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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.

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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:pcDNA3-HAND1-his was transfected into HEK293T cells and harvested after 48 hours. IMAC was carried out under denaturing conditions to enrich for HAND1,and samples were loaded onto SDS-PAGE gel with HAND1 gel band excised and submitted to LC-MS/MS.

2020-12-18 | PXD022407 | Pride

HAND1 knockdown disrupts trophoblast gene expression in vitro in Bewo cells

Project description:HAND1 knockdown disrupts trophoblast gene expression in vitro in Bewo cells

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

Project description:Hand1 and Hand2 are transcriptional factors, and knockout mice of these genes show left and right ventricular hypoplasia, respectively. However, their function and expression in human cardiogenesis are not well studied. To delineate their expressions and assess their functions in human cardiomyocytes (CMs) in vitro, we established two triple reporter human induced pluripotent stem cell lines, HAND1mCherry, HAND2EGFP, with MYH6-driven iRFP670 or constitutive tagBFP expression and investigated their expression dynamics during cardiac differentiation. On day 5 of the differentiation, HAND1 expression marked cardiac progenitor cells. We profiled the CM subpopulations on day 20 with RNA-sequencing and found that mCherry+ CMs showed higher proliferative ability than mCherry- CMs and identified CD105 as a surface marker of highly proliferative CMs. Finally, we revealed that LEF1 is a key regulator of proliferation and is repressively regulated by HAND1 and HAND2.

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Adgrg1 is a New Transcriptional Target of Hand1 During Trophoblast Giant Cell Differentiation

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.

2022-01-12 | GSE193214 | GEO

HAND1 knockdown disrupts trophoblast global gene expression

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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 .

Project description:Purpose: The goals of this study are to verify HAND1 overexpression is suffice to upregulate other MAGs in H1 cells during human early hematopoietic differentiation through comparing the transcriptome profilings in WT samples and HAND1-overexpressed samples collected at day 8 after hematopoietic differentiation. Methods: mRNA profiles of hESC samples collected at day 8 after hematopoiesis differentiation were generated by deep sequencing using Illumina GAIIx. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. qRT–PCR validation was performed using TaqMan and SYBR Green assays Conclusions: HAND1 overexpression is suffice to upregulate other MAGs during early hematopoietic differentiation of H1 cells.

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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