Multinucleated giant cells in atherosclerotic plaques of human carotid arteries: Identification of osteoclast-like cells and their specific proteins in artery wall

Human Alternative Macrophages Populate Calcified Areas of Atherosclerotic Lesions and Display Impaired RANKL-Induced Osteoclastic Bone Resorption Activity

“…5,18 Indeed, TRAP-positive multinucleated giant osteoclast-like cells have been detected in human atherosclerotic lesions. 19 Moreover, colocalization of CA2 staining with the macrophage marker CD68 has been reported in human atherosclerotic plaques. 20 In addition, cathepsin K expression and activity within the atherosclerotic lesions are mainly detected in macrophages.…”

Ferryl Hemoglobin Inhibits Osteoclastic Differentiation of Macrophages in Hemorrhaged Atherosclerotic Plaques

“…This hypothesis is further supported by the fact that Runx2, a key transcription factor that induces transition of VSMCs to osteoblast-like cells, directly binds to the promoter of RANKL and activates its expression leading to mineral deposition by VSMCs-derived osteoblasts and mineral resorption by OLCs [28]. Within the intramural compartment of the arteries, OLCs might degrade mineral deposits, thereby attenuating calcification and counterbalancing the activity of VSMC-derived osteoblasts [26]. The imbalance between bone formation by VSMC-derived osteoblasts and bone resorption by OLCs triggers pathological calcification process in the vessel walls.…”

“…In atherosclerotic plaques, calcification and bone formation are common phenomena characterized by the presence of vascular smooth muscle cells (VSMCs), osteoblasts, and osteoclast-like cells (OLCs) [25]. OLCs differentiate from infiltrating macrophages and colocalize with cholesterol deposition and mineralization [26]. An intriguing model has been raised by Doherty and coworkers suggesting that arterial calcium deposits represent a unique scenario which might favor the formation of OLCs from hematopoietic precursors possibly limiting calcification in atherosclerosis [27].…”

Biochemical Markers of Bone Tissue Metabolism Influence on Vulnerability of Atherosclerotic Lesions

“…V. 1 , Kashtanova E. V. Проблема сосудистого кальциноза в последнее время стала одной из приоритетных в кардиологии. Кальцификация коронарных артерий рассматрива-ется как маркер риска атеросклероза и его осложне-ний.…”

“…Сосудистая кальцификация -это сложный процесс, который во многом сопоставим с остеогене-зом и имеет те же регуляторные белки. Установлено, что компонентами сосудистого кальцификата явля-ются соли кальция, фосфаты, остеопонтин, остео-нектин, остеопротегерин, остеокальцин, коллаген 1 типа и другие соединения характерные для костной ткани [1,2]. В кальцифицированной атеросклероти-ческой бляшке идентифицированы остеобластопо-добные клетки, определено существование активной резорбции очагов эктопической сосудистой кальци-фикации.…”