VEGF enhancement of osteoclast survival and bone resorption involves VEGF receptor-2 signaling and β3-integrin

Yang, Qian; McHugh, Kevin P.; Patntirapong, Somying; Gu, Xuesong; Wunderlich, Lívius; Hauschka, Peter V.

doi:10.1016/j.matbio.2008.06.005

Cited by 125 publications

(88 citation statements)

References 57 publications

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“…64 Among the growth factors upregulated in AAA, vascular endothelial growth factor (VEGF) has been reported to enhance the survival, differentiation, maturation, and resorptive activity of osteoclasts. 65 Several experimental models of aneurysm have been utilized, including chemically induced aneurysms induced by intraluminal infusion of elastase and the periaortic application of calcium chloride (CaCl2). Aneurysmal changes in the carotid artery of hyperlipidemic rabbits resulting from periaortic application of CaCl2 was first described by Gertz et al 66 This method was further expanded and applied to the abdominal aortas of hyperlipidemic rabbits in combination with thioglycollate, as reported by Freestone et al 67 and subsequently adapted to mice.…”

Section: Aaa and Osteoclastogenesismentioning

confidence: 99%

Balanced Mineralization in the Arterial System

Yamanouchi

Takei

Komori

2012

Circ J

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Arterial calcification is the result of the same highly organized processes as seen in bone, which rely on a delicate balance between osteoblasts and osteoclasts. Although previously understood as passive precipitation, evidence has accumulated to suggest that arterial calcification is the result of organized, regulated processes bearing many similarities to osteogenesis in bone, including the presence of subpopulations of arterial wall cells that retain osteoblastic lineage potential. These cells have the potential to form mineralized nodules and express osteoblast markers, including bone morphogenetic protein-2, osteocalcin, osteopontin, and alkaline phosphatase. By contrast, osteoclastlike cells mediate the catabolic process of mineral resorption. Recent data shows that cells positive for tartrate-resistant acid phosphatase, a major marker for osteoclasts, have been histologically identified in atherosclerotic lesions and are referred to as osteoclast-like cells. Evidence has accumulated to suggest that initial arterial calcification through passive precipitation of calcium phosphate initiates balanced mineralization regulated by osteoclast-like and osteoblast-like cells. Subsequently, various pathogenic conditions may trigger an imbalance between osteoblastogenesis and osteoclastogenesis, leading to either calcification in stenotic/occlusive disease or destruction of the extracellular matrix in aneurysmal disease. Further elucidation of these newly emerging concepts could lead to a novel therapeutic approach to arterial stenotic/occlusive disease and/or abdominal aortic aneurysm. (Circ J 2012; 76: 2732 - 2737)

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Section: Aaa and Osteoclastogenesismentioning

confidence: 99%

Balanced Mineralization in the Arterial System

Yamanouchi

Takei

Komori

2012

Circ J

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“…The actions of the hormone that are initiated at the integrin receptor are distinctive because of the distribution of integrin ␣v␤3. The integrin is concentrated largely in plasma membranes of endothelial cells, vascular smooth muscle cells, cancer cells, (7) and osteoclasts (67). The integrin is an attractive target of attempts to manipulate tumor cell proliferation, tumor-related neovascularization, and angiogenesis unrelated to cancer (7).…”

Section: Integrin ␣V␤3 the Thyroid Hormone Plasma Membrane Receptormentioning

confidence: 99%

“…Unrelated to cancer, angiogenesis may be pathological, e.g., in certain retinopathies, or it may be desirable in the context of ischemic tissues. Expression of a TR on ␣v␤3 of osteoclasts appears to underlie a model of thyroid hormone-induced bone mass loss in the mouse (3,67) or rat (23). The integrin is displayed to a lesser extent on other cells, e.g., muscle cells (59), and on platelets (26), and specific thyroid hormone analogs have been shown to induce human platelet aggregation in vitro (44).…”

Section: Integrin ␣V␤3 the Thyroid Hormone Plasma Membrane Receptormentioning

confidence: 99%

Translational implications of nongenomic actions of thyroid hormone initiated at its integrin receptor

Davis

Davis²,

Lin³

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

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receptor on integrin ␣v␤3 that mediates cell surface-initiated nongenomic actions of thyroid hormone on tumor cell proliferation and on angiogenesis has been described. Transduction of the hormone signal into these recently recognized proliferative effects is by extracellular-regulated kinases 1/2 (ERK1/2). Other nongenomic actions of the hormone may be transduced by phosphatidylinositol 3-kinase (PI3K) and are initiated in cytoplasm or at the cell surface. PI3K-mediated effects are important to angiogenesis or other recently appreciated cell functions but apparently not to tumor cell division. For those actions of thyroid hormone [L-thyroxine (T4) and 3,3Ј-5-triiodo-L-thyronine (T3)] that begin at the integrin receptor, tetraiodothyroacetic acid (tetrac) is an inhibitor of and probe for the participation of the receptor in downstream intracellular events. In addition, tetrac has actions initiated at the integrin receptor that are unrelated to inhibition of the effects of T 4 and T3 but do involve gene transcription in tumor cells. Discussed here are the implications of translating these nongenomic mechanisms of thyroid hormone analogs into clinical cancer cell biology, tumor-related angiogenesis, and modulation of angiogenesis that is not related to cancer.

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“…The effects of VEGF are mediated by two signaling receptors that belong to the Class III tyrosine kinase receptor family [4,27], namely VEGFR-1 (flt-1, fms-like tyrosine kinase-1) and VEGFR-2 (kinase domain region/ flk-1, fetal liver kinase-1). For signal transduction of VEGF in bone, VEGFR-2 is more important [33]. Interestingly, the angiogenic potency of VEGF is splice variant specific [24].…”

Section: Introductionmentioning

confidence: 99%