Background: Over the years, a number of published studies showed that E-Selectin gene rs5361 (S128R, Ser128Arg, A561C) variants were associated with the risk of ischemic stroke (IS). However, the results of those case-control studies were still equivocal. Therefore, we performed this meta-analysis to clarify the relationship between E-Selectin gene rs5361 polymorphism and IS risk.
Methods: We searched the Web of Science, PubMed, VIP, CNKI (China National Knowledge Infrastructure) and Wanfang databases for obtainning the eligible studies according to the inclusion and exclusion criteria. Odds ratios (ORs) with its 95% confidence intervals (CIs) were calculated to evaluate the relationship of E-Selectin gene rs5361 polymorphism with IS susceptibility under the dominant and allelic model with fixed or random effects model.
Results: Totally, 13 studies with 2888 cases and 2976 controls were selected in this systematic review and meta-analysis This meta-analysis obtained that E-Selectin gene rs5361variants contributed to increase the risk of IS (C vs. A: OR = 2.23, 95%CI = 1.70-2.92, < 0.001). We also performed a sub-analysis by ethnicity, the results indicated that rs5361 variants were related to an increased risk of IS (East Asian population: C vs. A: OR = 1.97, 95%CI =1.58-2.45, < 0.001; African population: C vs. A: OR = 5.52, 95%CI = 3.48-8.76, < 0.001; Caucasian population: C vs. A: OR =1.67, 95%CI =1.32-2.10, < 0.001).
Conclusions: Therefore, our meta-analysis suggested that C allele, AA and AC genotypes of E-Selectin gene rs5361 variants were related to an increased risk of IS in overall populations.
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http://dx.doi.org/10.1080/00207454.2020.1750385 | DOI Listing |
Alzheimers Dement
December 2024
Neural Stem Cell Institute, Rensselaer, NY, USA.
Background: Up to 84% of patients with Alzheimer's Disease (AD) have vascular damage which precedes cognitive decline. Inflammation induces changes in blood-brain-barrier (BBB) integrity, though the link between induction of inflammation and AD is unclear. IL1β, a cytokine upregulated in patients with AD and in mouse models of the disease, is released and interacts with IL1R1 and its obligate co-receptor, IL1RAP, to induce downstream signaling.
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December 2024
M Maugham-Macan, Biomedical Science, University of the Sunshine Coast, Sippy Downs, Australia.
Bone is a common and debilitating site for metastatic cancer cell expansion. Skeletal metastasis is a multistage process, with primary stages of circulating tumour cells, progressing to a dormant state in vasculature and bone marrow niches, followed by tumorigenic reactivation, proliferation, and finally bone destruction. The frequency of bone metastasis is reconciled in Paget's "seed and soil" hypothesis, where a conducive microenvironment (bone niche) is essential for cancer cell colonisation.
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December 2024
Department of Respiratory Medicine Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Child Rare Diseases in Infection and Immunity, Chongqing, 400014, China.
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January 2025
Institute of Anatomy and Experimental Morphology, University Cancer Center Hamburg, University Medical Center Hamburg-Eppendorf, 20241, Hamburg, Germany; Institute of Anatomy I, Jena University Hospital, 07743, Jena, Germany; Comprehensive Cancer Center Central Germany (CCCG). Electronic address:
The commonly altered glycosylation of tumor cells is a hallmark of tumor progression and metastasis formation. One prominent example is the interaction of sialylated glycans at the tumor cell surface with endothelial (E)-selectin as an early event of an adhesion cascade that enables extravasation of circulating tumor cells (CTCs) into distant tissues. In a previous study, we identified GCNT3 (mucin-type core2/ core4 β1,6-N-acetylglucosaminyltransferase) highly over-expressed in gastrointestinal adenocarcinoma cells that facilitate the canonical E-selectin ligands sialyl-Lewis A and X (sLeA/X) for E-selectin binding and endothelial adhesion.
View Article and Find Full Text PDFInt J Mol Sci
October 2024
Optics & Imaging, Doris Duke Medical Research Institute, College of Health Sciences, University of KwaZulu-Natal, Durban 4041, South Africa.
Intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1), and E-selectin are cell adhesion molecules that play a significant role in inflammation and are implicated in the pathophysiology of preeclampsia development and HIV infection. More specifically, the immune expression of ICAM-1, VCAM-1, and E-selectin within cyto- and syncytiotrophoblast cells are dysregulated in preeclampsia, indicating their role in defective placentation. This study investigates the associations of ICAM-1, VCAM-1, and E-selectin gene variants (rs3093030, rs3783605, and rs1805193, respectively) with preeclampsia comorbid with HIV infection in women of African ancestry.
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