Nesfatin-1 Promotes Proliferation, Migration and Invasion of HTR-8/SVneo Trophoblast Cells and Inhibits Oxidative Stress via Activation of PI3K/AKT/mTOR and AKT/GSK3β Pathway

Li, Tingting; Wei, Sumei; Fan, Conghong; Tang, Dongmei; Luo, Di

doi:10.1007/s43032-020-00324-1

Cited by 17 publications

(11 citation statements)

References 39 publications

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“…28 During normal pregnancy, trophoblast cells infiltrate into the decidua to complete the spiral artery remodeling and placenta formation, while PE placenta uterine spiral artery recasting is impaired, and trophoblast cell proliferation is reduced. 29 30 Our study found that, in the hypoxic-treated cells, high expression of RORA inhibited cell proliferation and the expression of related proteins, while the knockdown of RORA had the opposite effect. Angiogenesis is a key factor in placenta formation and vascular remodeling, involving a variety of growth factors.…”

Section: Discussionmentioning

confidence: 64%

RAR-Related Orphan Receptor: An Accelerated Preeclampsia Progression by Activating the JAK/STAT3 Pathway

Zhu

2022

Yonsei Med J

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Purpose To investigate the effect and underlying mechanism of RAR related orphan receptor A (RORA) on preeclampsia (PE). Materials and Methods Differentially expressed genes (DEGs) in four datasets were obtained by using the Venn diagram method. RORA mRNA and protein expressions were detected by qRT-PCR, western blot, and immunohistochemistry. HTR-8/SVneo cell viability, proliferation, invasion, migration, and angiogenesis were detected by CCK-8 assay, EdU assay, Transwell, wound healing assay, and tube formation assay, respectively. The concentration of Ang-1 in cells was assessed using available ELISA kit. Epithelial-mesenchymal transition, proliferation, and angiogenesis-related proteins were detected by western blot. GSEA analysis were performed for common DEGs, and the expression of enriched pathway-related proteins was also detected. Results The expression of RORA was increased in PE tissue and HTR-8/SVneo cells. Silencing RORA could promote the migration, invasion, epithelial-mesenchymal transition, proliferation, and angiogenesis of hypoxia-treated HTR-8/SVneo cells. Mechanistically, RORA contributed to the deterioration of PE by activating the JAK2/STAT3 signaling pathway to promote cell proliferation, migration, invasion, and angiogenesis. Conclusion RORA was up-regulated in PE and affected HTR-8/SVneo cell proliferation, invasion, migration, apoptosis, and angiogenesis via the JAK2/STAT3 signaling pathway. This provided a novel strategy for the prevention and treatment of PE.

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Section: Discussionmentioning

confidence: 64%

RAR-Related Orphan Receptor: An Accelerated Preeclampsia Progression by Activating the JAK/STAT3 Pathway

Zhu

2022

Yonsei Med J

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“…Mechanistic studies on how nesfatin-1 stimulates GlP-1 secretion in vivo are required. Several studies have shown that the effects of nesfatin-1 involve the aKT pathway (42)(43)(44)(45)(46)(47). although various studies have been conducted on nesfatin-1 (48,49), the nesfatin-1 receptor has not yet been identified.…”

Section: Discussionmentioning

confidence: 99%

Intraperitoneal administration of nesfatin‑1 stimulates glucagon‑like peptide‑1 secretion in fasted mice

et al. 2022

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increasing endogenous secretion of glucagon-like peptide (GlP)-1 is considered a promising therapeutic approach for type 2 diabetes because decreased GlP-1 plasma concentrations have been observed in patients with this condition. nesfatin-1, which is a central and peripheral anorexigenic peptide, has been reported to release GlP-1 from enteroendocrine STc-1 cells, although whether nesfatin-1 stimulates GlP-1 secretion in vivo remains to be elucidated. Previous studies have indicated that nesfatin-1 has glucose-lowering and insulinotropic effects in mice and rats; however, the in vivo mechanism remains unclear. The present study aimed to investigate whether peripheral administration of nesfatin-1 increased blood concentrations of GlP-1 and insulin in food-deprived mice. nesfatin-1 was administered intraperitoneally to 18-h fasted mice. Plasma GlP-1 and insulin concentrations in the mice administered 2.5 µmol/kg nesfatin-1 were higher than those in saline-treated mice. Blood glucose concentrations in mice treated with 1.25 and 2.5 µmol/kg nesfatin-1 were lower than those in saline-treated mice. The mrna expression of preproglucagon in mouse ilea after treatment with 1.25 µmol/kg nesfatin-1 was higher than that in saline-treated mice. The administration of 1.25 µmol/kg nesfatin-1 raised GlP-1 concentrations at 30 and 60 min and insulin concentrations at 30 and 60 min after injection. Furthermore, the higher level of nesfatin-1-induced insulin was diminished by pre-administration of anti-GlP-1 antiserum. intraperitoneally administered nesfatin-1 increased insulin concentrations by accelerating GLP-1 secretion. The results are the first in vivo demonstration of promotion of GlP-1 secretion by nesfatin-1 in the mouse, suggesting the developmental potential of nesfatin-1 for GlP-1 release.

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“…PI3K/AKT signaling pathway has always been a hotspot for studying the mechanism of human tumorigenesis, and is associated with tumor cell migration, adhesion, angiogenesis, and extracellular matrix degradation 27,28 . Notably, the biological behaviors of trophoblasts are often compared with those of tumor cells, because they share many similar molecular mechanisms, moreover, appropriate activation of PI3K/AKT signaling pathway can promote trophoblast proliferation and migration 29,30 . The expression of ITGB1 is close related with the PI3K/Akt pathway in regulating tumor cell invasion 14 .…”

Section: Discussionmentioning

confidence: 99%

Integrin β1 regulates proliferation, apoptosis, and migration of trophoblasts through activation of phosphoinositide 3 kinase/protein kinase B signaling

Shu

Han

et al. 2021

J of Obstet and Gynaecol

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Aims Abnormal trophoblast invasion is one of the onsets of preeclampsia (PE). Studies found that integrin β1 (ITGB1) is closely related to PE, but the role of ITGB1 in the progression of trophoblast remained unclear. Therefore, we studied the functional role of ITGB1 in PE and its effects on trophoblast. Methods ITGB1 expression in placenta tissues was determined by quantitative real‐time polymerase chain reaction (qRT‐PCR). The effects of transfection on HTR‐8/SVneo cells were analyzed by qRT‐PCR and western blotting. After cell transfection, colony formation assay, flow cytometry, wound healing assay, and transwell assay were performed to detect cell proliferation, apoptosis, migration, and invasion. Western blotting assay was used for determining phosphoinositide 3 kinase (PI3K) and protein kinase B (Akt) signaling pathway. After inhibiting PI3K/Akt pathway, apoptosis‐regulated proteins were detected by western blotting, and the effects of inhibitor on the migration and invasion changes were examined. Results ITGB1 was downregulated in placenta tissues from PE patients, as compared with normal. ITGB1 overexpression in HTR‐8/SVneo cells enhanced cell proliferation, migration, and invasion, reduced cell apoptosis, and improved phosphorylation of PI3K and Akt. However, ITGB1 depletion resulted in an opposite effect to its overexpression. Inhibition of PI3K/Akt pathway completely blocked the effect of ITGB1 overexpression on cells, because we observed that apoptosis‐regulated proteins were highly upregulated, and that cell migration and invasion were reduced. Conclusion ITGB1 regulated HTR‐8/SVneo cell progression by activation of the PI3K/Akt pathway.

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Nesfatin-1 Promotes Proliferation, Migration and Invasion of HTR-8/SVneo Trophoblast Cells and Inhibits Oxidative Stress via Activation of PI3K/AKT/mTOR and AKT/GSK3β Pathway

Cited by 17 publications

References 39 publications

RAR-Related Orphan Receptor: An Accelerated Preeclampsia Progression by Activating the JAK/STAT3 Pathway

RAR-Related Orphan Receptor: An Accelerated Preeclampsia Progression by Activating the JAK/STAT3 Pathway

Intraperitoneal administration of nesfatin‑1 stimulates glucagon‑like peptide‑1 secretion in fasted mice

Integrin β1 regulates proliferation, apoptosis, and migration of trophoblasts through activation of phosphoinositide 3 kinase/protein kinase B signaling

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