Named after Academician V.I. Kulakov', Ministry of Healthcare of the Russian Federation, 4, Oparina Str., 117997 Moscow, Russia., Vysokikh MY; FSBI 'National Medical Research Center for Obstetrics, Gynecology and Perinatology Named after Academician V.I. Kulakov', Ministry of Healthcare of the Russian Federation, 4, Oparina Str., 117997 Moscow, Russia.; A.N. Belozersky Research Institute of Physico-Chemical Biology MSU, Leninskye Gory, House 1, Building 40, 119992 Moscow, Russia., Marey MV; FSBI 'National Medical Research Center for Obstetrics, Gynecology and Perinatology Named after Academician V.I. Kulakov', Ministry of Healthcare of the Russian Federation, 4, Oparina Str., 117997 Moscow, Russia., Sidorova KO; Faculty of Medicine and Biology, Pirogov Russian National Research Medical University, 1 Ostrovityanova Str., 117997 Moscow, Russia., Manukhova LA; FSBI 'National Medical Research Center for Obstetrics, Gynecology and Perinatology Named after Academician V.I. Kulakov', Ministry of Healthcare of the Russian Federation, 4, Oparina Str., 117997 Moscow, Russia., Shkavro NN; FSBI 'National Medical Research Center for Obstetrics, Gynecology and Perinatology Named after Academician V.I. Kulakov', Ministry of Healthcare of the Russian Federation, 4, Oparina Str., 117997 Moscow, Russia., Uvarova EV; FSBI 'National Medical Research Center for Obstetrics, Gynecology and Perinatology Named after Academician V.I. Kulakov', Ministry of Healthcare of the Russian Federation, 4, Oparina Str., 117997 Moscow, Russia.; Department for Obstetrics, Gynecology, Perinatology and Reproduction, Sechenov First Moscow State Medical University, Trubetskaya Str. 8, Bld. 2, 119991 Moscow, Russia., Chuprynin VD; FSBI 'National Medical Research Center for Obstetrics, Gynecology and Perinatology Named after Academician V.I. Kulakov', Ministry of Healthcare of the Russian Federation, 4, Oparina Str., 117997 Moscow, Russia., Fatkhudinov TK; FSBI 'National Medical Research Center for Obstetrics, Gynecology and Perinatology Named after Academician V.I. Kulakov', Ministry of Healthcare of the Russian Federation, 4, Oparina Str., 117997 Moscow, Russia.; Department of Histology, Cytology and Embryology, Peoples' Friendship University of Russia (RUDN), Miklukho-Maklaya Str. 6, 117997 Moscow, Russia., Adamyan LV; FSBI 'National Medical Research Center for Obstetrics, Gynecology and Perinatology Named after Academician V.I. Kulakov', Ministry of Healthcare of the Russian Federation, 4, Oparina Str., 117997 Moscow, Russia., Sukhikh GT; FSBI 'National Medical Research Center for Obstetrics, Gynecology and Perinatology Named after Academician V.I. Kulakov', Ministry of Healthcare of the Russian Federation, 4, Oparina Str., 117997 Moscow, Russia.; Department for Obstetrics, Gynecology, Perinatology and Reproduction, Sechenov First Moscow State Medical University, Trubetskaya Str. 8, Bld. 2, 119991 Moscow, Russia. |
| Abstrakt: |
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. |
