The hemosteoblast: friend or foe?
The hemosteoblast: friend or foe?
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造血成骨细胞:朋友还是敌人?
DOI:
10.1161/circresaha.111.244665
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发表时间:
2011
影响因子:
20.1
通讯作者:
Demer,Linda
中科院分区:
文献类型:
--
作者:
Tintut,Yin;Demer,Linda
Ectopic calcification arises in soft tissues in a variety of diseases. When it occurs in cardiovascular tissues, such as the aorta, cardiac valve leaflets, and coronary and renal arteries, it produces debilitating and sometimes fatal conditions, including coronary insufficiency, heart failure, calcific aortic stenosis, systolic hypertension, and left ventricular hypertrophy. Although calcific vasculopathy was long considered a passive process of aging, studies from the last 2 decades have revealed an active mechanism in which transcription factors drive osteochondrogenic differentiation of vascular cells.In the right context, a number of extraskeletal cells display osteochondrogenic potential, including (1) microvascular pericytes, 1 (2) adventitial myofibroblasts, 2 (3) calcifying vascular cells, 4 now known to be multipotent vascular stem cells, 5 (4) medial smooth muscle cells, 3 (5) valvular interstitial cells, 5b and (6) mesoangioblasts. 6 Because these cells are all of purely mesenchymal origin, mineralization has been considered, until recently, solely a mesenchymal attribute. Now, in this issue of Circulation Research, Fadini and colleagues7 report mineralization potential in cells of hematopoietic origin: circulating myeloid cells that produce calcium mineral when cultured in Matrigel, a solubilized basement membrane matrix derived from mouse sarcoma cells. These circulating cells also express monocyte/macrophage lineage markers (CD45, CD14, and CD68), as well as the osteoblastic markers alkaline phosphatase (BAP, also known as tissue-nonspecific alkaline phosphatase), osteocalcin and the osteochondrogenic transcription factors Runx2 and osterix. These findings indicate that some adult cells of hematopoietic origin, perhaps “hemosteoblasts” have the capacity to take over the distinctly mesenchymal function of extracellular mineralization.
影响因子:
15.9
作者:
WATSON, KE;BOSTROM, K;DEMER, LL
通讯作者:
DEMER, LL