Evaluation of protein levels of autophagy markers (Beclin 1 and SQSTM1/p62) and phosphorylation of cyclin E in the placenta of women with preeclampsia

Yildiz, Dilara Akçora; Kandemir, Sevgi İrtegün; Ağaçayak, Elif; Deveci, Engin

doi:10.14715/10.14715/cmb/2017.63.12.12

Cited by 10 publications

(4 citation statements)

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“…Recently, some scholars have found that trophoblast autophagy plays a role in the pathogenesis of severe pre‐eclampsia. Numerous studies have shown that pre‐eclampsia patients have severe placental ischaemia and that this environment can promote autophagy . When excessive autophagy occurs in placental chorionic trophoblasts, it causes the death of trophoblasts .…”

Section: Introductionmentioning

confidence: 99%

“…Numerous studies have shown that pre-eclampsia patients have severe placental ischaemia and that this environment can promote autophagy. 8,9 When excessive autophagy occurs in placental chorionic trophoblasts, it causes the death of trophoblasts. 10,11 Additionally, a report showed that damaged autophagy in extravillous trophoblast cells contributed to developing pre-eclampsia pathophysiology.…”

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confidence: 99%

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LRP6 regulates Rab7‐mediated autophagy through the Wnt/β‐catenin pathway to modulate trophoblast cell migration and invasion

Peng

Zhou

et al. 2019

J of Cellular Biochemistry

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Pre‐eclampsia is a common complication during pregnancy; however, the underlying mechanisms of the crosstalk between low‐density lipoprotein receptor‐related protein 6 (LRP6) and autophagy in trophoblast cells are still not fully explored. Messenger RNA (mRNA) and protein levels of LRP6, beclin 1, Unc‐51‐like autophagy activating kinase 1 (ULK1), p62, vimentin, matrix metallopeptidase‐9 (MMP‐9), β‐catenin, c‐Myc, and Rab7, as well as the ratio of LC3‐II/LC3‐I, were analysed by quantitative real‐time polymerase chain reaction or Western blot analysis, respectively. An MTT assay was used to measure cell growth, and transwell and wound healing assays were carried out to evaluate the invasion and migration abilities of the trophoblasts used. An immunofluorescence assay was used to measure LC3. The mRFP‐GFP‐LC3 tandem fluorescence assay was applied to detect autophagic flow. LRP6 overexpression was achieved by constructing pcDNA3.1‐LRP6 vectors. LRP6 was expressed at low levels in HTR‐8/SVneo cells under hypoxia/reoxygenation (H/R) conditions. H/R inhibited the activation of autophagy. LRP6 overexpression promoted cell proliferation and activated autophagy, which led to the upregulation of beclin 1 and ULK1, as well as the ratio of LC3‐II/LC3‐I and the downregulation of p62. Furthermore, LRP6 overexpression elevated the migration and invasion abilities of the indicated cells and increased vimentin and MMP‐9 expression levels. Furthermore, LRP6 upregulated Rab7 and activated autophagy through the Wnt/β‐catenin pathway. The late autophagy inhibitor bafilomycin A1 (Baf‐A1) and the Wnt/β‐catenin pathway inhibitor PKF115‐584 reversed the effects of LRP6 on trophoblast autophagy, migration and invasion. LRP6 promotes Rab7‐mediated autophagy by activating the Wnt/β‐catenin pathway, which leads to increasing migration and invasion of trophoblast cells. Our study paves a new avenue for clinical treatment, and LRP6 may serve as an essential target in pre‐eclampsia.

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Section: Introductionmentioning

confidence: 99%

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confidence: 99%

LRP6 regulates Rab7‐mediated autophagy through the Wnt/β‐catenin pathway to modulate trophoblast cell migration and invasion

Peng

Zhou

et al. 2019

J of Cellular Biochemistry

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“…They jointly regulate the generation of autophagosomes, and P62 is involved in autophagy degradation. The LC3-II to LC3-I ratio is currently recognized as an important marker of autophagy activation [ 26 , 27 ]. Because these factors are closely related to the activation and activity of autophagy, their expression levels in DCI patients are often used to infer autophagy activity.…”

Section: Resultsmentioning

confidence: 99%

Electroacupuncture improves cognitive impairment in diabetic cognitive dysfunction rats by regulating the mitochondrial autophagy pathway

Cui

Yan³

et al. 2022

J Physiol Sci

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Background Diabetes-associated cognitive dysfunction has become a major public health concern. However, the mechanisms driving this disease are elusive. Herein, we explored how electroacupuncture improves learning and memory function in diabetic rats. Methods The diabetic model was established by intraperitoneal injection of streptozotocin (STZ) in adult Sprague–Dawley rats. Rats were fed on high-fat and high-sugar diets. Learning and memory functions were assessed using behavioral tests. The hematoxylin and eosin (H&E) staining, Western blotting, real-time PCR, ELISA, immunohistochemistry, and transmission electronic microscopy (TEM) was performed to test related indicators. Results High-fat and high-sugar diets impaired learning and memory function in rats, while electroacupuncture treatment reversed these changes. The model group presented highly prolonged escape latency compared to the control group, indicating impaired learning and memory functions. The TEM examination showed that electroacupuncture enhanced Aβ clearance and mitochondrial autophagy in hippocampal neuronal cells by increasing DISC1 expression. Conclusions Electroacupuncture improves learning and memory function in diabetic rats by increasing DISC1 expression to promote mitophagy. This enhanced Aβ clearance, alleviating cytotoxicity in hippocampal neuronal cells.

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“…Each step of autophagic flux is tightly regulated by a myriad of evolutionally conserved proteins encoded by the autophagy-related genes ( Figure 1 A). However, which regulatory molecules in the autophagy–lysosomal pathway are dysregulated in the placenta or the cellular models of PE remain poorly understood [ 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 , 52 , 53 ].…”

Section: Introductionmentioning

confidence: 99%

Hypoxia-Reoxygenation Impairs Autophagy-Lysosomal Machinery in Primary Human Trophoblasts Mimicking Placental Pathology of Early-Onset Preeclampsia

Cheng

Huang

Jash

et al. 2022

IJMS

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We have previously described that placental activation of autophagy is a central feature of normal pregnancy, whereas autophagy is impaired in preeclampsia (PE). Here, we show that hypoxia–reoxygenation (H/R) treatment dysregulates key molecules that maintain autophagy–lysosomal flux in primary human trophoblasts (PHTs). Ultrastructural analysis using transmission electron microscopy reveals a significant reduction in autophagosomes and autolysosomes in H/R-exposed PHTs. H/R-induced accumulation of protein aggregates follows a similar pattern that occurs in PHTs treated with a lysosomal disruptor, chloroquine. Importantly, the placenta from early-onset PE deliveries exhibits the same features as seen in H/R-treated PHTs. Taken together, our results indicate that H/R disrupts autophagic machinery in PHTs and that impaired autophagy in the placenta from early-onset PE deliveries mimics the events in H/R-treated PHTs. Notably, assessment of key regulators at each stage of autophagic processes, especially lysosomal integrity, and verification of autophagic ultrastructure are essential for an accurate evaluation of autophagy activity in human trophoblasts and placental tissue from PE deliveries.

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Evaluation of protein levels of autophagy markers (Beclin 1 and SQSTM1/p62) and phosphorylation of cyclin E in the placenta of women with preeclampsia

Cited by 10 publications

References 0 publications

LRP6 regulates Rab7‐mediated autophagy through the Wnt/β‐catenin pathway to modulate trophoblast cell migration and invasion

LRP6 regulates Rab7‐mediated autophagy through the Wnt/β‐catenin pathway to modulate trophoblast cell migration and invasion

Electroacupuncture improves cognitive impairment in diabetic cognitive dysfunction rats by regulating the mitochondrial autophagy pathway

Hypoxia-Reoxygenation Impairs Autophagy-Lysosomal Machinery in Primary Human Trophoblasts Mimicking Placental Pathology of Early-Onset Preeclampsia

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