Details for: CL0000359

Cell ID: CL0000359

Cell Name: vascular associated smooth muscle cell

Description: A smooth muscle cell associated with the vasculature.

Synonyms: VSMC, vascular smooth muscle cell

Selected Context(s): Overall

Gene Significance Landscape

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Score:
Display
Genes

Contexts:

Cell Significance Index (CSI) is uniquely calculated to reveal cell-specific gene markers. More info here

Significant Genes List

Genes with the highest and lowest Percentile Rank Scores (PRS) for vascular associated smooth muscle cell within the selected context(s).

Gene ID: A unique numerical identifier for this specific gene.
Symbol: Shortened abbreviation or name that represents this gene.
Ensembl Gene ID: A unique identifier assigned by Ensembl for genomic data mapping.
CSI Score: A combined effect size and statistical significance measure for vascular associated smooth muscle cell. Higher scores indicate a stronger, more significant difference in expression.
(Previously described as "Fold Change", but now represents Cliff's Delta × –log10(p).)

Gene ID: A unique numerical identifier for this specific gene.
Symbol: Shortened abbreviation or name that represents this gene.
Ensembl Gene ID: A unique identifier assigned by Ensembl for genomic data mapping.
CSI Score: A combined effect size and statistical significance measure for vascular associated smooth muscle cell. Higher scores indicate a stronger, more significant difference in expression.
Average CSI: csi sum / gene count
Cell network configuration

This network visualizes key genes for vascular associated smooth muscle cell. It primarily includes:
1. Top genes highly significant for this cell (Num. Top Cell Genes - based on the 'Min. CSI' setting).
2. Any additional specific 'Context Genes' you add below.
The final network is a combined view. Choose an Interaction Source (pathways or protein interactions) and optionally compare CSI scores with a Baseline Cell Type.

Maximum number of selected genes.
Select a context for the baseline cell.
Select a context for the target cell.
Target Cell for CSI:  vascular associated smooth muscle cell (CL0000359)

 Legend
Nodes (Genes):
 Query Gene
Node size also reflects Target Cell CSI magnitude.
Node Color (Target Cell CSI in specific network):
 Very High
 High
 Medium
 Low
 Very Low
 N/A or Not Sig.
Edges (Interactions):
 STRING (Protein-Protein)
 ONTOLOGY (Shared Pathway)
 Colors vary by pathway category; default arrow applies.

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## Summary The [vascular associated smooth muscle cell](/details-cell/CL0000359) (VSMC) is an integral component of the vascular wall, traditionally known for its contractile function that regulates vessel tone and blood pressure. The gene significance profile for this cell type reveals a more complex identity. **Overall**, the high specificity score for [B2M](/details-gene/567), a key component of the MHC class I molecule, suggests that a primary defining characteristic of VSMCs is their capacity for immune presentation, positioning them as active participants in vascular immune surveillance. This is complemented by significant expression of genes involved in cytoskeletal organization ([MYL6](/details-gene/4637)), calcium-dependent signaling ([S100A6](/details-gene/6277)), and interaction with the extracellular matrix ([POSTN](/details-gene/10631)), underscoring their multifaceted role in maintaining vascular homeostasis and responding to pathological stimuli. ## Key Characteristics and Function The unique transcriptional signature of [vascular associated smooth muscle cells](/details-cell/CL0000359) is defined by a combination of genes reflecting their structural, signaling, metabolic, and immune-interactive roles. The analysis based on expression specificity (`csi_z`) highlights several functional clusters. * **Immune and Antigen Presentation:** The top marker, [B2M](/details-gene/567), is essential for presenting endogenous antigens via MHC class I molecules. Its high `csi_z` (37.30) strongly suggests that this immune function is a uniquely defining feature of VSMCs compared to other cell types in this biological context. This is consistent with roles in viral defense and autoimmune processes within the vasculature. * **Cytoskeletal and Contractile Machinery:** As expected for a muscle cell, genes related to the cytoskeleton are prominent. [MYL6](/details-gene/4637), a myosin alkali light chain involved in microfilament motor activity, is a significant marker. Additionally, the high specificity of [KRT8](/details-gene/170421) (Keratin 8) and [MAP1B](/details-gene/4131) (Microtubule-Associated Protein 1B) indicates that the intermediate filament and microtubule networks are also defining structural components, likely contributing to the cell's mechanical resilience and plasticity. * **Signaling and Cellular Regulation:** VSMCs appear to be highly responsive to their microenvironment, evidenced by markers like [S100A6](/details-gene/6277), a calcium-binding protein involved in growth regulation ([Link](https://doi.org/10.1016/s0021-9258(18)67137-6)), and [RGS6](/details-gene/9628), a regulator of G protein signaling. The presence of [NTRK3](/details-gene/4916), a neurotrophin receptor, suggests potential for neuro-vascular communication and signaling. * **Gene Expression and Metabolism:** The high specificity of generalist genes like the long non-coding RNA [NEAT1](/details-gene/283131), the RNA helicase [DDX5](/details-gene/1655), and the translation elongation factor [EEF1B2](/details-gene/1933) suggests that VSMCs possess a distinct and highly regulated machinery for gene expression and protein synthesis. Furthermore, the mitochondrial ADP/ATP transporter [SLC25A6](/details-gene/293) and iron-binding protein [FTL](/details-gene/2512) point to a specific metabolic profile. * **Extracellular Matrix Interaction:** The identification of [POSTN](/details-gene/10631) (Periostin) and [FMOD](/details-gene/2331) (Fibromodulin) as markers underscores the critical role of VSMCs in organizing and communicating with the vascular extracellular matrix, a process central to vascular development and pathological remodeling. Conversely, the anti-marker profile is particularly revealing. The strong negative `csi_z` for multiple core components of the mitochondrial electron transport chain, including [COX1](/details-gene/4512), [COX2](/details-gene/4513), and [COX3](/details-gene/4514), suggests that the expression of these mitochondrial genes is significantly less specific or prominent in VSMCs compared to other cell types. This may indicate a reliance on alternative energy pathways, such as glycolysis, which is a known feature of proliferating or synthetic VSMCs. The negative scores for [SARAF](/details-gene/51669), a negative regulator of store-operated calcium entry ([Link](https://doi.org/10.1016/j.cell.2012.01.055)), and [SH3BGRL3](/details-gene/83442) further refine the cell's unique signaling and metabolic landscape. ## Clinical Significance and Contextual Roles Although this analysis represents an **Overall** context, the specific gene markers for [vascular associated smooth muscle cells](/details-cell/CL0000359) carry significant clinical implications, particularly in cardiovascular disease and cancer. The prominence of genes involved in cell proliferation, adhesion, and matrix remodeling, such as [POSTN](/details-gene/10631) and [S100A6](/details-gene/6277), is highly relevant to atherosclerosis. In this disease, VSMCs undergo a phenotypic switch from a quiescent, contractile state to a proliferative, synthetic state, migrating into the intima, secreting extracellular matrix, and contributing to plaque formation. [POSTN](/details-gene/10631) is known to be a ligand for integrins and promotes cell motility, a function that could drive this pathological migration ([Link](https://pubmed.ncbi.nlm.nih.gov/12235007/)). The top marker, [B2M](/details-gene/567), links VSMCs to inflammatory aspects of vascular disease. Elevated levels of circulating beta-2-microglobulin are associated with cardiovascular mortality, and the local presentation of antigens by VSMCs could perpetuate chronic inflammation within atherosclerotic plaques. Several markers are also implicated in cancer biology. [PCLAF](/details-gene/9768), also known as KIAA0101, is overexpressed in various cancers and promotes growth and invasion ([Link](https://doi.org/10.1371/journal.pone.0026866)). Similarly, [GSTP1](/details-gene/2950), a glutathione S-transferase, is involved in detoxification and drug resistance, and its expression is often altered in tumors. The role of VSMCs in tumor angiogenesis, where they are recruited to stabilize newly formed vessels, makes the expression of such genes clinically significant. ## Potential Mechanisms and Research Directions 1. **Hypothesis: VSMCs function as non-professional antigen-presenting cells that actively shape local immune responses within the vascular wall.** The exceptionally high specificity of [B2M](/details-gene/567) suggests this is not a passive or background function but a core component of the VSMC identity. This challenges the view of VSMCs as purely structural or contractile cells and repositions them as key players in vascular inflammation. * **Surprising Findings:** It is unexpected that an immune-related gene like [B2M](/details-gene/567) would emerge as the single most specific marker for VSMCs, outranking classic smooth muscle genes. This implies that in a comparative multi-cell type context, the ability to present antigen is more unique to VSMCs than their contractile function. * **Testable Questions:** In co-culture systems, can VSMCs loaded with a specific viral or self-antigen induce the activation and proliferation of antigen-specific [CD8-positive, alpha-beta T cells](/details-cell/CL0000625)? How does this presentation capacity change when VSMCs are stimulated with pro-inflammatory cytokines like IFN-gamma or TNF-alpha? 2. **Hypothesis: The unique bioenergetic profile of VSMCs, characterized by a lower reliance on core mitochondrial respiratory gene expression, is a key determinant of their phenotypic plasticity.** The consistent negative `csi_z` for multiple essential mitochondrial genes ([COX1](/details-gene/4512), [COX2](/details-gene/4513), etc.) suggests VSMCs may be primed for metabolic switching towards glycolysis. This "Warburg-like" metabolic phenotype is characteristic of highly proliferative cells and could facilitate the rapid phenotypic changes required during vascular injury, repair, and diseases like atherosclerosis and restenosis. * **Surprising Findings:** A strong negative signature for fundamental energy-producing genes is counterintuitive for a cell type responsible for maintaining vascular tone. This suggests that their basal state may be metabolically distinct from other cells in the tissue, potentially to conserve resources or maintain a state of readiness for rapid proliferation. * **Testable Questions:** Using metabolic flux analysis, what is the basal ratio of glycolysis to oxidative phosphorylation in quiescent VSMCs compared to VSMCs stimulated to a proliferative/synthetic phenotype by growth factors like PDGF? Does pharmacologically inhibiting glycolysis prevent this phenotypic switch and subsequent cell migration?