Autophagy-related protein LC3 and Beclin-1 in the first trimester of pregnancy

Chifenti, Barbara; Locci, Maria Teresa Fernanda; Lazzeri, Gloria; Guagnozzi, Mariangela; Dinucci, D.; Chiellini, Emo; Filice, Maria Elena; Salerno, Maria Giovanna; Battini, Lorella

doi:10.5653/cerm.2013.40.1.33

Cited by 48 publications

(31 citation statements)

References 14 publications

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“…Autophagy is essential for normal placental development and for maintaining pregnancy at different gestational stages 49,50 and a protective role of autophagy in placental antiviral defense has been recently reported. 51 Placental autophagy is also induced under pathological conditions, such as preeclampsia and intrauterine growth restriction.…”

Section: Discussionmentioning

confidence: 99%

Sexual dimorphism in activation of placental autophagy in obese women with evidence for fetal programming from a placenta-specific mouse model

et al. 2016

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(2016) Sexual dimorphism in activation of placental autophagy in obese women with evidence for fetal programming from a placenta-specific mouse model, Autophagy, 12:5, 752-769, DOI: 10.1080/15548627.2016 ABSTRACTThe incidence of maternal obesity and its co-morbidities (diabetes, cardiovascular disease) continues to increase at an alarming rate, with major public health implications. In utero exposure to maternal obesity has been associated with development of cardiovascular and metabolic diseases in the offspring as a result of developmental programming. The placenta regulates maternal-fetal metabolism and shows significant changes in its function with maternal obesity. Autophagy is a cell-survival process, which is responsible for the degradation of damaged organelles and misfolded proteins. Here we show an activation of autophagosomal formation and autophagosome-lysosome fusion in placentas of males but not females from overweight (OW) and obese (OB) women vs. normal weight (NW) women. However, total autophagic activity in these placentas appeared to be decreased as it showed an increase in SQSTM1/p62 and a decrease in lysosomal biogenesis. A mouse model with a targeted deletion of the essential autophagy gene Atg7 in placental tissue showed significant placental abnormalities comparable to those seen in human placenta with maternal obesity. These included a decrease in expression of mitochondrial genes and antioxidants, and decreased lysosomal biogenesis. Strikingly, the knockout mice were developmentally programmed as they showed an increased sensitivity to high-fat diet-induced obesity, hyperglycemia, hyperinsulinemia, increased adiposity, and cardiac remodeling. In summary, our results indicate a sexual dimorphism in placental autophagy in response to maternal obesity. We also show that autophagy plays an important role in placental function and that inhibition of placental autophagy programs the offspring to obesity, and to metabolic and cardiovascular diseases.

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Section: Discussionmentioning

confidence: 99%

Sexual dimorphism in activation of placental autophagy in obese women with evidence for fetal programming from a placenta-specific mouse model

et al. 2016

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“…The autophagy markers LC3-II and Beclin-1 are highly expressed in villous cytotrophoblasts at the first trimester and they are prevalently activated in trophoblast cells during the whole gestation period (Chifenti et al, 2013). The cytotrophoblast and the syncytiotrophoblast, which form the placental barrier, function differently according to different gestational ages.…”

Section: Autophagy Inhibitors and The Clinical Effectsmentioning

confidence: 99%

The Role of Secretory Autophagy in Zika Virus Transfer through the Placental Barrier

Zhang

Yuan

2017

Front. Cell. Infect. Microbiol.

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Recent studies indicated that the Zika virus genome could be detected in the amniotic fluid and the fetal brain, which confirms that the virus can cross the placental barrier. Secretory autophagy or exosome pathways may participate in this virus transfer. Autophagy modulators regulate autophagosome formation or membrane fusion with lysosomal vesicles and therefore inhibit viral nucleocapsid releasing or virus transfer to the fetus hypothetically. However, some autophagy modulators may enhance virus replication. Autophagy inhibitors may arrest placental development; while exaggeration of autophagy in human placenta may be associated with the fetal growth restriction. Therefore, autophagy modulators should be used carefully due to their complex clinical effects. Alternatively, exosome-specific inhibitors might be also considered, although their safety of both maternal and fetal conditions must be carefully assessed before any advancement to human clinical trials.

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“…Autophagy is a complex catabolic mechanism involving the transport of cytoplasmic components to the lysosome (Sever & Demir, 2017). Key proteins of the autophagic pathway, such as Beclin1 and microtubule-associated protein light chain 3 (Lc3), are conserved among species and are widely used as autophagic markers (Chifenti et al, 2013;Mathai, Meijer, & Simonsen, 2017). Beclin1 promotes autophagic nucleation and the recruitment of cytosolic proteins essential for autophagosome formation (Kang, Zeh, Lotze, & Tang, 2011).…”

Section: Introductionmentioning

confidence: 99%

Autophagy and Cathepsin D mediated apoptosis contributing to ovarian follicular atresia in the Nile tilapia

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Melo

Pinheiro

et al. 2019

Molecular Reproduction Devel

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Follicular atresia is a hormonally controlled degenerative process involving apoptosis of the somatic and germ cells. Since different signaling pathways can induce cell death, the aim of the present study was to investigate cell death signaling and crosstalk between autophagic, apoptotic, and lysosomal proteins during follicular atresia in Nile tilapia. For this, females were kept in controlled conditions for 21 days, and ovary samples were collected weekly. The atretic follicles (AF) were analyzed in three regression phases: Early, advanced, and late. Under electron microscopy, the follicular cells exhibited numerous protein synthesis organelles in the early AF. Immunoreactivity for Bcl2, Beclin1, Lc3, and Cathepsin D increased significantly in advanced AF (p < .001), when follicular cells were in intense yolk phagocytosis. In this phase, autophagosomes and autolysosomes were frequently observed. In the late AF, follicular cells had a markedly electron‐lucid cytoplasm and immunoreactivity for Bax and TUNEL assay indicated an elevated apoptosis rate. Colocalisation of Lamp1/Cathepsin D and Lc3/Caspase‐3 suggests dynamic crosstalk between the autophagy, apoptosis, and lysosome pathways. Taken together, the data indicate that autophagy plays a role in the homeostasis and clearance of the follicular cells preceding Cathepsin D mediated apoptosis during follicular atresia in Nile tilapia.

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Autophagy-related protein LC3 and Beclin-1 in the first trimester of pregnancy

Cited by 48 publications

References 14 publications

Sexual dimorphism in activation of placental autophagy in obese women with evidence for fetal programming from a placenta-specific mouse model

Sexual dimorphism in activation of placental autophagy in obese women with evidence for fetal programming from a placenta-specific mouse model

The Role of Secretory Autophagy in Zika Virus Transfer through the Placental Barrier

Autophagy and Cathepsin D mediated apoptosis contributing to ovarian follicular atresia in the Nile tilapia

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