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RNA-seq analysis of pulmonary arterial smooth muscle cells (PASMCs), bronchial smooth muscle cells(BSMCs) and venous SMCs in the lung

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE301478 | GEO | 2026/04/11

REPOSITORIES: GEO

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Project description:Tissue Factor Pathway Inhibitor-2 is Induced by Fluid Shear Stress in Vascular Smooth Muscle Cells and Affects Cell Proliferation and Survival Introduction: Vascular smooth muscle cells (SMCs) are exposed to fluid shear stress (FSS) after interventional procedures such as balloon-angioplasty. Whereas the effects of hemodynamic forces on endothelial cells are explored in detail, the influence of FSS on smooth muscle cell function is poorly characterized. Here, we investigated the effect of FSS on SMC gene expression and function. Methods: Laminar FSS of arterial level (14 dynes/cm2) was applied to SMC cultures for 24 h in a parallel-plate flow chamber. The effect of FSS on gene expression was first screened with microarray technology and the results further verified by real time (RT) PCR and immunoblotting. Protein expression was also studied in the rat carotid artery after balloon-injury and DNA synthesis and apoptosis was examined in SMCs in vitro. Results: Microarrays identified tissue-pathway inhibitor-2 (TFPI-2) as the most differentially expressed gene by FSS in cultured SMCs. The regulatory effect of FSS on the expression of TFPI-2 was confirmed by RT-PCR and immunobloting demonstrating a more than 400-fold increase in TFPI-2 expression in SMCs exposed to FSS compared to static controls and a consistent upregulation at the protein level. Functionally, SMC proliferation was decreased by FSS and recombinant TFPI-2 was found to inhibit SMC proliferation and induce SMC apoptosis as indicated by activation of caspase-3. In vivo, TFPI-2 expression was found to be up-regulated 5, 10 and 20 h after rat carotid balloon-injury and immunohistochemistry demonstrated TFPI-2 protein in luminal SMCs exposed to FSS in rat carotid intimal hyperplasia 10 days after balloon-injury. Conclusion: FSS strongly influence gene expression in cultured SMCs and induce TFPI-2 expression, which is also expressed after rat carotid balloon injury in luminal SMCs exposed to FSS. Functionally, TFPI-2 may play an important role in vessel wall repair by regulating SMC proliferation and survival. Further studies are needed to elucidate the mechanisms by which TFPI-2 control SMC function. 3 x 2 samples from a paired fluid shear stress experiment on smooth muscle cells.

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RNA-seq analysis of pulmonary arterial smooth muscle cells (PASMCs), bronchial smooth muscle cells(BSMCs) and venous SMCs in the lung

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