Neovascular capacity of endothelial progenitor cells in the adult pulmonary circulation.
Neovascular capacity of endothelial progenitor cells in the adult pulmonary circulation.
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成人肺循环中内皮祖细胞的新血管能力。
DOI：
10.1152/ajplung.00103.2009
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发表时间：
2009
期刊：
影响因子：
--
通讯作者：
Alvarez,DiegoF
中科院分区：
文献类型：
--
作者：
Majka,Susan;Alvarez,DiegoF
PULMONARY POSTNATAL NEOVASCULARIZATION or formation of de novo vessels in the adult lung has been controversial. Most of the argument has been focused on findings in the systemic circulation, which exhibits diverse degrees of angiogenesis (vessel formation from preexisting vessels) and arteriogenesis (collateral development proximal to a site of arterial occlusion). With the advent of stem cell plasticity, neovascularization was demonstrated to occur postnatally in skeletal and cardiac muscle, peripheral vasculature, adipose tissue, and the endometrium and during pathological conditions such as expansion of solid tumors. Furthermore, remodeling of the tunica intima and media is observed in the systemic circulation during atherosclerosis. Interestingly, parallel angiogenic responses are not frequently observed in the pulmonary circulation leading early investigators to theorize that the pulmonary circulation was quiescent, lacking the capacity to generate de novo vessels or undergo vascular remodeling. Moreover, during focal tissue hypoxia in the setting of idiopathic pulmonary arterial hypertension (IPAH), PAH secondary to fibrosis, or chronic obstructive pulmonary disease (COPD), the native pulmonary vasculature experiences a series of perturbations, which results in the loss, instead of the formation, of vessels. In 1847, Virchow (17) observed that under regional ischemia in the human lung, the systemic circulation restored circulation to nonperfused areas. From early studies, it was clear that the ischemic lung depends on the adjacent systemic circulation to provide necessary collateral circulation. More recently, neoangiogenesis by systemic vessels in the pulmonary artery vaso vasorum has been shown to occur in response to a variety of physiological and pathological stimuli (6). Despite the compelling support indicating that neovascularization of the pulmonary circulation occurs by extension of the systemic circulation, there are many studies supporting mechanisms that do not involve contribution of the systemic vasculature. Patients with scleroderma-induced vasculitis (4), pulmonary venoocclusive disease (15), idiopathic interstitial pneumonia (14), and acute respiratory distress syndrome (ARDS) survivors are important examples of lung neoangiogenesis that occur independent of the contribution from the systemic circulation. Moreover, experimental models of pneumonectomy in rats (9), caloric restriction in mice (13), intermittent levels of chronic hypoxia in rats (8), and lung tumorigenesis in dogs (11) further support that pulmonary neoangiogenesis arises in a systemic vasculature-independent manner. Although it is clear that neoangiogenesis and vascular remodeling develops within the pulmonary circulation, the origin of the cellular constituents that facilitate or contribute to this process is inconclusive. Recent evidence implicates several progenitors with the potential to engineer a proangiogenic environment or induce de novo vessel formation, including resident lung vascular cells (1, 10, 21), circulating bone marrow-derived cells such as endothelial progenitors (cEPCs; Ref. 16), and mesenchymal progenitors (fibrocytes; Ref. 7). Consistent with the concept that vascular progenitor cells arise from the bone marrow, pioneering work by Asahara et al.(2) resolved that isolated cells from the mononuclear fraction of the peripheral blood regulated neoangiogenesis in an ischemic experimental model. The cells identified by Asahara et al.(2) have been further characterized by their expression of the membrane proteins CD34, VEGFR2 (Flk-1), and CD133. In the lung, vascular progenitor cells are hypothesized to be recruited from the bone …
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芳香氨基酸和维生素生物合成的调控
DOI：
--
发表时间：
1970
期刊：
影响因子：
--
作者：
J. Pittard;F. Gibson
通讯作者：
F. Gibson
DOI：
--
发表时间：
1978
期刊：
影响因子：
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作者：
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通讯作者：
J. Forest
影响因子：
3.9
作者：
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通讯作者：
JENSEN, RA
影响因子：
3.9
作者：
B. Singh;J. A. Connelly;E. Conn
通讯作者：
B. Singh;J. A. Connelly;E. Conn
预苯酸酯、芳酸酯和螺芳酸酯的差别酸催化芳构化
影响因子：
1.8
作者：
L. Zamir;R. Tiberio;R. Jensen
通讯作者：
R. Jensen