Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adhesion molecules play a significant role in leukocyte migration across the endothelium and are also involved in regulating immune system. It is shown that diabetic patients have an increase of soluble adhesion molecules (sICAM-1, sICAM-2, sVCAM-1, sE-selectin, sL-selectin, sP-selectin) considered an integral part of inflammatory state. This inflammation is responsible for the increased cardiovascular risk of these patients. There is a close link between hyperglycemia, oxidative stress, coagulopathy and inflammation and between these factors and the vascular damage. Various studies have showed the potential role of adhesion molecules in the pathogenesis of diabetic vasculopathy. They promote leukocyte recruitment, which is one of the initial steps in the genesis of atherosclerotic plaque. Adhesion molecules are also involved in the pathogenesis of diabetes mellitus type 1; sICAM-1 would have a particular immunomodulatory role in the process of destroying beta-cells and could be used as a subclinical marker of insulitis. Plasma levels of soluble adhesion molecules correlate with hyperglycemia, insulin resistance, dyslipidemia and obesity; they are associated with the development of nephropathy, retinopathy, myocardial infarction, stroke and obliterant peripheral arterial disease in diabetic type 1 and 2. Given the role of these molecules in endothelial dysfunction genesis and tissue damage associated with diabetes, they could constitute a therapeutic target for the prevention of genesis and progression of chronic complications of diabetic disease.
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PMID:[Adhesion molecules and diabetes mellitus]. 2054 49

Emerging evidence has demonstrated that long non-coding RNAs (lncRNAs) are related to the pathogenesis of atherosclerosis (AS). We aimed to investigate the roles and molecular mechanisms of myocardial infarction-associated transcript (MIAT) in the proliferation, migration and invasion of oxidized low-density lipoprotein (ox-LDL)-induced vascular smooth muscle cells (VSMCs). Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to determine the levels of MIAT, microRNA490-3p (miR-490-3p) and Intercellular Adhesion Molecule 1 (ICAM1). Cell Counting Kit-8 (CCK-8) assay was carried out to assess cell proliferation. Transwell assay was employed to evaluate cell migration and invasion. Western blot assay was performed to measure the protein levels of proliferating cell nuclear antigen (PCNA), N-cadherin, matrix metalloprotein-9 (MMP9) and ICAM1. Dual-luciferase reporter, RNA immunoprecipitation (RIP) and RNA pull-down assays were conducted to verify the relationship between miR-490-3p and MIAT or ICAM1. MIAT was elevated in AS patients' serum and ox-LDL-induced VSMCs. MIAT knockdown suppressed cell proliferation, migration and invasion in ox-LDL-stimulated VSMCs. MIAT acted as a sponge of miR-490-3p and miR-490-3p deficiency overturned the inhibition of MIAT knockdown on VSMC proliferation, migration and invasion. ICAM1 was a direct target of miR-490-3p and ICAM1 silencing repressed the proliferation, migration and invasion of ox-LDL-stimulated VSMCs. Moreover, ICAM1 overexpression reversed the impacts of MIAT knockdown on ox-LDL-induced VSMC proliferation, migration and invasion. MIAT knockdown could depress cell proliferation, migration and invasion via miR-490-3p/ICAM1 axis in ox-LDL-induced VSMCs.
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PMID:MIAT knockdown inhibits cell proliferation, migration and invasion via miR-490-3p/ICAM1 axis in ox-LDL-induced vascular smooth muscle cells. 3283 4


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