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Sphingosine kinase 1 regulates the pulmonary vascular immune response

ABSTRACT: Sphingosine kinase 1 regulates the pulmonary vascular immune response

PROVIDER: PRJNA729260 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14506889_1.fastq.gz	Fastqsanger.gz
	SRR14506889_2.fastq.gz	Fastqsanger.gz
	SRR14506890_1.fastq.gz	Fastqsanger.gz
	SRR14506890_2.fastq.gz	Fastqsanger.gz
	SRR14506891_1.fastq.gz	Fastqsanger.gz

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Sphingosine kinase 1 regulates the pulmonary vascular immune response

Project description:Aberrant proliferation of pulmonary arterial smooth muscle (PASMCs) cells are a defining characteristic of pulmonary arterial hypertension (PAH) and leads to increased vascular resistance, elevated pulmonary pressure, and right heart failure. The Sphingosine kinase 1 (SPHK1)/Sphingosine-1 phosphate/ Sphingosine-1 phosphate receptor 2 pathway promotes vascular remodeling and induces PAH. The aim of this study was to identify genes and cellular processes that are modulated by over-expression of SPHK1 in human PASMCs (hPASMCs). RNA was purified and submitted for RNA sequencing to identify differentially expressed genes. Using a corrected p-value threshold of <0.05, there were 294 genes significantly up-regulated while 179 were significantly down-regulated. Predicted effects of these differentially expressed genes was evaluated using the freeware tool Enrichr to assess general gene set over-representation (enrichment) and Ingenuity Pathway Analysis (IPA™) for upstream regulator predictions. We found a strong change in genes that regulated the cellular immune response. IL6, STAT1, and PARP9, were elevated in response to SPHK1 over-expression in hPASMCs. The gene set enrichment mapped to a few immune modulatory signaling networks, including IFNG. Furthermore, STAT1 protein was elevated in primary hPASMCs isolated from PAH patients. In conclusion, these data suggest a role of Sphk1 regulates pulmonary vascular immune response in PAH.

2021-06-22 | GSE174304 | GEO

Sphingosine Kinase 1 Regulates the Pulmonary Vascular Immune Response.

Project description:The aberrant proliferation of pulmonary artery smooth muscle (PASMCs) cells is a defining characteristic of pulmonary arterial hypertension (PAH) and leads to increased vascular resistance, elevated pulmonary pressure, and right heart failure. The sphingosine kinase 1 (SPHK1)/sphingosine-1 phosphate/sphingosine-1 phosphate receptor 2 pathway promotes vascular remodeling and induces PAH. The aim of this study was to identify genes and cellular processes that are modulated by over-expression of SPHK1 in human PASMCs (hPASMCs). RNA was purified and submitted for RNA sequencing to identify differentially expressed genes. Using a corrected p-value threshold of <0.05, there were 294 genes significantly up-regulated while 179 were significantly down-regulated. Predicted effects of these differentially expressed genes were evaluated using the freeware tool Enrichr to assess general gene set over-representation (enrichment) and ingenuity pathway analysis (IPA™) for upstream regulator predictions. We found a strong change in genes that regulated the cellular immune response. IL6, STAT1, and PARP9 were elevated in response to SPHK1 over-expression in hPASMCs. The gene set enrichment mapped to a few immune-modulatory signaling networks, including IFNG. Furthermore, PARP9 and STAT1 protein were elevated in primary hPASMCs isolated from PAH patients. In conclusion, these data suggest a role of Sphk1 regulates pulmonary vascular immune response in PAH.

| S-EPMC8206894 | biostudies-literature

Impact of Sphingosine Kinase-1 knock out in neonatal mice lungs

Project description:Sphingosine Kinase-1 knock out protects against hyperoxic lung injury One day old Wild type (WT) control and Sphingosine Kinase-1 knock out (SphK-1 KO)pups exposed to room air (RA) or hyperoxia (HO). Microarray based profiling of lung tissue after 7 days of hyperoxia of 75%

2016-10-30 | GSE87350 | GEO

PDZ-Binding Kinase, a Novel Regulator of Vascular Remodeling in Pulmonary Arterial Hypertension

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Vascular remodeling following pulmonary hypertension

Project description:Hypoxia can induce vasoconstriction followed by vascular remodeling including hypertrophy and hyperplasia of pulmonary vascular smooth muscle and proliferation of endothelial cells. The goal of this project is to elucidate the genes involved in vascular remodeling following pulmonary hypertension. Total RNA was isolated from lungs of normoxic and hypoxic treated animals. Keywords: other

2003-07-16 | GSE482 | GEO

Sphingosine kinase 2 regulates CD4+ T cell responses following LCMV Cl 13 infection

Project description:Sphingosine kinase 2 regulates CD4+ T cell responses following LCMV Cl 13 infection

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Pulmonary Vascular Disease Phenomics Program (PVDOMICS)

Project description:Pulmonary Vascular Disease Phenomics Program (PVDOMICS)

| PRJNA740364 | ENA

Th2 cytokine IL-4 is critical in initiating pulmonary vascular inflammation under hypoxic conditions and induces pulmonary vascular endothelial cell activation.

Project description:IL-4-mediated pro-inflammatory vascular responses have been implicated in the pathogenesis of chronic cardiopulmonary diseases. Our results show that hypoxia-induced collagen synthesis and early recruitment of inflammatory cells are significantly less in the lungs of IL-4 knockout (KO) mice than in those of wild-type mice. In addition, we found that IL-4 significantly increased pro-inflammatory genes in primary pulmonary microvascular endothelial cells. This study was designed to identify the gene expression profile of IL-4-dependent pulmonary vascular inflammation induced by hypoxia.

2013-09-19 | E-GEOD-40999 | biostudies-arrayexpress

Sphingosine kinase 2 signaling modulates altered expression profile of host genome in a murine model of Pseudomonas aeruginosa pneumonia.

Project description:We present the set of pseudomonas responsive genes activated in the WT mice in comparison with Sphk2-/- thereby revealing the genes that could contribute to the protection seen in Sphk2-/- mice. Methods: Lung mRNA profiles of 8 week old male wild-type (WT) and Sphingosine kinase 2 knock out (Sphk2−/−) mice were generated by deep sequencing, in triplicate, using Illumina GAIIx. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two way ANOVA (ANOVA). qRT–PCR validation was performed using SYBR Green assays Genetic deletion of Sphk2-/-resisted alteration of host pulmonary genome by PA infection of the lungs promoting its own virulence thereby conferring significant protection against PA pneumonia.

2019-01-01 | GSE121359 | GEO

Sphingosine kinase 2 regulates CD4+ T cell responses following LCMV Cl 13 infection

Project description:Viruses often establish persistent infections by interrupting immune cell responses. Sphingosine kinase 2 (SphK2) generates sphingosine 1-phsophate, which is known to regulate versatile cellular processes, including immune responses. However, little is known about the role of SphK2 in the immune response to viral infections. Here, we demonstrate that during lymphocytic choriomeningitis virus (LCMV) clone 13 infection, a virus known to establish a persistent infection in mice, SphK2 functions to limit CD4+ T cell responses, which aids in the establishment of virus-induced immunosuppression and viral persistence. The infection of SphK2-deficient (Sphk2-/-) mice with LCMV resulted in kidney disease and ultimately mortality. Following infection, Sphk2-/- mice were shown to have increased LCMV-specific CD4+ and CD8+ T cell responses. With the use of LCMV epitope-specific TCR transgenic mouse lines in adoptive transfer studies, SphK2 was shown to have intrinsic negative function in CD4+ T cells, but not CD8+ T cells. Furthermore, Sphk2-/- CD4+ T cells were able to promote endogenous, virus-specific CD8+ T cell responses more efficiently than Sphk2+/+ CD4+ T cells. Our results suggest that SphK2 is a novel regulator of the immune response during LCMV clone 13 infection and targeting SphK2 may provide a promising immunotherapeutic strategy for the control of persistent viral infections. This study incorporated the use of RNA sequencing to determine what pathways SphK2 was involved in to affect CD4+ T cell activity and proliferation. Sphk2+/+ or Sphk2-/- LCMV epitope-recognizing tg CD4+ T cells were transferred into C57BL/6 mice and recovered 7 days following LCMV Cl 13 infection. RNA sequencing revealed several pathways upregulated in Sphk2-/- CD4+ T cells relating to cell cycle progression, regulation of transcription, and regulation of nucleic acid binding.

2020-10-29 | GSE155030 | GEO

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