Adiponectin/T-cadherin and apelin/APJ expression in human arteries and periadventitial fat: implication of local adipokine signaling in atherosclerosis?

Kostopoulos, C.; Spiroglou, S.; Varakis, John; Apostolakis, Efstratios; Papadaki, Helen

doi:10.1016/j.carpath.2014.02.003

Cited by 44 publications

(30 citation statements)

References 59 publications

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“…T-cadherin, a membrane-associated adiponectin-binding protein lacking intracellular domain [134,135] seems to be a main mediator of the antiatherogenic adiponectin actions, and maybe a component of insulin granules [136]. Both adiponectin and T-cadherin were found to be inversely associated with human aortic and coronary atherosclerosis [59], and it appears that a majority of the whole body adiponectin is conveyed to cardiovascular tissues by T-cadherin [134,137,138]. T-cadherin seems to be a clue novel signaling pathway at the crossroads of vascular and metabolic disorders [139,140].…”

Section: Discussionmentioning

confidence: 99%

“…These effects seem responsible for the lowering of glucose levels in vivo, via glucose utilization and fatty-acid oxidation by activating AMP-activated protein kinase [58]. T-cadherin, a membrane-associated adiponectin-binding protein localized in vascular smooth muscle cells and endothelial cells, seems to be the mediator of adiponectin activity [59]. …”

Section: Introductionmentioning

confidence: 99%

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Adiponectin: a manifold therapeutic target for metabolic syndrome, diabetes, and coronary disease?

Fisman

Tenenbaum

2014

Cardiovasc Diabetol

206

157

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Adiponectin is the most abundant peptide secreted by adipocytes, being a key component in the interrelationship between adiposity, insulin resistance and inflammation. Central obesity accompanied by insulin resistance is a key factor in the development of metabolic syndrome (MS) and future macrovascular complications. Moreover, the remarkable correlation between coronary artery disease (CAD) and alterations in glucose metabolism has raised the likelihood that atherosclerosis and type 2 diabetes mellitus (T2DM) may share a common biological background. We summarize here the current knowledge about the influence of adiponectin on insulin sensitivity and endothelial function, discussing its forthcoming prospects and potential role as a therapeutic target for MS, T2DM, and cardiovascular disease. Adiponectin is present in the circulation as a dimer, trimer or protein complex of high molecular weight hexamers, >400 kDa. AdipoR1 and AdipoR2 are its major receptors in vivo mediating the metabolic actions. Adiponectin stimulates phosphorylation and AMP (adenosin mono phosphate) kinase activation, exerting direct effects on vascular endothelium, diminishing the inflammatory response to mechanical injury and enhancing endothelium protection in cases of apolipoprotein E deficiency. Hypoadiponectinemia is consistently associated with obesity, MS, atherosclerosis, CAD, T2DM. Lifestyle correction helps to favorably modify plasma adiponectin levels. Low adiponectinemia in obese patients is raised via continued weight loss programs in both diabetic and nondiabetic individuals and is also accompanied by reductions in pro-inflammatory factors. Diet modifications, like intake of fish, omega-3 supplementation, adherence to a Mediterranean dietary pattern and coffee consumption also increase adiponectin levels. Antidiabetic and cardiovascular pharmacological agents, like glitazones, glimepiride, angiotensin converting enzyme inhibitors and angiotensin receptor blockers are also able to improve adiponectin concentration. Fibric acid derivatives, like bezafibrate and fenofibrate, have been reported to enhance adiponectin levels as well. T-cadherin, a membrane-associated adiponectin-binding protein lacking intracellular domain seems to be a main mediator of the antiatherogenic adiponectin actions. The finding of novel pharmacologic agents proficient to improve adiponectin plasma levels should be target of exhaustive research. Interesting future approaches could be the development of adiponectin-targeted drugs chemically designed to induce the activaton of its receptors and/or postreceptor signaling pathways, or the development of specific adiponectin agonists.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Adiponectin: a manifold therapeutic target for metabolic syndrome, diabetes, and coronary disease?

Fisman

Tenenbaum

2014

Cardiovasc Diabetol

206

157

View full text Add to dashboard Cite

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“…In addition, chemerin and CMKLR1 genes are both expressed by cells of the walls of the aortic and coronary arteries, and the levels of both proteins are positively correlated with the severity of atherosclerosis [32]. Our purpose was to clarify if chemerin could also affect cardiac cells viability, since cardiomyocyte apoptosis plays a crucial role in the pathophysiological development of a wide diversity of heart diseases including ischemic heart disease, acute myocardial infarction and congestive heart failure [50][51][52].…”

Section: Cellular Physiology and Biochemistry Cellular Physiology Andmentioning

confidence: 99%

“…Moreover, chemerin and CMKLR1 genes are both expressed by cells of the cardiovascular system, in which their levels have been shown to be positively correlated with the severity of cardiac pathologies such as atherosclerosis [32].…”

Section: Cellular Physiology and Biochemistrymentioning

confidence: 99%

The Adipokine Chemerin Induces Apoptosis in Cardiomyocytes

Rodríguez-Penas¹,

Feijóo‐Bandín²,

García-Rúa³

et al. 2015

Cell Physiol Biochem

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Background: The adipokine chemerin has been associated with cardiovascular disease. We investigated the effects of chemerin on viability and intracellular signalling in murine cardiomyocytes, and the effects of insulin and TNF-α on cardiomyocyte chemerin production. Methods: Hoechst dye vital staining and cell cycle analysis were used to analyse the viability of murine cardiac cells in culture. Western blot was used to explore the phosphorylation of AKT and caspase-9 activity in neonatal rat cardiomyocytes and HL-1 cells. Finally, RT-qPCR, ELISA and western blot were performed to examine chemerin and CMKLR1 expression after insulin and TNF-α treatment in cardiac cells. Results: Chemerin treatment increased apoptosis, reduced phosphorylation of AKT at Thr308 and increased caspase-9 activity in murine cardiomyocytes. Insulin treatment lowered chemerin and CMKLR1 mRNA and protein levels, and the amount of chemerin in the cell media, while TNF-α treatment increased chemerin mRNA and protein levels but decreased expression of the CMKLR1 gene. Conclusion: Chemerin induces apoptosis, reduces AKT phosphorylation and increases the cleavage of caspase-9 in murine cardiomyocytes. The expression of chemerin is regulated by important metabolic (insulin) and inflammatory (TNF-α) mediators at cardiac level. Our results suggest that chemerin could play a role in the physiopathology of cardiac diseases.

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“…In vivo, the overexpression of T-cadherin has the potential of producing pathological changes, such as atherosclerosis and restenosis. [14,15] Kyriakakis et al, investigated the interaction between T-cadherin and epidermal growth factor receptor (EGFR) in A431 squamous cell carcinoma. They found that EGFR activation may be impacted by T-cadherin and that epidermal growth factor induced redistribution of T-cadherin from cell-cell contact results in the activation of EGFR.…”

Section: T-cadherinmentioning

confidence: 99%

The significance of cadherin for cell–cell interactions and cell adhesions on biomaterials

Shen

et al. 2015

Journal of Adhesion Science and Technology

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Cadherins are surface glycoproteins on plasma membranes and exist in many forms: T-cadherin, neuronal cadherin (N-cadherin), epithelial cadherin (E-cadherin), and vascular endothelial (VE-cadherin). Cadherins play critical roles in cell-cell interactions and are involved in multiple functions related to cell growth and proliferation. Findings from numerous reports have indicated that VE-cadherin regulates the remodeling, gating, and maturation of vascular vessels. The surface morphology of materials also impacts endothelial cell adhesion. This report is an overview of recent research on the effects of cadherins on cell-cell interactions, along with cell adhesions as examined on different materials. This summary will provide novel insights and approaches for research on cell-cell and cell-material interactions and illuminate some of the mechanisms of cell growth on different materials.

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Adiponectin/T-cadherin and apelin/APJ expression in human arteries and periadventitial fat: implication of local adipokine signaling in atherosclerosis?

Cited by 44 publications

References 59 publications

Adiponectin: a manifold therapeutic target for metabolic syndrome, diabetes, and coronary disease?

Adiponectin: a manifold therapeutic target for metabolic syndrome, diabetes, and coronary disease?

The Adipokine Chemerin Induces Apoptosis in Cardiomyocytes

The significance of cadherin for cell–cell interactions and cell adhesions on biomaterials

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