Details for: CL0002543

Cell ID: CL0002543

Cell Name: vein endothelial cell

Description: An endothelial cell that is part of the vein.

Synonyms: endothelial cell of vein, venous endothelial cell

Selected Context(s): Overall

Gene Significance Landscape

Display Options
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 vein endothelial 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 vein endothelial 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 vein endothelial 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 vein endothelial 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:  vein endothelial cell (CL0002543)

 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.

Loading network (please wait)...

## Summary The [vein endothelial cell](/details-cell/CL0002543) is a specialized endothelial cell type that forms the inner lining of veins. Based on its gene significance profile, this cell is characterized by exceptionally high activity in protein synthesis and RNA metabolism, as indicated by top markers such as the translationally controlled tumor protein [TPT1](/details-gene/7178) and the poly(A) binding protein [PABPC1](/details-gene/26986). Furthermore, the specific expression of genes involved in immune presentation, such as [B2M](/details-gene/567) and [HLA E](/details-gene/3133), suggests a crucial role in interacting with the immune system within the low-pressure venous environment. This profile paints a picture of a metabolically active cell that is not merely a passive conduit but a key player in maintaining vascular homeostasis, managing cytoskeletal integrity, and regulating immune surveillance. ## Key Characteristics and Function Analysis of the top marker genes, ranked by expression specificity (**Overall** context), reveals several core functional clusters that define the [vein endothelial cell](/details-cell/CL0002543). * **Protein Synthesis and RNA Processing:** A dominant characteristic of this cell type is its robust machinery for protein production and regulation. The high significance of [TPT1](/details-gene/7178), [PABPC1](/details-gene/26986), [SRP14](/details-gene/6727), [EEF1B2](/details-gene/1933), and [EEF1D](/details-gene/1936) highlights a state of high translational activity. This is further supported by the specificity of genes involved in RNA binding and splicing, such as [DDX5](/details-gene/1655), and transcription, like [BTF3](/details-gene/689). This suggests these cells are actively synthesizing a wide array of proteins required for self-maintenance, communication, and responding to hemodynamic and inflammatory cues. * **Immune Presentation and Modulation:** [Vein endothelial cells](/details-cell/CL0002543) appear to be actively engaged in immune surveillance. The high specificity of [B2M](/details-gene/567), the light chain of MHC class I molecules, and the non-classical MHC class I molecule [HLA E](/details-gene/3133) is particularly noteworthy. [HLA E](/details-gene/3133) is known to present a restricted set of peptides and primarily interacts with inhibitory receptors on NK cells and subsets of T cells. This suggests that venous endothelium plays a specialized role in modulating local immune responses, potentially preventing inappropriate activation in the low-flow venous system. * **Cytoskeletal Dynamics and Mechanotransduction:** The cell's structural integrity and responsiveness to physical forces are underscored by the specific expression of several myosin light chain genes ([MYL6](/details-gene/4637), [MYL12A](/details-gene/10627), [MYL12B](/details-gene/103910)) and the actin-binding protein [CFL1](/details-gene/1072). This machinery is essential for maintaining cell shape, managing intercellular junctions, and responding to the unique shear stress conditions found in veins. * **Metabolic Activity and Ion Homeostasis:** The profile indicates significant metabolic function. High specificity of ferritin subunits [FTL](/details-gene/2512) and [FTH1](/details-gene/2495) points to an important role in iron storage and management, which is crucial for controlling oxidative stress. The expression of [ATP5F1E](/details-gene/514), a component of ATP synthase, and the glycolytic enzyme [GAPDH](/details-gene/2597) are consistent with the high energy demands of this active cell type. The calcium-binding protein [S100A6](/details-gene/6277) further suggests involvement in calcium-dependent signaling pathways. * **Extracellular Environment Interaction:** The high specificity of [SPARCL1](/details-gene/8404), a secreted calcium-binding protein related to SPARC, suggests that these cells actively modulate their surrounding extracellular matrix. [SPARCL1](/details-gene/8404) (also known as hevin) has been described as an anti-adhesive protein, potentially regulating leukocyte-endothelial interactions ([Link](https://doi.org/10.1016/1074-7613(95)90083-7)). The anti-marker profile, although showing high p-values for many genes, is notable for the low relative significance of mitochondrial genes involved in the electron transport chain, such as [MTCO3P18](/details-gene/107075215) and [COX3](/details-gene/4514). This may suggest a preference for glycolysis over oxidative phosphorylation under basal conditions, a known feature of some endothelial cell types. ## Clinical Significance and Contextual Roles The gene expression profile of [vein endothelial cells](/details-cell/CL0002543) provides insights into their potential involvement in various pathological processes, particularly those related to vascular inflammation, immune-mediated diseases, and neurodegeneration. * **Vascular Inflammation and Thrombosis:** The prominent role of [B2M](/details-gene/567) and [HLA E](/details-gene/3133) suggests that dysregulation of antigen presentation by venous endothelium could be a factor in autoimmune vasculitides or in the initiation of venous thrombosis (phlebitis), where inappropriate immune cell activation is a key event. The cell's robust cytoskeletal machinery ([MYL6](/details-gene/4637), [CFL1](/details-gene/1072)) is critical for maintaining barrier function, and its failure could contribute to edema and inflammation. * **Systemic Disease and Amyloidopathy:** A striking finding is the high specificity of [ITM2B](/details-gene/9445), a gene whose mutations are directly causal for Familial British Dementia and Familial Danish Dementia, both of which are cerebral amyloid angiopathies ([Link](https://doi.org/10.1038/21637), [Link](https://doi.org/10.1073/pnas.080076097)). The specific expression of this gene in a peripheral vascular cell type like the [vein endothelial cell](/details-cell/CL0002543) may indicate a systemic contribution to these diseases, where the endothelium could act as a source for the amyloidogenic ABri or ADan peptides. This finding bridges vascular biology with neurodegenerative disease. * **Iron Metabolism and Oxidative Stress:** The significant expression of ferritin genes ([FTL](/details-gene/2512), [FTH1](/details-gene/2495)) highlights the cell's role in managing iron, a potent pro-oxidant. In conditions like chronic venous insufficiency, where oxidative stress is implicated, the capacity of these cells to sequester iron may be a critical protective mechanism. Dysregulation of this process could exacerbate endothelial damage and inflammation. ## Potential Mechanisms and Research Directions 1. **Hypothesis:** Based on the high expression specificity of the non-classical MHC molecule [HLA E](/details-gene/3133) and its partner [B2M](/details-gene/567), we hypothesize that [vein endothelial cells](/details-cell/CL0002543) utilize the HLA-E pathway as a primary mechanism to constitutively inhibit NK cell and T cell activation, thereby maintaining an anti-inflammatory state and immune tolerance in the low-shear venous environment. * **Surprising Findings:** The prominence of a non-classical, primarily inhibitory, MHC molecule like [HLA E](/details-gene/3133) over classical antigen-presenting molecules suggests that the default function of these cells may be to actively suppress, rather than activate, immune responses. This is particularly relevant in the venous system where blood flow is slower, increasing the contact time between leukocytes and the endothelium. * **Testable Questions:** Does inflammatory stimulation (e.g., with TNF-alpha or IL-1beta) alter the surface expression ratio of HLA-E to classical MHC-I molecules on primary human venous endothelial cells, and how does this shift impact their susceptibility to NK cell-mediated lysis? 2. **Hypothesis:** The highly specific expression of the anti-adhesive matricellular protein [SPARCL1](/details-gene/8404) suggests that [vein endothelial cells](/details-cell/CL0002543) secrete this factor to finely tune leukocyte adhesion, preventing aberrant cell attachment in low-flow conditions while permitting regulated diapedesis during inflammation. * **Surprising Findings:** It is counterintuitive for an endothelial cell, which must support leukocyte trafficking, to specifically express a potent anti-adhesive protein. This suggests a more sophisticated regulatory role than simple adhesion, where [SPARCL1](/details-gene/8404) might create a non-stick surface that requires strong, specific inflammatory signals to be overcome, thus raising the threshold for leukocyte transmigration. * **Testable Questions:** Does the addition of recombinant [SPARCL1](/details-gene/8404) to an in vitro flow chamber assay inhibit basal leukocyte rolling and adhesion to venous endothelial monolayers, and can this inhibition be reversed by pre-treating the endothelial cells with inflammatory cytokines?