SMAD1/5 binding regions and expression data of human umbilical vein endothelial cells (HUVECs) and pulmonary arterial smooth muscle cells (PASMCs) treated with BMPs
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ABSTRACT: This SuperSeries is composed of the SubSeries listed below.
Project description:Smad1/5 are transcription factors that engage in BMP-induced transcription. We determined and analyzed Smad1/5 binding sites by ChIP-sequencing. We used expression microarrays to compare the Smad1/5 binding sites identified by ChIP-seq to BMP-induced gene expressions.
Project description:Smad1/5 binding regions were identified by ChIP-seq. HUVECs were treated with BMP for 1.5 h and anti-SMAD1/5 ChIP-seq analyses were performed using Illumina genome analyzer.
Project description:Previous studies to determine transcriptional changes in PASMCs during PAH were affected by the inevitable contamination with BSMCs and venous SMCs. To specific target ASMCs, we generated an ASMC-effector mouse line by combining Cspg4/Acta2 intersectional genetics, enabling specific targeting of vascular SMCs, including PASMCs. To target non-vascular SMCs, including BSMCs, we generated the NVSMC-effector mouse line using Chrm2/Acta2 intersectional genetics. The development of ASMC-effector mice, excluding venous and BSMCs, enabled us to avoid such problems and determine PASMC-specific reactions after induction of PAH.
Project description:Smad1/5 are transcription factors that engage in BMP-induced transcription. We determined and analyzed Smad1/5 binding sites by ChIP-sequencing. We used expression microarrays to compare the Smad1/5 binding sites identified by ChIP-seq to BMP-induced gene expressions. PASMCs were treated with 50 ng/ml BMP-4 for 0, 2, or 24 hrs. RNA was extracted and hybridized on Affymetrix microarrays.
Project description:Smad1/5 are transcription factors that engage in BMP-induced transcription. We determined and analyzed Smad1/5 binding sites by ChIP-sequencing. We used expression microarrays to compare the Smad1/5 binding sites identified by ChIP-seq to BMP-induced gene expressions.
Project description:Inactivation of BMP9/10 in mice leads to attenuated contractility of smooth muscle cells and decreased blood pressure.Treatment of de-differentiated PASMCs with BMP9/10 resulted in a strong increase of ACTA2 expression as measured by immunofluorescence and RT-PCR, indicating a switch from the de-differentiated, synthetic to a differentiated, contractile state. To further study the role of BMP9/10 in smooth muscle cells, we isolate PSAMCs and stimulate cells with or without BMP9/10 and perform the RNA-seq analysis.
Project description:Information about the differences among arterial, venous, and bronchial smooth muscle cells (SMCs) in the lung is particularly valuable, as these distinct SMC populations are differentially affected in pulmonary diseases such as asthma, chronic obstructive pulmonary disease (COPD), and pulmonary arterial hypertension (PAH). To directly compare these SMC subtypes, we employed a combination of genetic tools and fluorescence-activated cell sorting (FACS) isolation strategies.We generated an ASMC-effector mouse line by combining Cspg4/Acta2 intersectional genetics, enabling specific targeting of vascular SMCs, including pulmonary arterial SMCs (PASMCs). To target non-vascular SMCs, including bronchial SMCs (BSMCs), we generated the NVSMC-effector mouse line using Chrm2/Acta2 intersectional genetics. As no driver specific to venous vascular SMCs (VVSMCs) is currently available, we used the transgenic reporter line [Tg(Acta2-GFP)], which labels all pulmonary SMCs, including venous SMCs.