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Pericytes, which share markers with smooth muscle cells (SMCs), are heterogenous cells. Pericytes in the brain and skeletal muscle have different embryonic origins, representing distinct subpopulations. One challenge in the field is that there are no subpopulation-specific pericyte markers. Here, we compared the transcriptomes of muscle pericytes and SMCs, and identified 741 muscle pericyte-enriched genes and 564 muscle SMC-enriched genes. Gene ontology analysis uncovered distinct biological processes and molecular functions in muscle pericytes and SMCs. Interestingly, the Venn diagram revealed only one gene shared by brain and muscle pericytes, suggesting that they are indeed distinct subpopulations with different transcriptional profiles. We further validated that GSN co-localized with PDGFRβSMA cells in small and large blood vessels but not PDGFRβSMA cells, indicating that GSN predominantly marks pericytes and fibroblasts rather than SMCs in skeletal muscle. Negligible levels of GSN were detected in the brain. These findings indicate that GSN may serve as a selective marker for muscle pericytes.
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http://dx.doi.org/10.1038/s41598-025-14225-3 | DOI Listing |
Unlabelled: Facioscapulohumeral muscular dystrophy (FSHD) is an autosomal dominant myopathy caused by aberrant expression of the retrogene, and it affects skeletal muscles primarily in the face, shoulder, and limbs. In healthy individuals, is expressed in early development and is subsequently silenced in most somatic tissues. The spatiotemporal pattern of DUX4 mis-expression beyond the cleavage stage in FSHD is poorly understood because is not well conserved beyond primates.
View Article and Find Full Text PDFJ Cachexia Sarcopenia Muscle
October 2025
Department of Rheumatology and Immunology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Background: Idiopathic inflammatory myopathies (IIMs) exhibit diverse cellular microenvironments in muscle tissues, yet the full spectrum of cell populations and changes remains unclear. This study aimed to characterize cellular heterogeneity, explore cell-cell interactions and assess the prognostic value of cell subtype abundances across IIM subtypes in Han Chinese.
Methods: Muscle samples from six IIMs and three normal controls (NC) underwent single-cell RNA sequencing (scRNA-seq), whereas bulk RNA sequencing was performed on 203 IIMs and 19 NC.
Front Cardiovasc Med
August 2025
Experimental Cardiovascular Medicine, University of Bristol, Bristol, United Kingdom.
Background: Endothelial cells (ECs) induce vascular smooth muscle cells (VSMCs) relaxation via nitric oxide (NO), prostacyclin (PGI₂) and hyperpolarizing factors. Recent whole-genomic, single-cell transcriptomic analysis of human vascular cells has revealed angiotypic heterogeneity. However, it remains unknown whether vasorelaxant mediators reiterate this pattern.
View Article and Find Full Text PDFCardiovasc Res
August 2025
Ottawa Hospital Research Institute, Sinclair Centre for Regenerative Medicine Program, Ottawa, ON, Canada.
Background: Pulmonary arterial hypertension (PAH) is a lethal pulmonary vascular disease characterized by arteriolar pruning and occlusive vascular remodeling leading to increased pulmonary vascular resistance and eventually right heart failure. While endothelial cell (EC) injury and apoptosis are known triggers for this disease, the mechanisms by which they lead to complex arterial remodeling remain obscure.
Aims: We employed multiplexed single-cell RNA sequencing at multiple timepoints during the onset and progression of disease in a model of severe PAH to identify mechanisms involved in the development of occlusive arterial lesions.
Biomaterials
August 2025
State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases & Engineering Research Center of Oral Translational Medicine, Ministry of Education &National Engineering Laboratory for Oral Regenerative Medicine, West China Hospital of Stomatology, Sichuan University, Che
Skeletal muscle regeneration mediated by muscle satellite cells (MuSCs) is supported by the specific vascular niche containing endothelial cells, pericytes, and mesenchymal stem cells. Volumetric muscle loss (VML) severely disrupts the vascular niche and impairs the ability of MuSCs to regenerate functional skeletal muscle. Until now, it remains a great challenge to reconstruct the vascular niche for muscle regeneration.
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