Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (680 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Cell adhesion molecule and CD antigen that mediates neutrophil, monocyte, and memory T-cell adhesion to cytokine-activated endothelial cells. E-selectin recognizes sialylated carbohydrate groups related to the Lewis X or Lewis A family.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Endothelial Leukocyte Adhesion Molecule-1; E Selectin; Selectin, E; ELAM-1; LECAM-2; CD62E Antigen; Antigen, CD62E; Antigens, CD62E.
Where it fits in the MeSH classification
- Broader topics
- Selectins
Research landscape
PubMed indexes 6,142 records tagged with the MeSH heading “E-Selectin” (counts retrieved 2026-10-31). 386 of them (6.3%) were published from 2020 onward, and the busiest period so far is 2000-2009 with 2,348 records.
Reviews account for 227 records (3.7%) and meta-analyses for 31. Randomized controlled trials number 250 (4.1%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 1,916 |
| 2000-2009 | 2,348 |
| 2010-2019 | 1,492 |
| 2020 onward | 386 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 227 | 3.7% |
| Meta-analyses | 31 | 0.5% |
| Randomized controlled trials | 250 | 4.1% |
Method: PubMed query "E-Selectin"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
Vascular and blood-brain barrier-related changes underlie stress responses and resilience in female mice and depression in human tissue [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Prevalence, symptoms, and treatment of depression suggest that major depressive disorders (MDD) present sex differences.
- Closing excerpt
- Altogether, we propose that BBB dysfunction plays an important role in modulating stress responses in female mice and possibly MDD.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (175 words)
Prevalence, symptoms, and treatment of depression suggest that major depressive disorders (MDD) present sex differences. Social stress-induced neurovascular pathology is associated with depressive symptoms in male mice; however, this association is unclear in females. Here, we report that chronic social and subchronic variable stress promotes blood-brain barrier (BBB) alterations in mood-related brain regions of female mice. Targeted disruption of the BBB in the female prefrontal cortex (PFC) induces anxiety- and depression-like behaviours. By comparing the endothelium cell-specific transcriptomic profiling of the mouse male and female PFC, we identify several pathways and genes involved in maladaptive stress responses and resilience to stress. Furthermore, we confirm that the BBB in the PFC of stressed female mice is leaky. Then, we identify circulating vascular biomarkers of chronic stress, such as soluble E-selectin. Similar changes in circulating soluble E-selectin, BBB gene expression and morphology can be found in blood serum and postmortem brain samples from women diagnosed with MDD. Altogether, we propose that BBB dysfunction plays an important role in modulating stress responses in female mice and possibly MDD.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 35013188 · DOI · PMC8748803
Endothelial E-selectin inhibition improves acute myeloid leukaemia therapy by disrupting vascular niche-mediated chemoresistance [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The endothelial cell adhesion molecule E-selectin is a key component of the bone marrow hematopoietic stem cell (HSC) vascular niche regulating balance between HSC self-renewal and commitment.
- Closing excerpt
- Absence (in Sele-/- hosts) or therapeutic blockade of E-selectin using small molecule mimetic GMI-1271/Uproleselan effectively inhibits this niche-mediated pro-survival signaling, dampens AML blast regeneration, and strongly synergizes with chemotherapy, doubling the duration of mouse survival over chemotherapy alone, whilst protecting endogenous HSC.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (150 words)
The endothelial cell adhesion molecule E-selectin is a key component of the bone marrow hematopoietic stem cell (HSC) vascular niche regulating balance between HSC self-renewal and commitment. We now report in contrast, E-selectin directly triggers signaling pathways that promote malignant cell survival and regeneration. Using acute myeloid leukemia (AML) mouse models, we show AML blasts release inflammatory mediators that upregulate endothelial niche E-selectin expression. Alterations in cell-surface glycosylation associated with oncogenesis enhances AML blast binding to E-selectin and enable promotion of pro-survival signaling through AKT/NF-κB pathways. In vivo AML blasts with highest E-selectin binding potential are 12-fold more likely to survive chemotherapy and main contributors to disease relapse. Absence (in Sele-/- hosts) or therapeutic blockade of E-selectin using small molecule mimetic GMI-1271/Uproleselan effectively inhibits this niche-mediated pro-survival signaling, dampens AML blast regeneration, and strongly synergizes with chemotherapy, doubling the duration of mouse survival over chemotherapy alone, whilst protecting endogenous HSC.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32341362 · DOI · PMC7184728
E-selectin-targeting delivery of microRNAs by microparticles ameliorates endothelial inflammation and atherosclerosis [3]
Abstract reading summary — source excerpts
- Opening excerpt
- E-selectin is a surface marker of endothelial cell (EC) inflammation, one of the hallmarks of atherogenesis.
- Closing excerpt
- Our data supported our hypothesis that ESTA-MSV microparticle-mediated delivery of miR-146a/-181b ameliorates endothelial inflammation and atherosclerosis.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (198 words)
E-selectin is a surface marker of endothelial cell (EC) inflammation, one of the hallmarks of atherogenesis. Thus, we tested the hypothesis that delivery of microRNA (miR)-146a and miR-181b with an E-selectin-targeting multistage vector (ESTA-MSV) to inflamed endothelium covering atherosclerotic plaques inhibits atherosclerosis. Cy5-conjugated miR-146a and miR-181b were packaged in polyethylene glycol-polyethyleneimine (PEG/PEI) nanoparticles and loaded into ESTA-MSV microparticles. Both miRs were downregulated in tumor necrosis factor (TNF)-α-treated ECs. Transfection of TNF-α-treated mouse aortas and cultured ECs with miRs was more efficient with ESTA-MSV than with the PEG/PEI. Likewise, miR-146a/-181b packaged in ESTA-MSV efficiently suppressed the chemokines, CCL2, CCL5, CCL8, and CXCL9, and monocyte adhesion to ECs. Complementary in vivo tests were conducted in male apolipoprotein E-deficient mice fed a Western diet and injected intravenously with the particles prepared as above biweekly for 12 weeks. Treatment with miRs packaged in ESTA-MSV but not in PEG/PEI reduced atherosclerotic plaque size. Concurrently, vascular inflammation markers, including macrophages in aortic root lesions and chemokine expression in aortic tissues were reduced while the vascular smooth muscle cells and collagen increased in plaques from ESTA-MSV/miRs-treated vs. vehicle-treated mice. Our data supported our hypothesis that ESTA-MSV microparticle-mediated delivery of miR-146a/-181b ameliorates endothelial inflammation and atherosclerosis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 26956647 · DOI · PMC4783714
High CD44 expression and enhanced E-selectin binding identified as biomarkers of chemoresistant leukemic cells in human T-ALL [4]
Abstract reading summary — source excerpts
- Opening excerpt
- T-cell acute lymphoblastic leukemia (T-ALL) is a hematopoietic malignancy characterized by increased proliferation and incomplete maturation of T-cell progenitors, for which relapse is often of poor prognosis.
- Closing excerpt
- These characteristics of chemoresistant T-ALL CLCs provide key insights for prognostic stratification and novel therapeutic options.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (157 words)
T-cell acute lymphoblastic leukemia (T-ALL) is a hematopoietic malignancy characterized by increased proliferation and incomplete maturation of T-cell progenitors, for which relapse is often of poor prognosis. To improve patient outcomes, it is critical to understand the chemoresistance mechanisms arising from cell plasticity induced by the bone marrow (BM) microenvironment. Single-cell RNA sequencing of human T-ALL cells from adipocyte-rich and adipocyte-poor BM revealed a distinct leukemic cell population defined by quiescence and high CD44 expression (Ki67neg/lowCD44high). During in vivo treatment, these cells evaded chemotherapy, and were further called Chemotherapy-resistant Leukemic Cells (CLCs). Patient sample analysis revealed Ki67neg/lowCD44high CLCs at diagnosis and during relapse, with each displaying a specific transcriptomic signature. Interestingly, CD44high expression in T-ALL Ki67neg/low CLCs was associated with E-selectin binding. Analysis of 39 human T-ALL samples revealed significantly enhanced E-selectin binding activity in relapse/refractory samples compared with drug-sensitive samples. These characteristics of chemoresistant T-ALL CLCs provide key insights for prognostic stratification and novel therapeutic options.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39580584 · DOI · PMC11794132
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Leukocyte ligands for endothelial selectins: specialized glycoconjugates that mediate rolling and signaling under flow [5]
- Research article Carbohydrate-mediated cell adhesion involved in hematogenous metastasis of cancer [6]
- Research article Soluble E-selectin in cardiovascular disease and its risk factors. A review of the literature [7]
- Research article Immune cell entry into the central nervous system: involvement of adhesion molecules and chemokines [8]
- Research article Selectin ligands, leukocyte trafficking, and fucosyltransferase genes [9]
- Research article Vascular endothelial adhesion molecules and tissue inflammation [10]
References
- Dion-Albert L, Cadoret A, Doney E, Kaufmann FN, Dudek KA, Daigle B, et al.. Vascular and blood-brain barrier-related changes underlie stress responses and resilience in female mice and depression in human tissue. . 2022. PMID 35013188 · DOI · PMC8748803
- Barbier V, Erbani J, Fiveash C, Davies JM, Tay J, Tallack MR, et al.. Endothelial E-selectin inhibition improves acute myeloid leukaemia therapy by disrupting vascular niche-mediated chemoresistance. . 2020. PMID 32341362 · DOI · PMC7184728
- Ma S, Tian XY, Zhang Y, Mu C, Shen H, Bismuth J, et al.. E-selectin-targeting delivery of microRNAs by microparticles ameliorates endothelial inflammation and atherosclerosis. . 2016. PMID 26956647 · DOI · PMC4783714
- Calvo J, Naguibneva I, Kypraios A, Gilain F, Uzan B, Gaillard B, et al.. High CD44 expression and enhanced E-selectin binding identified as biomarkers of chemoresistant leukemic cells in human T-ALL. . 2025. PMID 39580584 · DOI · PMC11794132
- Zarbock A, Ley K, McEver RP, Hidalgo A. Leukocyte ligands for endothelial selectins: specialized glycoconjugates that mediate rolling and signaling under flow. Blood. 2011. PMID 22021370 · DOI · PMC3245201
- Kannagi R. Carbohydrate-mediated cell adhesion involved in hematogenous metastasis of cancer. Glycoconj J. 1997. PMID 9298690 · DOI
- Roldán V, Marín F, Lip GY, Blann AD. Soluble E-selectin in cardiovascular disease and its risk factors. A review of the literature. Thromb Haemost. 2003. PMID 14652631 · DOI
- Engelhardt B. Immune cell entry into the central nervous system: involvement of adhesion molecules and chemokines. J Neurol Sci. 2008. PMID 18573502 · DOI
- Lowe JB. Selectin ligands, leukocyte trafficking, and fucosyltransferase genes. Kidney Int. 1997. PMID 9150453 · DOI
- Malik AB, Lo SK. Vascular endothelial adhesion molecules and tissue inflammation. Pharmacol Rev. 1996. PMID 8804104 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.