Long non-coding RNA FAM99A modulated YAP1 to affect trophoblast cell behaviors in preeclampsia by sponging miR-134-5p

Xu, Bingnv; Geng, Xiaofang; Liu, Xiaodan; Liu, Ying

doi:10.1590/1414-431x20209732

Cited by 6 publications

(15 citation statements)

References 21 publications

(27 reference statements)

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“…HG induction increased the miR-134-5p expression and reduced the cell viability, proliferation, and migration, while miR-134-5p inhibition facilitated cell proliferation and migration. Consistently, the miR-134 inhibitor could evidently weaken the invasiveness of trophoblast cells and loss of miR-134-5p could exacerbate the proliferation and migration of trophoblast cells in preeclampsia [ 15 , 32 ]. Collectively, our findings elicited that miR-134-5p downregulation enhances the cell proliferation and migration of trophoblast cells.…”

Section: Discussionmentioning

confidence: 98%

“…GDM is a dangerous condition during pregnancy that progresses to inflammation and apoptosis in the trophoblast [ 4 ]. Recently, the functionality of miR-134-5p has been identified as a potential diagnostic marker of GDM with notable function in the regulation of trophoblast cell metabolism [ 12 , 15 ]. Accumulating evidence has highlighted that FOXP2is targeted by miR-134-5p and can explicitly manipulate cellular in diabetes [ 16 , 19 ].…”

Section: Discussionmentioning

confidence: 99%

“…Our results illustrated that HG could elevate the release of TNF-α, IL-1β, and Bax and inhibit the release of IL-10 and Bcl-2, where miR-134-5p inhibition could annul molecular alternations, indicating that miR-134-5p had induced inflammation and apoptosis. Previously, an existing study demonstrated the capacity of miR-134-5p to induce the apoptosis of trophoblast cells in preeclampsia via down-regulation of Yes-associated protein 1 [ 15 ]. Moreover, miR-134 has been identified as an effective target that facilitates proinflammatory cytokine production in atherosclerosis [ 10 ].…”

Section: Discussionmentioning

confidence: 99%

“…Extensive research has highlighted the role of miR-134-5p in cellular metabolism, particularly the proliferation, migration, and apoptosis of cancer cells [ 13 , 14 ]. Notably, an existing study demonstrated the ability of miR-134-5p to regulate trophoblast cell behaviors in preeclampsia, such as apoptosis, migration, and invasion [ 15 ]. Nevertheless, the molecular mechanism of miR-134-5p in GDM remains elusive.…”

Section: Introductionmentioning

confidence: 99%

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RETRACTED ARTICLE: miR-134-5p promotes inflammation and apoptosis of trophoblast cells via regulating FOXP2 transcription in gestational diabetes mellitus

Chen

Zheng

et al. 2021

Bioengineered

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Gestational diabetes mellitus (GDM) is a prevalent and risky pregnant complication which warrants targeted therapy for restriction the inflammation and apoptosis of trophoblast cells. This study sought to analyze the aberrant expression and regulatory mechanism of microRNA (miR)-134-5p in GDM. The miR-134-5p expression in the serum of GDM patients and normal participants was detected via qRT-PCR, followed by receiver operating characteristic (ROC) curve analysis. In vitro GDM cell model was established in the HTR-8/SVneo cells using 25 mmol/L glucose, followed by transfection with miR-134-5p inhibitor and si-Forkhead box p2(FOXP2). The miR-134-5p and FOXP2 expressions, TNF-α, IL-1β, and IL-10 levels, cell proliferation, migration, and apoptosis were determined by a combination of qRT-PCR, western blot, ELISA, and cell counting Kit-8, Transwell assay, and flow cytometry. The binding relationship between miR-134-5p and FOXP2 was predicted and verified. Our results revealed that miR-134-5p was increased in the serum of GDM patients and could serve as a critical diagnostic marker for GDM. Moreover, miR-134-5p was upregulated in the high glucose (HG)-induced HTR-8/SVneo cells. The miR-134-5p inhibition suppressed the inflammation and apoptosis of HG-induced HTR-8/SVneo cells. miR-134-5p inhibited FOXP2 expression. FOXP2 expression was decreased in GDM. FOXP2 inhibition attenuated the function of miR-134-5p in HG-induced HTR-8/SVneo cells. Overall, miR-134-5p inhibited the FOXP2 expression to facilitate the inflammation and apoptosis of trophoblast cells, thereby exacerbating GDM.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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RETRACTED ARTICLE: miR-134-5p promotes inflammation and apoptosis of trophoblast cells via regulating FOXP2 transcription in gestational diabetes mellitus

Chen

Zheng

et al. 2021

Bioengineered

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“…Importantly, the participation of lncRNAs in HDCP is of vital importance and has been extensively reported [8]. The gene of the lncRNA FAM99A is located on the 11th chromosome, which links to the maternal circulating lipid of pregnant women [9]. LncRNA FAM99A is downregulated in PE and plays pivotal roles in cell metastasis, growth, and apoptosis in PE, suggestive of a potential biomarker for PE [1].…”

Section: Introductionmentioning

confidence: 99%

Expression of serum long noncoding RNA FAM99A in patients with hypertensive disorder complicating and its clinical significance

Zhao

2022

Blood Pressure Monitoring

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Objective Hypertensive disorder complicating pregnancy (HDCP) consists of various heterogeneous conditions. Long noncoding RNAs (LncRNA) FAM99A is implicated in HDCP diagnosis. This study discussed the diagnostic efficiency of lncRNA FAM99A in HDCP. Methods Totally 130 singleton HDCP patients including 50 patients of gestation hypertension (GH), 44 of mild preeclampsia (mPE), and 36 of severe preeclampsia (sPEz) were enrolled, with 70 healthy pregnant women as the control. Serum lncRNA FAM99A expression was detected and its diagnostic efficiency in HDCP was analyzed using the receiver operating characteristic curve. The influencing factors of PE grade were analyzed using the logistic regression model. Results Serum lncRNA FAM99A was downregulated in HDCP patients. The SBP/DBP, 24-h urinary protein, and serum creatinine (SCr), AST and ALT contents were elevated, and platelet count (PLT) was diminished in HDCP patients. Relative to the high-expression group, SBP/DBP, 24-h urinary protein, SCr, AST, and ALT contents were raised, and PLT was lowered in the low-expression group. The area under curve of lncRNA FAM99A for HDCP diagnosis was 0.9514, and the cutoff value was 0.8450, with 83.85% sensitivity and 94.29% specificity. LncRNA FAM99A expression was downregulated in the GH group, then mPE group, and sPEz group the least. LncRNA FAM99A had diagnostic efficiency for GH and mPE, and mPE and sPEz. DBP, urinary protein, PLT, and lncRNA FAM99A were independent risk factors for PE severity. Conclusion LncRNA FAM99A was diminished in HDCP patients and was related to HDCP severity, which might be used as a potential diagnostic marker of HDCP.

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HDAC4 regulates the proliferation, migration, and invasion of trophoblasts in pre‐eclampsia through the miR‐134‐5p/FOXM1 axis

Xu,

Kang,

Jiang

et al. 2023

Molecular Reproduction Devel

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Epigenetics, including histone modifications and noncoding RNAs, affects abnormal placental function in pre‐eclampsia (PE). This study was conducted to explore the role of histone deacetylase 4 (HDAC4) in trophoblast invasion and migration. The expression levels of HDAC4, microRNA (miR)‐134‐5p, and forkhead box protein M1 (FOXM1) in placentas from PE patients and healthy controls and their correlations were examined. HTR8/SVneo cells were cultured and underwent gene intervention. Then, trophoblast proliferation, invasion, and migration were evaluated by 5‐ethynyl‐2ʹdeoxyuridine, Transwell, and scratch assays. The enrichments of HDAC4 and acetylated histone H3 at lysine 9 (H3K9Ac) on the miR‐134‐5p promoter were quantified by chromatin immunoprecipitation. The binding of miR‐134‐5p to FOXM1 was analyzed by dual‐luciferase assay. HDAC4 and FOXM1 were downregulated while miR‐134‐5p was upregulated in PE placentas. HDAC4 downregulation impaired trophoblast proliferation, invasion, and migration while HDAC4 overexpression played the opposite role. Mechanically, HDAC4 deacetylated H3K9Ac to repress miR‐134‐5p expression by erasing H3K9Ac, reduced the binding of miR‐134‐5p to FOXM1, and then promoted FOXM1 transcription. miR‐134‐5p overexpression or FOXM1 downregulation abrogated the promotive role of HDAC overexpression in trophoblast invasion and migration. Our study unraveled a novel mechanism of trophoblast proliferation, invasion, and migration and proposed that HDAC4 may be a promising target for the treatment of PE.

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Long non-coding RNA FAM99A modulated YAP1 to affect trophoblast cell behaviors in preeclampsia by sponging miR-134-5p

Cited by 6 publications

References 21 publications

RETRACTED ARTICLE: miR-134-5p promotes inflammation and apoptosis of trophoblast cells via regulating FOXP2 transcription in gestational diabetes mellitus

RETRACTED ARTICLE: miR-134-5p promotes inflammation and apoptosis of trophoblast cells via regulating FOXP2 transcription in gestational diabetes mellitus

Expression of serum long noncoding RNA FAM99A in patients with hypertensive disorder complicating and its clinical significance

HDAC4 regulates the proliferation, migration, and invasion of trophoblasts in pre‐eclampsia through the miR‐134‐5p/FOXM1 axis

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