The association of cell adhesion molecules and selectins (VCAM-1, ICAM-1, E-selectin, L-selectin, and P-selectin) with microvascular complications in patients with type 2 diabetes: A follow-up study

Siddiqui, Khalid; George, Teena P.; Mujammami, Muhammad; Isnani, Arthur; Alfadda, Assim A.

doi:10.3389/fendo.2023.1072288

Cited by 15 publications

(10 citation statements)

References 34 publications

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“…IL-1β and TNF-α can induce inflammation and apoptosis of endothelial cells, leading to endothelial cell injury and death, and causing abnormal proliferation and leakage of blood vessels [23] . ICAM-1 is an adhesion molecule that can increase the adhesion and infiltration of endothelial cells and inflammatory cells, leading to abnormal proliferation and leakage of retinal microvessels [24] . MCP-1 is a chemotactic factor that can attract inflammatory cells to the lesion area [25] .…”

Section: Discussionmentioning

confidence: 99%

Trimethylamine N-oxide aggravates vascular permeability and endothelial cell dysfunction under diabetic condition: in vitro and in vivo study

Jiang,

Zhang,

Ren

et al. 2024

Int J Ophthalmol

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AIM: To provide the direct evidence for the crucial role of trimethylamine N-oxide (TMAO) in vascular permeability and endothelial cell dysfunction under diabetic condition. METHODS: The role of TMAO on the in vitro biological effect of human retinal microvascular endothelial cells (HRMEC) under high glucose conditions was tested by a cell counting kit, wound healing, a transwell and a tube formation assay. The inflammation-related gene expression affected by TMAO was tested by real-time polymerase chain reaction (RT-PCR). The expression of the cell junction was measured by Western blotting (WB) and immunofluorescence staining. In addition, two groups of rat models, diabetic and non-diabetic, were fed with normal or 0.1% TMAO for 16wk, and their plasma levels of TMAO, vascular endothelial growth factor (VEGF), interleukin (IL)-6 and tumor necrosis factor (TNF)-α were tested. The vascular permeability of rat retinas was measured using FITC-Dextran, and the expression of zonula occludens (ZO)-1 and claudin-5 in rat retinas was detected by WB or immunofluorescence staining. RESULTS: TMAO administration significantly increased the cell proliferation, migration, and tube formation of primary HRMEC either in normal or high-glucose conditions. RT-PCR showed elevated inflammation-related gene expression of HRMEC under TMAO stimulation, while WB or immunofluorescence staining indicated decreased cell junction ZO-1 and occludin expression after high-glucose and TMAO treatment. Diabetic rats showed higher plasma levels of TMAO as well as retinal vascular leakage, which were even higher in TMAO-feeding diabetic rats. Furthermore, TMAO administration increased the rat plasma levels of VEGF, IL-6 and TNF-α while decreasing the retinal expression levels of ZO-1 and claudin-5. CONCLUSION: TMAO enhances the proliferation, migration, and tube formation of HRMEC, as well as destroys their vascular integrity and tight connection. It also regulates the expression of VEGF, IL-6, and TNF-α.

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Section: Discussionmentioning

confidence: 99%

Trimethylamine N-oxide aggravates vascular permeability and endothelial cell dysfunction under diabetic condition: in vitro and in vivo study

Jiang,

Zhang,

Ren

et al. 2024

Int J Ophthalmol

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“…In our study, patients in the study group had significantly higher L-selectin concentrations than healthy volunteers; comparable results to ours were obtained by Nomura and colleagues [ 53 ]. Recent scientific reports show the association of elevated L-selectin values with microvascular complications in type 2 diabetes individuals [ 54 ]. In our cohort, we obtained a statistically significant reduction in serum L-selectin levels after 180 days of GLP-RA therapy; to the best of our knowledge, there are no results available evaluating the effect of this group of drugs on L-selectin adhesion molecule levels.…”

Section: Discussionmentioning

confidence: 99%

Effect of GLP-1RA Treatment on Adhesion Molecules and Monocyte Chemoattractant Protein-1 in Diabetic Patients with Atherosclerosis

Hachuła,

Basiak,

Kosowski

et al. 2024

Life

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Cardiovascular disease (CVD) remains a prominent cause of global mortality, primarily driven by atherosclerosis. Diabetes mellitus, as a modifiable risk factor, significantly contributes to atherogenesis. Monocyte recruitment to the intima is a critical step in atherosclerotic plaque formation, involving chemokines and adhesion molecules such as selectins, ICAM-1, and MCP-1. Glucagon-like peptide 1 receptor agonists (GLP-1RAs) are a promising group of drugs for reducing cardiovascular risk in diabetic patients, prompting investigation into their mechanisms of action. This interventional study enrolled 50 diabetes patients with atherosclerotic plaque, administering GLP-1RA for 180 days. Serum concentrations of MCP-1, ICAM-1, and L-selectin were measured before and after treatment. Anthropometric and biochemical parameters were also assessed. GLP-1RA treatment resulted in significant improvements in anthropometric parameters, glycemic control, blood pressure, and biochemical markers of liver steatosis. Biomarker laboratory analysis revealed higher baseline levels of MCP-1, ICAM-1, and L-selectin in diabetic patients with atherosclerotic plaque compared to healthy controls. Following treatment, MCP-1 and L-selectin levels decreased significantly (p < 0.001), while ICAM-1 levels increased (p < 0.001). GLP-1RA treatment in diabetic patients with atherosclerotic plaque leads to favorable changes in serum molecule levels associated with monocyte recruitment to the endothelium. The observed reduction in MCP-1 and L-selectin suggests a potential mechanism underlying GLP-1RA-mediated cardiovascular risk reduction. Further research is warranted to elucidate the precise mechanisms and clinical implications of these findings in diabetic patients with atherosclerosis.

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“…Hyperglycemia leads to the impairment of retinal endothelial cells (RECs) by ischemia, oxidative stress, and the release of proinflammatory factors. Patients with DR may experience increased vessel wall permeability and capillary occlusion as a result of increased adhesion molecule expression and decreased vasodilation found in retinal microvessels (121). Retinal binding protein 3 (RBP3) reduces inflammatory cytokines and inhibits VEGF's activities in the retina, which may prevent the advancement of DR (122).…”

Section: Diabetic Retinopathymentioning

confidence: 99%

Endothelial dysfunction in vascular complications of diabetes: a comprehensive review of mechanisms and implications

Yang,

Wang,

Zhang

et al. 2024

Front. Endocrinol.

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Diabetic vascular complications are prevalent and severe among diabetic patients, profoundly affecting both their quality of life and long-term prospects. These complications can be classified into macrovascular and microvascular complications. Under the impact of risk factors such as elevated blood glucose, blood pressure, and cholesterol lipids, the vascular endothelium undergoes endothelial dysfunction, characterized by increased inflammation and oxidative stress, decreased NO biosynthesis, endothelial-mesenchymal transition, senescence, and even cell death. These processes will ultimately lead to macrovascular and microvascular diseases, with macrovascular diseases mainly characterized by atherosclerosis (AS) and microvascular diseases mainly characterized by thickening of the basement membrane. It further indicates a primary contributor to the elevated morbidity and mortality observed in individuals with diabetes. In this review, we will delve into the intricate mechanisms that drive endothelial dysfunction during diabetes progression and its associated vascular complications. Furthermore, we will outline various pharmacotherapies targeting diabetic endothelial dysfunction in the hope of accelerating effective therapeutic drug discovery for early control of diabetes and its vascular complications.

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The association of cell adhesion molecules and selectins (VCAM-1, ICAM-1, E-selectin, L-selectin, and P-selectin) with microvascular complications in patients with type 2 diabetes: A follow-up study

Cited by 15 publications

References 34 publications

Trimethylamine N-oxide aggravates vascular permeability and endothelial cell dysfunction under diabetic condition: in vitro and in vivo study

Trimethylamine N-oxide aggravates vascular permeability and endothelial cell dysfunction under diabetic condition: in vitro and in vivo study

Effect of GLP-1RA Treatment on Adhesion Molecules and Monocyte Chemoattractant Protein-1 in Diabetic Patients with Atherosclerosis

Endothelial dysfunction in vascular complications of diabetes: a comprehensive review of mechanisms and implications

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