ArticleSurgery2017
Effects of diabetes and cardiopulmonary bypass on expression of adherens junction proteins in human peripheral tissue.
Article in Surgery, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Uncontrolled hypertension contributes to vascular permeability after cardioplegic arrest and cardiopulmonary bypass.JTCVS open · 2026Article
- Common mechanisms underlying diabetic vascular complications: focus on the interaction of metabolic disorders, immuno-inflammation, and endothelial dysfunction.Cell communication and signaling : CCS · 2023Review
- Glycemic control is not associated with neurocognitive decline after cardiac surgery.Journal of cardiac surgery · 2022Article
- Endothelial Dysfunction and Coronary Vasoreactivity - A Review of the History, Physiology, Diagnostic Techniques, and Clinical Relevance.Current cardiology reviews · 2021Review
- Impaired coronary contraction to phenylephrine after cardioplegic arrest in diabetic patients.The Journal of surgical research · 2018Article
- Decreased coronary arteriolar response to KMolecular and cellular biochemistry · 2018Article
- Cyclooxygenase 2 contributes to bradykinin-induced microvascular responses in peripheral arterioles after cardiopulmonary bypass.The Journal of surgical research · 2017Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundWe investigated the changes in adherens junction proteins, such as vascular endothelial-cadherin and β-catenin, of skeletal muscle and vessels in patients with or without diabetes in the setting of cardiopulmonary bypass and cardiac operation.
methodsSkeletal muscle tissue samples were harvested pre- and post-cardiopulmonary bypass from nondiabetic (hemoglobin A1c: 5.4 ± 0.1), controlled diabetic (hemoglobin A1c: 6.3 ± 0.1), and uncontrolled diabetic patients (hemoglobin A1c: 9.6 ± 0.3) undergoing coronary artery bypass grafting operation (n = 8 per group). The expression/phosphorylation of adherens junction proteins vascular endothelial-cadherin and β-catenin were assessed by immunoblotting and immuno-histochemistry. Endothelial function of skeletal muscle arterioles was determined by videomicroscopy in response to the vasodilator substance P.
resultsThe protein expression of total vascular endothelial-cadherin was not changed at baseline or between pre-and post-cardiopulmonary bypass among groups. The pre-cardiopulmonary bypass level of phospho-vascular endothelial-cadherin was found to be significantly increased in the uncontrolled diabetic patients group compared with the nondiabetic or controlled diabetic groups (P < .05). The post-cardiopulmonary bypass levels of phospho-vascular endothelial-cadherin were significantly increased compared with pre-cardiopulmonary bypass in all groups (P < .05 each), and this increase was greater in the uncontrolled diabetic patients group than that of the nondiabetic or controlled diabetic groups (P < .05). Expression of basal β-catenin protein in the uncontrolled diabetic group was decreased compared with nondiabetic or controlled diabetic groups (P < .05). There were significant decreases in the β-catenin protein expression between pre- and post-cardiopulmonary bypass in all 3 groups (P < .05 each), and this decrease was greater in the uncontrolled diabetic patients group than the nondiabetic group (P < .05). There were decreases in the relaxation response of skeletal muscle arterioles to substance P after cardiopulmonary bypass in all 3 groups (P < .05), and this alteration was more pronounced in the uncontrolled diabetic patients (P < .05).
conclusionUncontrolled diabetes causes inactivation and reduction in the expression of endothelial adherens junction proteins in the arterioles of skeletal muscle early after cardiopulmonary bypass. The enhanced phosphorylation of vascular endothelial-cadherin and degradation of β-catenin indicate deterioration of these proteins and damage of the cell-cell endothelial junctions, specifically in the diabetic peripheral vessels. These alterations may contribute to the increases in peripheral vascular permeability and endothelial dysfunction.
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