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HAND1 knockdown disrupts trophoblast gene expression in vitro in Bewo cells

ABSTRACT: Congenital heart disease (CHD) affects nearly 1% of births annually, and neonatal and perinatal outcomes in cases of CHD are strongly impacted by pregnancy outcomes. CHD pregnancies carry increased risk of developing pathologies of abnormal placentation including fetal growth restriction, preeclampsia, preterm birth, and stillbirth. HAND1 is a gene associated with CHD. In this study, we aimed characterize the mechanistic impacts of disrupting HAND1 on human placenta trophoblast cell lines.

ORGANISM(S): Homo sapiens

PROVIDER: GSE209620 | GEO | 2022/08/02

REPOSITORIES: GEO

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HAND1 knockdown disrupts trophoblast gene expression in vitro- human vascular endothelial cell

Project description:Congenital heart disease (CHD) affects nearly 1% of births annually, and neonatal and perinatal outcomes in cases of CHD are strongly impacted by pregnancy outcomes. CHD pregnancies carry increased risk of developing pathologies of abnormal placentation including fetal growth restriction, preeclampsia, preterm birth, and stillbirth. HAND1 is a gene associated with CHD. In this study, we aimed characterize the mechanistic impacts of disrupting HAND1 on human vascular endothelial cell gene expression.

2022-08-03 | GSE210318 | GEO

HAND1 Ubiquitination and Phosphorylation sites

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2020-12-18 | PXD022407 | Pride

E11.5 Hand1 myocardial knockout RNA-Seq

Project description:Aims: To examine the role of the basic Helix-loop-Helix (bHLH) transcription factor HAND1 in embryonic and adult myocardium. Methods and Results: Hand1 is expressed within the cardiomyocytes of the left ventricle (LV) and myocardial cuff between embryonic days (E) 9.5-13.5. Hand gene dosage plays an important role in ventricular morphology and the contribution of Hand1 to congenital heart defects requires further interrogation. Conditional ablation of Hand1 was carried out using either Nkx2.5 knockin Cre (Nkx2.5Cre) or a-myosin heavy chain Cre (aMhc-Cre) driver. Interrogation of transcriptome data via Ingenuity Pathway Analysis (IPA) reveals several gene regulatory pathways disrupted including translation and cardiac hypertrophy-related pathways. Embryo and adult hearts were subjected to histological, functional and molecular analyses. Myocardial deletion of Hand1 results in morphological defects that include cardiac conduction system defects, survivable interventricular septal defects (VSDs), and abnormal LV papillary muscles (PM). Resulting Hand1 conditional mutants are born at Mendelian frequencies; but the morphological alterations acquired during cardiac development result in, the mice developing diastolic heart failure. Conclusions: Collectively, these data reveal that Hand1 contributes to the morphogenic patterning and maturation of cardiomyocytes during embryogenesis and although survivable, indicate a role for Hand1 conduction system and papillary morphogenesis.

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Project description:E11.5 Hand1 myocardial knockout RNA-Seq

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Expression dynamics of HAND1/2 in in vitro human cardiomyocyte differentiation

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Project description:The placenta, forming the maternal–fetal interface, is essential for the survival and development of the fetus. It has been shown that the basic helix-loop-helix (bHLH) transcription factor Hand1 plays an important role in trophoblast giant cells (TGCs) differentiation during placental development in mice. However, the underlying molecular mechanism remains elusive. We hereby report that Adgrg1 (GPR56), a G protein coupled receptor, was a new transcriptional target of Hand1. Hand1 activated the expression of Adgrg1 by binding to its promoter region during TGCs differentiation. Double in situ hybridization revealed co-expression of Hand1 and Adgrg1 in TGCs, and Adgrg1 was located to Prl2c2+ TGCs in the junctional zone of the placenta. Knockdown of Adgrg1 not only led to increased expression of Prl2c2, but also the improvement of cell migration during TGC differentiation. Moreover, the ligands of Adgrg1, Tgm2 and Col3a1, were expressed in Prl2c2+ TGCs located in the placental junctional zone and maternal spiral arteries, respectively, further providing preconditions for the function of Adgrg1 in TGCs. Collectively, these results demonstrate that Adgrg1 is a new transcriptional target of Hand1, affecting Prl2c2 expression and cell migration during TGCs differentiation. Tgm2 and Col3a1 may be involved in TGC differentiation regulated by Adgrg1 in the manners of autocrine or paracrine. As a transmembrane receptor, Adgrg1 perhaps could act as a potential therapeutic target for placental-associated diseases caused by abnormal trophoblast migration, providing new insights for the preventions and therapies of placenta-related diseases.

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RNA Sequencing Facilitates Quantitative Analysis of Transcriptomes of H1 derived CD31+ cells and H1 after HAND1-overexpression derived CD31+ cells at Day8 after human early hematopoietic differentiation .

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2019-07-26 | GSE134906 | GEO

Transcriptomic Profiling of Trophoblast Subpopulations in Severe Preeclampsia Reveals Novel Aspects of RNA Dysregulation

Project description:The maternal signs of preeclampsia, principally the new onset of high blood pressure, are thought to occur secondary to faulty placentation. Previous studies profiled the gene expression patterns of chorionic villi, the maternal-fetal interface or isolated cytotrophoblasts in this pregnancy complication. We theorized that transcriptomic analyses of trophoblast subpopulations in situ would give us new insights into the role of these cells in preeclampsia pathogenesis.

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2008-06-14 | E-GEOD-6573 | biostudies-arrayexpress

A Hidden Proteome Encoded by circRNAs in Human Placentas: Implications for Uncovering Preeclampsia Pathogenesis

Project description:Circular RNAs (circRNAs) are consistently overlooked as translational templates due to computational and experimental limitations. Here, we used multi-omics approaches to identify new translational events of circRNAs in human placentas, and assessed the roles of circRNA-encoded proteins in placentation and associated disorders based on the recently proposed protein bait hypothesis. The combination of placental circRNA sequencing and bioinformatics analysis revealed 219607 circRNAs, of which 35% were identified by the Coding Potential Assessment Tool (CPAT) as having >50% coding probability. Ribosomal profiling further identified 528 novel coding circRNAs, including 217 that coded for microproteins verified by LC-MS/MS. Based on these data, we established the Placental Microprotein Bank (PMB) for coding circRNAs and their coded proteins. These proteins have lower molecular weights, higher stable indices and hydrophobicity compared to the canonical proteins, and potentially link to placental development and adverse pregnancy outcomes such as pre-eclampsia. Furthermore, we identified circPRKCB119aa as a novel preeclampsia-related microprotein that enhanced trophoblast autophagy by inhibiting phosphorylation of its cognate linear-spliced isoform protein kinase C (PKC) β. In summary, we discovered a hidden circRNA-encoded proteome in the human placenta, which offers new insights into the mechanisms underlying placentation and its disorders such as, but not limited to, preeclampsia.

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