Metastasis-associated lung adenocarcinoma transcript 1 induces methyl-CpG-binding domain protein 4 in mice with recurrent spontaneous abortion caused by anti-phospholipid antibody positivity

Han, Yongmei; Wang, Ying; Zhang, Chenyu; Li, Yanru; Guo, Jìng; Tian, Chao

doi:10.1016/j.placenta.2023.04.008

Cited by 2 publications

(6 citation statements)

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“…Furthermore, aPL-positive RPL mouse model was generated [172]. The embryo resorption rate was increased in aPL-positive RPL mice compared both to RPL mice negative for aPL and control mice [172]. Placental MALAT1 overexpression by adenoviral transfection in aPL-positive RPL mice significantly decreased embryo resorption rate compared to untreated aPL-RPL mice [172].…”

Section: Non-coding Rnas-emerging Players In Oaps Pathophysiologymentioning

confidence: 99%

“…Effects of decreased MALAT1 expression on trophoblast cell function were investigated in vitro by downregulation of this lncRNA in HTR-8/SVneo and JAR cells. The results showed that trophoblast cells with decreased MALAT1 levels proliferated less than unmodified cells and their migrating and invasive abilities were decreased as well as expression of EMT-related proteins [158,[169][170][171][172][173]. Different mechanisms of action were proposed for MALAT1-dependent regulation of trophoblast cell function.…”

Section: Non-coding Rnas-emerging Players In Oaps Pathophysiologymentioning

confidence: 99%

“…As mentioned above, APS is one of the main risk factors for RPL [168] but underlying mechanisms of aPL-induced RPL are still not completely elucidated. Recent studies identified lncRNA MALAT1 as one of the major regulators of the processes important for the adequate placental development and function in early pregnancy [158,[169][170][171][172][173]. Namely, MALAT1 levels were significantly downregulated in placentas of the patients experiencing RPL of unknown etiology compared to the healthy controls [158,174].…”

Section: Non-coding Rnas-emerging Players In Oaps Pathophysiologymentioning

confidence: 99%

“…Namely, MALAT1 levels were significantly downregulated in placentas of the patients experiencing RPL of unknown etiology compared to the healthy controls [158,174]. Furthermore, recent research showed that trophoblast and placental MALAT1 levels of aPL-positive RPL patients were even lower than MALAT1 levels of aPL-negative RPL patients [172]. Furthermore, aPL-positive RPL mouse model was generated [172].…”

Section: Non-coding Rnas-emerging Players In Oaps Pathophysiologymentioning

confidence: 99%

“…Furthermore, recent research showed that trophoblast and placental MALAT1 levels of aPL-positive RPL patients were even lower than MALAT1 levels of aPL-negative RPL patients [172]. Furthermore, aPL-positive RPL mouse model was generated [172]. The embryo resorption rate was increased in aPL-positive RPL mice compared both to RPL mice negative for aPL and control mice [172].…”

Section: Non-coding Rnas-emerging Players In Oaps Pathophysiologymentioning

confidence: 99%

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Trophoblast Cell Function in the Antiphospholipid Syndrome

Vrzić Petronijević,

Vilotić,

Bojić-Trbojević

et al. 2023

Biomedicines

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Antiphospholipid syndrome (APS) is a complex thrombo-inflammatory autoimmune disease characterized by the presence of antiphospholipid antibodies (aPL). Women with APS are at high risk of recurrent early pregnancy loss as well as late obstetrical complications—premature birth due to placental insufficiency or severe preeclampsia. Accumulating evidence implies that vascular thrombosis is not the only pathogenic mechanism in obstetric APS, and that the direct negative effect of aPL on the placental cells, trophoblast, plays a major role. In this review, we summarize the current findings regarding the potential mechanisms involved in aPL-induced trophoblast dysfunction. Introduction on the APS and aPL is followed by an overview of the effects of aPL on trophoblast—survival, cell function and aPL internalization. Finally, the implication of several non-coding RNAs in pathogenesis of obstetric APS is discussed, with special emphasis of their possible role in trophoblast dysfunction and the associated mechanisms.

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Section: Non-coding Rnas-emerging Players In Oaps Pathophysiologymentioning

confidence: 99%