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Chemerin is Present in the Adrenal Gland and Causes Release of Adrenal Catecholamines
Author(s) -
Moore Abigail Elizabeth,
Burnett Robert,
Zabel Brian A,
Watts Stephanie W
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1201.15
Subject(s) - chemerin , endocrinology , medicine , adrenal gland , adrenal medulla , sympathetic nervous system , catecholamine , adipokine , receptor , blood pressure , leptin , obesity
Chemerin (also known as tazarotene induced gene 2 or TIG2) is an adipokine typically known for its role in inflammation. Recent studies have shown that it may also play a part in the development of hypertension and obesity. Chemerin has exhibited several mechanisms by which it may influence blood pressure; we questioned whether there were other chemerin‐influenced avenues that may modify blood pressure. Since the sympathetic nervous system is unquestionably important to blood pressure regulation, we hypothesized that chemerin would be present in the adrenal glands and is active in the sympathetic nervous system. We further hypothesized that chemerin could cause a release of catecholamines through activation of its main receptor, Chemokine‐Like Receptor 1 or CMKLR1 (also known as ChemR23). Immunohistochemistry was used to assess the presence of chemerin and two of its receptors, CMKLR1 and GPR1 (G Protein‐Coupled Receptor 1), in the adrenals of male Sprague Dawley rats. The images were ranked on a scale from 1 (no staining) to 6 (very dark staining); the rankings were then averaged to find representative images for chemerin and its receptors. Chemerin and GPR1 were found in the cortex and medulla of the adrenal, while CMKLR1 was only found in the medulla. There was a moderate level of staining for chemerin (3±0.14, whole adrenal) ( Figure 1) and CMKLR1 (3±0.15, cortex only), as well as a high level of staining for GPR1 (5±0.17, whole adrenal). High‐performance liquid chromatography was used to measure norepinephrine and epinephrine released by the adrenal medulla when exposed to chemerin compared to vehicle release. Using only adrenal medulla, 100 nM chemerin‐9 (a shorter, more stable chemerin analog with known affinity for CMKLR1) caused a significant increase of norepinephrine (90% ± 24.2%, p<0.05) and epinephrine (69% ± 3.4%, p<0.05) over vehicle (n=24). However, the CMKLR1 antagonist, CCX832, was unable to reduce catecholamine levels significantly (p>0.05) in the presence of chemerin. These data suggest that chemerin is able to interact with the sympathetic nervous system, but that it may be through the action of GPR1 rather than CMKLR1. This work supports another mechanism by which chemerin could potentially modify blood pressure. 1