Endocrine Abstracts

Introduction: Periadventitial adipose tissue has been implicated in vascular physiology and pathology, including atherosclerosis, through paracrine and endocrine mechanisms, mainly adipokine production. We investigated the expression of adipokines chemerin and adiponectin and their receptors CMKLR1 and T-cadherin, respectively, in human aortic arterial wall and periaortic fat as well as their correlation with aortic atherosclerosis.

Methods: Paraffin embedded samples of human aortas (n=37) including periadventitial fat were evaluated for chemerin, adiponectin, CMKLR1 and T-cadherin expression using immunohistochemistry. AHA classification was used for atherosclerosis assessment. PASW Statistics was used for statistical analysis.

Results: Atherosclerosis was detected in 31/37 aortas. Chemerin was expressed in periaortic fat (34/37 samples), aortic vascular smooth muscle cells (VSMCs; 37/37 samples) and foam cells in aortic atherosclerotic lesions (25/31 samples). Adiponectin was expressed by periadventitial fat in 34/37 samples. CMKLR1 was expressed in aortic VSMCs (9/37 samples) and foam cells (28/31 samples). T-cadherin was detected in VSMCs (37/37 samples) and endothelia (32/37 samples). Periaortic fat chemerin expression was negatively correlated to adiponectin expression (r=−0.620, P<0.001). Foam cell chemerin expression and CMKLR1 expression were positively interrelated in aortic atherosclerotic lesions (r=0.456, P=0.01). Periadventitial fat adiponectin expression was positively correlated with endothelial T-cadherin expression (r=0.326, P=0.049). Aortic atherosclerosis was positively correlated with periaortic fat chemerin (r=0.813, P<0.001), aortic VSMC chemerin (r=0.654, P<0.001), aortic foam cell chemerin (r=0.639, P<0.001) and aortic foam cell CMKLR1 expression (r=0.399, P=0.026), while negatively correlated with periaortic fat adiponectin (r=−0.690, P<0.001), VSMC T-cadherin (r=−0.413, P=0.011) and endothelial T-cadherin (r=−0.396, P=0.015) expression.

Conclusions: Our data suggest a putative role for chemerin and its receptor in the atherosclerotic process, probably with opposite effects to adiponectin’s. T-cadherin may also serve as a receptor that mediates adiponectin’s actions regarding atherosclerosis deceleration.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This work was supported, however funding details unavailable.