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Single-cell gene expression profiling of interstitial macrophages exposed to hypoxia

ABSTRACT: Single-cell gene expression profiling of interstitial macrophages exposed to hypoxia

PROVIDER: PRJNA1071130 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27788900_1.fastq.gz	Fastqsanger.gz
	SRR27788900_2.fastq.gz	Fastqsanger.gz
	SRR27788901_1.fastq.gz	Fastqsanger.gz
	SRR27788901_2.fastq.gz	Fastqsanger.gz
	SRR27788902_1.fastq.gz	Fastqsanger.gz

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Single-cell gene expression profiling of interstitial macrophages exposed to hypoxia

Project description:Employing single-cell transcriptomic analyses, we investigated the repertoire and functional profiles of pulmonary interstitial macrophages in response to exposure at 0, 1, 3, 7, and 21 days of hypobaric hypoxia (at an altitude of 5,486 meters). The repertoire and functional profiles of interstitial macrophages (IMs) undergo dynamic changes based on the duration of hypoxia exposure. Acute hypoxia leads to type 1 acute inflammatory responses in most IM populations, which largely subside by Day 7. The resolution of the inflammatory phase is succeeded by the accumulation of dysregulated IMs, contributing to abnormal pulmonary vascular repair and remodeling. The classical and alternative complement pathways may play distinct roles in regulating early inflammation and later vascular remodeling phases in pulmonary hypertension (PH) pathogenesis. These findings highlight the dynamic nature of IMs, emphasizing that understanding the timing and mechanisms through which they influence PH pathogenesis will contribute to the development of IM-specific therapeutic targets.

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Project description:Dysregulated redox signaling contributes to pulmonary hypertension (PH) and vascular-selective depletion of the redox enzyme EC-SOD (EC-SOD SMC KO) worsens chronic hypoxic PH. Given the important role of macrophages in vascular remodeling and PH, this study aimed to determine if interstitial macrophages (IMs) and their interactions with the extracellular matrix (ECM) component, hyaluronan, are modulated by vascular EC-SOD. Floxed wild-type (WT), EC-SOD SMC KO, and EC-SOD mimetic- or vehicle-treated mice were exposed to hypobaric hypoxia (~10% FiO2), for 4, 14, or 21 days. Using flow cytometry, we demonstrated that the transient increase in IMs at day 4 was exacerbated in EC-SOD SMC KO mice and prevented with EC-SOD mimetic (5 mg/kg, subcutaneous, day 1). Highlighting the importance of targeting vascular oxidative stress in the early response to hypoxia, pretreatment with this single dose of EC-SOD mimetic decreased right ventricular systolic pressure, right ventricular hypertrophy, and small vessel muscularization at day 21. To assess IM phenotypic reprogramming in this model, RNAseq was performed on flow-sorted IMs revealing baseline proinflammatory activation and enhanced activation of vascular and ECM remodeling pathways in response to hypoxia in EC-SOD SMC KO IMs compared to controls. To further investigate the ECM remodeling response, we quantified IMs expressing the hyaluronan receptor Lyve1, and IM-hyaluronan binding. Lyve1+IMs and Lyve1+HA+IMs were increased in response to hypoxia in EC-SOD SMC KO mice and accumulated in the perivascular space. In conclusion, vascular EC-SOD limits IM accumulation and proinflammatory profibrotic IM signaling, including perivascular accumulation of Lyve1+IMs and their binding to hyaluronan.

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Project description:The extracellular isoform of superoxide dismutase (SOD3) is decreased in patients and animals with pulmonary hypertension (PH). The human R213G single nucleotide polymorphism (SNP) in SOD3 causes its release from tissue extracellular matrix (ECM) into extracellular fluids, without modulating enzyme activity, and increases cardiovascular disease risk in humans and chronic hypoxic PH in mice. Given the importance of interstitial macrophages (IM) to PH pathogenesis, this study aimed to determine whether R213G SOD3 worsens PH via increased IM accumulation and altered reprogramming. R213G mice and wild-type (WT) controls were exposed to hypobaric hypoxia for 4 or 14 days compared to normoxia. Flow cytometry demonstrated a transient increase in IMs at day 4 in both strains. Contrary to our hypothesis, the R213G SNP did not augment IM accumulation. To determine strain differences in the IM reprogramming response to hypoxia, we performed RNAsequencing on IMs isolated at each time point. We found that IMs from R213G mice exposed to hypoxia activated ECM-related pathways and a combination of alternative macrophage and proinflammatory signaling. Furthermore, when compared to WT responses, IMs from R213G mice lacked metabolic remodeling and demonstrated a blunted anti-inflammatory response between the early (day 4) and later (day 14) time points. We confirmed metabolic responses using Agilent Seahorse assays whereby WT, but not R213G, IMs upregulated glycolysis at day 4 that returned to baseline at day 14. Finally, we identify differential regulation of several redox-sensitive upstream regulators that could be investigated in future studies.

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