ADAM-9, ADAM-15, and ADAM-17 are upregulated in macrophages in advanced human atherosclerotic plaques in aorta and carotid and femoral arteries—Tampere vascular study

Abstract

Present findings provide strong evidence for the involvement of catalytically active ADAM-9, ADAM-15, and ADAM-17 in advanced atherosclerosis, most notably associated with cells of monocytic origin.

Association of Neuroimmune Guidance Cue Netrin-1 and Its Chemorepulsive Receptor UNC5B With Atherosclerotic Plaque Expression Signatures and Stability in Human(s)

“…Vascular sample series from Tampere Vascular Study (TVS), [17][18][19][20][21] including femoral arteries, carotid arteries, and abdominal aortas, were obtained during open vascular procedures from 2005 to 2009 from patients fulfilling the following inclusion criteria: (1) carotid endarterectomy because of asymptomatic or symptomatic and hemodynamically significant (>70%) carotid stenosis or (2) femoral or (3) aortic endarterectomy with aortoiliac or aortobifemoral bypass because of symptomatic peripheral arterial disease. The left internal thoracic artery (LITA) samples serving as controls were obtained during coronary artery bypass surgery because of symptomatic coronary artery disease (CAD).…”

Expression of a Disintegrin and Metalloprotease in Human Abdominal Aortic Aneurysms

“…The effect of ADAMs on the pathology of AAA is as yet unknown, although some researchers have proposed the role of ADAMs 9, 15 or 17 in atherosclerosis [25,26,27,28]. No recent studies have been performed in human AAAs with the exception of ADAM-17 [9,24]. …”

“…There is a plethora of proteolytic enzymes belonging to the family of metalloproteinases such as ADAMs with multiple biological roles including cell-matrix interaction, zymogen activation (shedding) and cell adhesion. These processes contribute to cell migration, proteolysis and angiogenesis [24]. The effect of ADAMs on the pathology of AAA is as yet unknown, although some researchers have proposed the role of ADAMs 9, 15 or 17 in atherosclerosis [25,26,27,28].…”

Preventive Effects of Heregulin-β 1 on Macrophage Foam Cell Formation and Atherosclerosis

“…We speculate that the expression of heregulin-␤ 1 in macrophages within extremely advanced atherosclerotic plaques may be reduced by its secretion because of upregulation of ADAM-17 (a disintegrin and metalloproteinase 17), which is required for cleavage of heregulin-␤ 1 . 29 Moreover, heregulin-␤ 1 may be exhausted by the activation of coagulation system during thrombus formation after rupture. Further analyses are required to clarify the relationship between decreased levels of heregulin-␤ 1 expression and coronary plaque destabilization and rupture ( Figure 8C through 8E).…”