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Transcriptomics revealed sex differences in human pulmonary microvascular endothelial cells in normoxia and hypoxia

ABSTRACT: Transcriptomics revealed sex differences in human pulmonary microvascular endothelial cells in normoxia and hypoxia

PROVIDER: PRJNA976643 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24745900_1.fastq.gz	Fastqsanger.gz
	SRR24745900_2.fastq.gz	Fastqsanger.gz
	SRR24745901_1.fastq.gz	Fastqsanger.gz
	SRR24745901_2.fastq.gz	Fastqsanger.gz
	SRR24745902_1.fastq.gz	Fastqsanger.gz

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Transcriptomics revealed sex differences in human pulmonary microvascular endothelial cells in normoxia and hypoxia

Project description:To investigate sex differences at the transcriptome level in human pulmonary microvascular endothelial cells (HPMECs) from healthy male and female donors basally (in normoxia) and in hypoxic conditions. RNA-seq was performed on male (n=3) and female (n=4) HPMECs that were cultured in conditions of physiological shear stress (PMID: 36730645) in normoxia (21% O2) or in hypoxia (1% O2) for either 24 or 48 hours.

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Transcriptomics and proteomics revealed sex differences in human pulmonary microvascular endothelial cells

Project description:There is marked sexual dimorphism displayed in the onset and progression of pulmonary hypertension (PH). Females more commonly develop pulmonary arterial hypertension (PAH), however, females with PAH and other types of PH have better survival than males. Pulmonary microvascular endothelial cells play a crucial role in the pulmonary vascular remodelling and increased pulmonary vascular resistance of PH. Given this background, we hypothesized that there are sex differences in the pulmonary microvascular endothelium basally and in response to hypoxia that are independent of the sex hormone environment.

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Physiological shear stress markedly alters the proteomic response to hypoxia in human pulmonary microvascular endothelial cells

Project description:Physiological shear stress, produced by blood flow, homeostatically regulates the phenotype of pulmonary endothelial cells exerting anti-inflammatory and anti-thrombotic actions and maintaining normal barrier function. In the pulmonary circulation hypoxia, due to high altitude or diseases such as COPD, causes vasoconstriction, increased vascular resistance and pulmonary hypertension. Hypoxia-induced changes in endothelial function play a central role in the development of this pulmonary hypertension. However, the direct interactive effects of hypoxia and shear stress on the pulmonary endothelial phenotype have not been extensively studied. We cultured human pulmonary microvascular endothelial cells (HPMEC) in normoxia or hypoxia while subjected to physiological shear stress or in static conditions. Unbiased proteomics was used to identify hypoxia-induced changes in protein expression. Using publicly available single cell RNA-seq datasets, differences in gene expression between the alveolar endothelial cells from COPD and healthy lungs were identified. 60 proteins were identified in HPMEC lysates whose expression changed in response to hypoxia in sheared but not in static conditions. mRNA for five of these (ERG, MCRIP1, EIF4A2, HSP90AA1 and DNAJA1) showed similar changes in the endothelial cells of COPD compared to healthy lungs. These data show that the proteomic responses of the pulmonary microvascular endothelium to hypoxia are significantly altered by shear stress and suggest that these differences are important in the development of hypoxic pulmonary vascular disease.

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