PMID- 36629523 OWN - NLM STAT- MEDLINE DCOM- 20230113 LR - 20230113 IS - 1414-431X (Electronic) IS - 0100-879X (Print) IS - 0100-879X (Linking) VI - 55 DP - 2023 TI - Down-regulation of autophagy proteins is associated with higher mTOR expression in the placenta of pregnant women with preeclampsia. PG - e12283 LID - S0100-879X2022000100683 [pii] LID - 10.1590/1414-431X2022e12283 [doi] LID - e12283 AB - Autophagy is a lysosomal degradation pathway that removes protein aggregates and damaged organelles maintaining cellular integrity. It seems to be essential for cell survival during stress, starvation, hypoxia, and consequently to the placenta implantation and development. Preeclampsia (PE) is a multisystemic disorder characterized by the onset of hypertension associated or not with proteinuria and other maternal complications. Considering that the placenta seems to play an important role in the pathogenesis of PE, the objective of the present study was to evaluate protein levels of light chain protein (LC3), beclin-1, and the mammalian target of rapamycin (mTOR) in the placenta of pregnant women with PE. Placental tissues collected from 20 women with PE and 20 normotensive (NT) pregnant women were evaluated for LC3, beclin-1, and mTOR expression by qPCR and immunohistochemistry. The mRNA for LC3 and beclin-1 were significantly lower, while mTOR gene expression was significantly higher in the placenta of pregnant women with PE than in the NT group. Placentas of PE women showed significantly decreased protein expression of LC3-II and beclin-1, whereas mTOR was significantly increased compared with the NT pregnant women. There was a negative correlation between protein expression of mTOR and LC3-II in the placental tissue of PE women. In conclusion, the results showed autophagy deficiency suggesting that failure in this degradation process may contribute to the pathogenesis of PE; however, new studies involving cross-talk between autophagy and inflammatory molecular mechanisms might help to better understand the autophagy process in this obstetric pathology. FAU - Weel, I C AU - Weel IC AUID- ORCID: 0000-0002-8267-5911 AD - Departamento de Ciencias Quimicas e Biologicas, Instituto de Biociencias, Universidade Estadual Paulista, Botucatu, SP, Brasil. FAU - Ribeiro, V R AU - Ribeiro VR AUID- ORCID: 0000-0001-7629-7689 AD - Departamento de Ciencias Quimicas e Biologicas, Instituto de Biociencias, Universidade Estadual Paulista, Botucatu, SP, Brasil. FAU - Romao-Veiga, M AU - Romao-Veiga M AUID- ORCID: 0000-0002-8990-0237 AD - Departamento de Ciencias Quimicas e Biologicas, Instituto de Biociencias, Universidade Estadual Paulista, Botucatu, SP, Brasil. FAU - Fioratti, E G AU - Fioratti EG AUID- ORCID: 0000-0002-1982-0119 AD - Departamento de Ciencias Quimicas e Biologicas, Instituto de Biociencias, Universidade Estadual Paulista, Botucatu, SP, Brasil. FAU - Peracoli, J C AU - Peracoli JC AUID- ORCID: 0000-0002-3273-3001 AD - Departamento de Ginecologia e Obstetricia, Faculdade de Medicina de Botucatu, Universidade Estadual Paulista, Botucatu, SP, Brasil. FAU - Peracoli, M T S AU - Peracoli MTS AUID- ORCID: 0000-0002-0936-9512 AD - Departamento de Ciencias Quimicas e Biologicas, Instituto de Biociencias, Universidade Estadual Paulista, Botucatu, SP, Brasil. AD - Departamento de Ginecologia e Obstetricia, Faculdade de Medicina de Botucatu, Universidade Estadual Paulista, Botucatu, SP, Brasil. LA - eng PT - Journal Article DEP - 20230109 PL - Brazil TA - Braz J Med Biol Res JT - Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas JID - 8112917 RN - 0 (Beclin-1) RN - EC 2.7.11.1 (TOR Serine-Threonine Kinases) RN - EC 2.7.1.1 (MTOR protein, human) SB - IM MH - Female MH - Pregnancy MH - Humans MH - *Placenta MH - Pregnant Women MH - *Pre-Eclampsia/genetics MH - Beclin-1/genetics/metabolism MH - Down-Regulation MH - TOR Serine-Threonine Kinases/metabolism MH - Autophagy/physiology PMC - PMC9828864 EDAT- 2023/01/12 06:00 MHDA- 2023/01/14 06:00 PMCR- 2023/01/09 CRDT- 2023/01/11 10:05 PHST- 2022/07/27 00:00 [received] PHST- 2022/11/09 00:00 [accepted] PHST- 2023/01/11 10:05 [entrez] PHST- 2023/01/12 06:00 [pubmed] PHST- 2023/01/14 06:00 [medline] PHST- 2023/01/09 00:00 [pmc-release] AID - S0100-879X2022000100683 [pii] AID - 10.1590/1414-431X2022e12283 [doi] PST - epublish SO - Braz J Med Biol Res. 2023 Jan 9;55:e12283. doi: 10.1590/1414-431X2022e12283. eCollection 2023.