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A single-cell transcriptomic inventory of murine smooth muscle cells [aorta]

ABSTRACT: Smooth muscle cells (SMC) execute important physiological functions in numerous vital organ systems, including the vascular, gastrointestinal, respiratory and urogenital tracts. SMC differ morphologically and functionally at different anatomical locations, but the molecular underpinnings of these differences remain poorly understood. Here, using deep single-cell RNA sequencing combined with in situ gene and protein expression analysis in four organs - heart, aorta, lung and colon - we reveal the molecular basis for high-level differences between vascular, visceral and airway SMC, and more subtle differences between SMC in elastic versus muscular arteries as well as zonation of elastic artery SMC along the direction of blood flow. Arterial SMC exhibit extensive organotypic heterogeneity, whereas venous SMC conversely display high similarity across organs. We further identify a unique SMC phenotype of terminal pulmonary arterioles. This study provides the first comparative SMC cross-organ resource, offering new insight into SMC subtypes and their specific functions.

ORGANISM(S): Mus musculus

PROVIDER: GSE210000 | GEO | 2022/09/26

REPOSITORIES: GEO

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A single-cell transcriptomic inventory of murine smooth muscle cells [heart]

Project description:Smooth muscle cells (SMC) execute important physiological functions in numerous vital organ systems, including the vascular, gastrointestinal, respiratory and urogenital tracts. SMC differ morphologically and functionally at different anatomical locations, but the molecular underpinnings of these differences remain poorly understood. Here, using deep single-cell RNA sequencing combined with in situ gene and protein expression analysis in four organs - heart, aorta, lung and colon - we reveal the molecular basis for high-level differences between vascular, visceral and airway SMC, and more subtle differences between SMC in elastic versus muscular arteries as well as zonation of elastic artery SMC along the direction of blood flow. Arterial SMC exhibit extensive organotypic heterogeneity, whereas venous SMC conversely display high similarity across organs. We further identify a unique SMC phenotype of terminal pulmonary arterioles. This study provides the first comparative SMC cross-organ resource, offering new insight into SMC subtypes and their specific functions.

2022-09-26 | GSE210087 | GEO

A single-cell transcriptomic inventory of murine smooth muscle cells [colon]

2022-09-26 | GSE210013 | GEO

A single-cell transcriptomic inventory of murine smooth muscle cells [lung]

2022-09-26 | GSE210100 | GEO

RNA sequencing of CTRL and siFBLN4 HAECs

Project description:Fibulin-4 (Fbln4) is an extracellular protein, expressed throughout the aortic wall including endothelial cells (EC), smooth muscle cells (SMC) and fibroblasts. SMC-specific deletion of Fbln4 in mice led to formation of ascending aortic aneurysm with disruption of elastic fibers and Fbln4 is known to play role in elastic fiber formation. However, the function of Fbln4 in EC is unknown. To examine if Fbln4 deletion induces any changes in cellular phenotype of EC, we knocked down FBLN4 in human aortic endothelial cells (HAECs) by FBLN4 siRNA (siFBLN4) compared with scramble siRNA-treated control cells (CTRL). RNA sequencing was performed to compare the differences in gene expression between CTRL and siFBLN4 cells.

2023-03-08 | GSE204771 | GEO

Vascular proteome responses precede organ dysfunction in a murine model of Staphylococcus aureus bacteremia

Project description:Vascular dysfunction and organ failure are two distinct, albeit highly interconnected clinical outcomes linked to morbidity and mortality in human sepsis. The mechanisms driving vascular and parenchymal damage are dynamic and display significant molecular crosstalk between organs and tissues. Therefore, assessing their individual contribution to disease progression is technically challenging. Here, we hypothesize that dysregulated vascular responses predispose the organism to organ failure. To address this hypothesis, we have evaluated four major organs in a murine model of S. aureus sepsis by combining in vivo labeling of the endothelial proteome, data-independent acquisition (DIA) mass spectrometry, and an integrative computational pipeline. The data reveal, with unprecedented depth and throughput, that a septic insult evokes organ-specific proteome responses that are highly compartmentalized, synchronously coordinated, and significantly correlated with the progression of the disease. This includes abundant vascular shedding, dysregulation of the intrinsic pathway of coagulation, compartmentalization of the acute phase-response, and abundant upregulation of glycocalyx components. Vascular proteome changes were also found to precede bacterial invasion and leukocyte infiltration into the organs, as well as to precede changes in various well-established cellular and biochemical correlates of systemic coagulopathy and tissue dysfunction. Importantly, our data suggests a potential role for the vascular proteome as a determinant of the susceptibility of the organs to undergo failure during sepsis.

2022-03-10 | MSV000089030 | MassIVE

Transcription profiling of aorta from mice underexpressing Fibulin-4 to investigate its role in elastic fibre assembly and cardio-vasuclar disease

Project description:Extracellular elastic fibres apply structure and mechanical elasticity to organs such as large arteries, lungs and skin 1. Elastic fibres are assembled through polymerization of tropoelastin monomers and loss of elastin is associated with aneurysmal degeneration of the aorta 2. The Fibulins are a six-member protein family hypothesized to function as intermolecular bridges that stabilize the organization of extracellular matrix structures such as elastic fibres and basement membranes 3. Fibulin-4 is found in the medial layers of arteries and moderately expressed in heart valves 4. To examine a potential role of Fibulin-4 in elastic fibre assembly and cardio-vascular disease we generated a mouse model underexpressing Fibulin-4. To get insight into the underlying molecular pathways involved in aneurysm formation, we determined the aorta transcriptome of Fibulin-4R/R animals and identified biological processes that were significantly overrepresented including apoptosis and cell death as well as several novel gene targets implicated in the response to aortic failure. We conclude that decreased Fibulin-4 expression causes aberrant composition of the elastin layers in the aorta and valvular leaflets, resulting in aortic aneurysms and heart abnormalities.

2007-01-01 | E-MEXP-840 | biostudies-arrayexpress

Specification of fetal liver endothelial progenitors to functional zonated adult sinusoids requires c-Maf induction [development stage]

Project description:Endothelial cell heterogeneity shapes the unique attributes of organ-specific blood vessels; however, how intra-organ vascular cell diversity is established remains unsolved. Liver vascular network is patterned by sinusoidal and hepatocyte co-zonation, however how intra-liver vessels acquire their hierarchical specialized functions is unknown. Here, we resolve the heterogeneity of hepatic vascular cells during development through functional and single-cell RNA sequencing. We show that acquisition of sinusoidal endothelial cell identity is initiated during early development and is completed postnatally, originating from a pool of undifferentiated vascular progenitors at E12. Notably, we identify the peri-natal induction of the transcription factor c-Maf as a critical switch for sinusoidal identity determination. Endothelium-restricted deletion of c-Maf disrupts liver sinusoidal development, aberrantly expands postnatal liver hematopoiesis, promotes excessive postnatal sinusoidal proliferation, and aggravates liver pro-fibrotic sensitivity to chemical insult. Notably, c-Maf overexpression in generic differentiated endothelial cells switches on a liver sinusoidal transcriptional zonation program that maintains hepatocyte function. Therefore, c-Maf represents an inducible intra-organotypic and niche-responsive molecular determinant of sinusoidal cell identity and lays the foundation for designing strategies to initiate vasculature-driven liver repair.

2022-04-02 | GSE174209 | GEO

Specification of fetal liver endothelial progenitors to functional zonated adult sinusoids requires c-Maf induction [c-Maf KO]

2022-04-02 | GSE174208 | GEO

Proteomic atlas of organ vasculopathies triggered by Staphylococcus aureus sepsis

Project description:Sepsis is a life-threatening condition triggered by a dysregulated host response to microbial infection resulting in vascular dysfunction, organ failure and death. Here we provide a semi-quantitative atlas of the murine vascular cell-surface proteome at the organ level, and how it changes during sepsis. Using in-vivo chemical labeling, multi-dimensional liquid chromatography, and high-resolution mass spectrometry, we demonstrate the presence of a vascular proteome that is perfusable and shared across multiple organs. This proteome was enriched in membrane-anchored proteins, including multiple regulators of endothelial barrier functions and the innate immunity. Further, we automated our workflows and applied them to a murine model of methicillin-resistant Staphylococcus aureus sepsis to unravel changes during systemic inflammatory responses. We provide an organ-specific atlas of both systemic and local changes of the vascular proteome triggered by sepsis. The data indicates that upon a septic challenge, the different organ vasculatures undergo unique and extensive remodeling.

2019-04-15 | MSV000083690 | MassIVE

RNA-seq transcriptome analysis of Nestin-GFP-peri and -GFP-retic bone marrow stromal cells

Project description:Cell cycle quiescence is a critical feature contributing to haematopoietic stem cell (HSC) maintenance. Although various candidate stromal cells have been identified as potential HSC niches, the spatial localization of quiescent HSC in the bone marrow (BM) remains unclear. Here, using a novel approach that combines whole-mount confocal immunofluorescence imaging technique and computational modelling to analyse significant tridimensional associations among vascular structures, stromal cells and HSCs, we show that quiescent HSCs associate specifically with small arterioles that are preferentially found in endosteal BM. These arterioles are ensheathed exclusively by rare Nestin-GFP-peri/NG2+ pericytes, distinct from sinusoid-associated Nestin-GFP-retic/LepR+ cells. The present RNA-seq study sought to obtain a comprehensive understanding of the differences between the two distinct HSC cellular niches. mRNA profiles of sorted Nestin-GFP-peri and -GFP-retic bone marrow stromal cells were generated from pooled mice in triplicate by Illumina HiSeq 2000 sequencing.

2013-10-10 | E-GEOD-48764 | biostudies-arrayexpress

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