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Omentina-1 e aterogenesi

L'omentina-1 è una nuova adipochina identificata per la prima volta nel grasso omentale. E' prodotta principalmente nel tessuto adiposo viscerale, ma se ne trovano tracce anche nel tessuto adiposo sottocutaneo, nel grasso epicardico e nelle cellule endoteliali. Studi sperimentali hanno dimostrato che è in grado di indurre vasodilatazione per incremento della ossido nitrico sintetasi e di stimolare la rivascolarizzazione indotta da ischemia, di inibire il tumor necrosis factor alfa, varie molecole di adesione cellulare e la produzione di superossido. Ha dunque le carte in regola per ipotizzare un suo ruolo soppressivo in alcune fasi del processo aterogenetico. Watanabe e Coll, l'hanno studiata nei monociti-macrofagi e nelle cellule muscolari lisce dell'aorta di pazienti con e senza cardiopatia ischemica. In sintesi, i risultati delle loro ricerche dimostrano che l'omentina-1 promuove la differenziazione dei macrofagi nel fenotipo antinfiammatorio M2, sopprime la risposta infiammatoria, la formazione di cellule schiumose indotta da LDL ossidate, la migrazione, la proliferazione e la produzione di collagene delle cellule muscolari lisce.

Counteractive effects of omentin-1 against atherogenesis

Watanabe K, Watanabe R, Konii H, Shirai R, Sato K, Matsuyama TA, Ishibashi-Ueda H, Koba S, Kobayashi Y, Hirano T, Watanabe T

Cardiovasc Res 2016;110:118-128

AIMS: Omentin-1, a novel adipocytokine expressed in visceral fat tissue, is negatively correlated with obesity, insulin resistance, and stable coronary artery disease (CAD). However, there have been no previous reports regarding the effects of omentin-1 on atherogenesis.
METHODS AND RESULTS: This study was performed to evaluate the atheroprotective effects of omentin-1 on human monocyte-derived macrophages, human aortic smooth muscle cells (HASMCs) in vitro, and aortic lesions in Apoe(-/-) mice in vivo. The histological expression of omentin-1 in coronary artery lesions and epicardial adipose tissues and its plasma levels were compared between CAD and non-CAD patients. Omentin-1 was abundantly expressed in human umbilical vein endothelial cells, macrophages, HASMCs, and human coronary artery SMCs in vitro. Omentin-1 promoted anti-inflammatory M2 phenotype during differentiation of human monocytes into macrophages. Omentin-1 suppressed oxidized low-density lipoprotein-induced foam cell formation associated with down-regulation of CD36, scavenger receptor class A, and acyl-CoA:cholesterol acyltransferase-1 and up-regulation of neutral cholesterol ester hydrolase in human macrophages. Omentin-1 suppressed angiotensin II-induced migration and platelet-derived growth factor-BB-induced proliferation, and collagen-1 and -3 expression in HASMCs. Four-week infusion of omentin-1 into Apoe(-/-) mice retarded the development of aortic atherosclerotic lesions with reduced contents of monocytes/macrophages, SMCs, and collagen fibres along with peritoneal M2-activated macrophages with inflammasome down-regulation and lowered plasma total cholesterol levels. Omentin-1 levels were markedly reduced in coronary endothelium and epicardial fat but increased in plasma and atheromatous plaques (macrophages/SMCs) in CAD patients compared with non-CAD patients.
CONCLUSION: This study provided the first evidence that omentin-1 may serve as a novel therapeutic target for atherosclerosis and CAD.

Cardiovasc Res 2016;110:118-128