Details for: CL0002591

Cell ID: CL0002591

Cell Name: smooth muscle cell of the pulmonary artery

Description: A smooth muscle of the pulmonary artery.

Selected Context(s): Overall

Gene Significance Landscape

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Genes

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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 smooth muscle cell of the pulmonary artery 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 smooth muscle cell of the pulmonary artery. 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 smooth muscle cell of the pulmonary artery. 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 smooth muscle cell of the pulmonary artery. 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:  smooth muscle cell of the pulmonary artery (CL0002591)

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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 [smooth muscle cell of the pulmonary artery](/details-cell/CL0002591) is a specialized contractile cell type responsible for regulating vascular tone and blood flow within the pulmonary circulation. **Overall**, the gene significance profile highlights a cell with a highly developed contractile apparatus, substantial metabolic activity, and robust systems for managing calcium signaling and iron homeostasis. The defining markers include myosin light chains such as [MYL6](/details-gene/4637), numerous components of the mitochondrial respiratory chain (e.g., [COX1](/details-gene/4512)), and several calcium-binding proteins, underscoring its primary function in sustained, energy-intensive contraction. ## Key Characteristics and Function The functional identity of the [pulmonary artery smooth muscle cell](/details-cell/CL0002591) is strongly defined by several key biological themes that emerge from its top marker genes. * **Contractile Machinery and Regulation:** The most specific markers are components of the actomyosin contractile apparatus. High significance scores for myosin light chains [MYL6](/details-gene/4637) (CSI: 12.76) and [MYL9](/details-gene/10398) (CSI: 9.42) directly reflect the cell's primary role in generating mechanical force. This is further supported by the high significance of [PPP1R14A](/details-gene/94274), an inhibitory phosphoprotein for myosin phosphatase, which suggests a tightly regulated system for controlling the phosphorylation state of myosin and thus the contractility of the cell ([Link](https://doi.org/10.1006/bbrc.2001.5290)). * **High Metabolic Energy Production:** A striking feature is the prominence of genes encoding subunits of the mitochondrial electron transport chain. [COX1](/details-gene/4512), [CYTB](/details-gene/4519), [COX4I1](/details-gene/1327), [ND2](/details-gene/4536), and [ND4](/details-gene/4538) all rank as top markers. This indicates a very high capacity for aerobic respiration, which is necessary to generate the large amounts of ATP required to power sustained vascular contraction and ion pumping. * **Calcium-Dependent Signaling:** Smooth muscle contraction is critically dependent on intracellular calcium levels. The high significance of calcium ion-binding proteins like [TPT1](/details-gene/7178) and [S100A6](/details-gene/6277) highlights the importance of calcium buffering and signaling. These proteins may serve not only to modulate contractile responses but also to integrate calcium signals with other cellular processes. The extracellular matrix protein [SPARCL1](/details-gene/8404), which also binds calcium, is another top marker, suggesting a link between the extracellular environment and intracellular calcium dynamics. * **Iron Homeostasis and Oxidative Stress Management:** The high significance of both ferritin heavy chain ([FTH1](/details-gene/2495)) and light chain ([FTL](/details-gene/2512)) is noteworthy. Ferritin sequesters intracellular iron, which is essential as a cofactor for mitochondrial enzymes but can also generate harmful reactive oxygen species. This, combined with the high rank of [GSTP1](/details-gene/2950), a glutathione transferase involved in detoxification, suggests a well-developed system to manage iron and mitigate oxidative stress, which is likely high in such a metabolically active cell. * **Distinct Lineage Identity:** The anti-marker profile helps to define what this cell is not. The low significance of genes associated with inflammation ([IL6](/details-gene/3569)), angiogenesis ([ANGPT1](/details-gene/284)), adipogenesis ([FABP4](/details-gene/2167)), and neuronal processes ([SEMA5A](/details-gene/9037)) confirms its specialized smooth muscle identity, distinct from immune, endothelial, fat, or neural lineages. ## Clinical Significance and Contextual Roles The gene signature of the [pulmonary artery smooth muscle cell](/details-cell/CL0002591) provides insights into its role in both health and disease, particularly in the context of pulmonary vascular diseases like pulmonary hypertension. The core identity of this cell revolves around maintaining pulmonary vascular resistance. The strong expression of contractile elements ([MYL6](/details-gene/4637), [MYL9](/details-gene/10398)) is central to this physiological function. Pathological conditions often involve the hyper-contractility and proliferation of these cells, leading to vessel narrowing and increased pressure. The regulatory protein [PPP1R14A](/details-gene/94274) represents a potential target for modulating this contractile state. The profound metabolic signature, characterized by numerous mitochondrial genes, is also clinically relevant. A metabolic shift from oxidative phosphorylation to glycolysis (the Warburg effect) has been described in the proliferating smooth muscle cells of pulmonary hypertension. The high basal expression of oxidative phosphorylation machinery suggests that perturbations in this energetic pathway could be a key event in the initiation or progression of vascular remodeling. Furthermore, the cell's robust machinery for handling oxidative stress ([FTH1](/details-gene/2495), [FTL](/details-gene/2512), [GSTP1](/details-gene/2950)) may be critical for its resilience under conditions of hypoxia or inflammation, common stimuli in lung pathology. Dysregulation of iron metabolism and subsequent oxidative damage could contribute to the cellular dysfunction seen in pulmonary vascular diseases. ## Potential Mechanisms and Research Directions 1. **Hypothesis: Pulmonary artery smooth muscle cells possess an integrated iron-energy axis to balance high metabolic demand with the mitigation of oxidative stress, and its disruption is a potential driver of vascular pathology.** The co-expression of a full suite of mitochondrial respiratory components alongside major iron-storage proteins ([FTH1](/details-gene/2495), [FTL](/details-gene/2512)) suggests a tightly coordinated system. This axis likely ensures a sufficient supply of iron for mitochondrial enzyme function while preventing iron-catalyzed oxidative damage, a significant risk in these highly aerobic cells. * **Surprising Findings:** The prominence of ferritin subunits as top identity markers is unexpected for a cell primarily defined by its contractility. This implies that managing iron homeostasis is as fundamental to this cell's specialized state as its myosin machinery. * **Testable Questions:** How does experimental modulation of [FTH1](/details-gene/2495) or [FTL](/details-gene/2512) expression affect mitochondrial function, ATP production, and contractile responses to vasoconstrictors in cultured [pulmonary artery smooth muscle cells](/details-cell/CL0002591)? Does iron chelation or overload alter the cell's proliferative response to mitogens like PDGF? 2. **Hypothesis: The specific repertoire of calcium-binding proteins, particularly [TPT1](/details-gene/7178) and [S100A6](/details-gene/6277), serves not only to buffer calcium for contraction but also to act as a signaling node that links calcium dynamics to gene expression and cell phenotype.** These proteins may function as sensors that translate the frequency and amplitude of calcium transients into distinct downstream signals, potentially influencing the switch between a quiescent, contractile phenotype and a proliferative, synthetic phenotype observed in disease. * **Surprising Findings:** While calcium's role in contraction is well-established, the high significance of [TPT1](/details-gene/7178), a protein often associated with cell growth and tumors, suggests a non-canonical role in this differentiated cell type, potentially linking its metabolic state or contractile activity to long-term phenotypic stability. * **Testable Questions:** What are the specific protein interaction partners of [TPT1](/details-gene/7178) and [S100A6](/details-gene/6277) in [pulmonary artery smooth muscle cells](/details-cell/CL0002591) under basal versus stimulated (e.g., endothelin-1) conditions? Does silencing these genes alter not only the acute contractile response but also the long-term expression of contractile-phenotype markers like alpha-smooth muscle actin?