Induction of vascular endothelial growth factor expression by prostaglandin E2 and E1 in osteoblasts.

Harada, Satoru; Nagy, Janice A.; Sullivan, Kathleen; Thomas, Kenneth A.; Endo, Naoto; Rodan, Gideon A.; Rodan, Sevgi B.

doi:10.1172/jci117258

Cited by 361 publications

(212 citation statements)

References 49 publications

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“…Determination of ALP activity was performed as described previously, 12 and the activity was expressed as nanomoles of p-nitrophenol formed per minute per milligram of protein. Hyp contents were evaluated by Woessner's method 13 and were expressed as mg/10 5 cells. von Kossa's staining was processed to monitor the mineralized nodules by using 5% silver nitrate, as described previously.…”

Section: Methodsmentioning

confidence: 99%

“…7 Prostaglandins (PGs) are produced both in skeletal tissue and bone cell culture in response to various stimulus, and are among the most important local factors with autocrine/ paracrine roles in bone. 13 Among the various PGs produced in bone tissue, the most abundant one is prostaglandin E2 (PGE2), and it appears to be of utmost importance in bone physiology. Although PGE2 is initially described as a potent bone-resorbing substance, 14,15 accumulated evidence indicates that PGE2 is a potent stimulator of bone formation in vivo and in vitro.…”

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confidence: 99%

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Activation of PKA and phosphorylation of sodium-dependent vitamin C transporter 2 by prostaglandin E2 promote osteoblast-like differentiation in MC3T3-E1 cells

Taniguchi

et al. 2007

Cell Death Differ

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Sodium-dependent vitamin C transporter (SVCT) 2-mediated L-ascorbic acid (AA) uptake is required in osteoblast-like differentiation of MC3T3-E1 cells, and prostaglandin E2 (PGE2) is among the most important local factors in bone formation, but the detailed mechanism by which PGE2 induces osteoblast differentiation remains obscure. We revealed that PGE2 induced AA uptake and osteoblast-like differential markers including alkaline phosphatase, collagen, osteocalcin expression, and mineralization in MC3T3-E1 cells. Inhibition of AA uptake by SVCT2 short isoform functioning as a dominant-negative mutant not only robustly attenuated PGE2-induced markers expression and mineralization, but also decreased their basal levels. However, upregulation of AA uptake resulted from PGE2-induced plasma membrane translocation of cytoplasm SVCT2, and this effect was abolished by pretreatment with EP4 receptor antagonist, AH-23848B or cAMP-dependent protein kinase A (PKA) inhibitor, H-89. Moreover, we showed SVCT2 physically interacted with PKA in immunoprecipitates, and PKA phosphorylated SVCT2 in vitro and in intact cells at Ser402 and Ser639 sites; however, mutation of Ser402 or/and Ser639 in SVCT2 severely diminished SVCT2 translocation in response to PGE2. Together, these results suggest that PGE2-induced SVCT2 plasma membrane translocation through EP4 receptor and subsequent phosphorylation of SVCT2 at Ser402 and Ser639 sites by PKA results in an increase of AA uptake and consequent promotion of osteoblast-like differentiation in MC3T3-E1 cells.

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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

Activation of PKA and phosphorylation of sodium-dependent vitamin C transporter 2 by prostaglandin E2 promote osteoblast-like differentiation in MC3T3-E1 cells

Taniguchi

et al. 2007

Cell Death Differ

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“…The host microenvironment is thought to influence tumor progression (Fukumura et al, 1997;Gohongi et al, 1999). Immunohistochemical examination of human colorectal cancer tissue has revealed that the marked COX-2 expression was detectable not only in tumor cells but also in inflammatory cells and fibroblasts in the stroma (Harada et al, 1994). It was also reported that COX-2 is abundant in the stromal cells that surround intestinal polyps in mice with a mutated APC gene (Ohshima et al, 1996).…”

Section: Cox-2/vegf and Tumor Angiogenesismentioning

confidence: 99%

COX-2/VEGF-Dependent Facilitation of Tumor-Associated Angiogenesis and Tumor Growth in vivo

Yoshida

Aoki

Hayashi

et al. 2003

Laboratory Investigation

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SUMMARY:Nonsteroidal anti-inflammatory drugs are known to suppress the occurrence and progression of malignancies such as colorectal cancers. However, the precise mechanism of these actions remains unknown. We have evaluated the role of an inducible cyclo-oxygenase (COX-2) in tumor-associated angiogenesis and tumor growth, and identified the downstream molecules involved using a ddy mouse model of sponge angiogenesis, which mimics tumor angiogenesis and is COX-2 and vascular endothelial growth factor (VEGF) dependent. In this model, VEGF expression was down-regulated by selective COX-2 inhibition with NS-398. To find out the involvement of COX-2/VEGF pathway in tumor-associated angiogenesis, we estimated angiogenesis occurring around implanted Millipore chambers containing sarcoma-180 (S-180) cells or Lewis lung carcinoma cells. Daily oral administration of NS-398 or of aspirin, a nonselective COX inhibitor, suppressed angiogenesis seen around the Millipore chambers. S-180 cells implanted in ddy mice formed substantial tumors with extensive angiogenesis markedly suppressed by aspirin and COX-2 inhibitors NS-398 and JTE522, but not by mofezolac, an inhibitor of constitutive COX-1. Tumor-associated angiogenesis was also significantly suppressed by a neutralizing antibody against VEGF. S-180 tumor growth in the subcutaneous tissues was also suppressed by aspirin, COX-2 selective inhibitors, and the VEGF antibody, but not by the COX-1 inhibitor. These results demonstrate that the inhibition of the COX-2/VEGF-dependent pathway was effective in tumor-associated angiogenesis, tumor growth, and tumor metastasis. (Lab Invest 2003, 83:1385-1394.

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“…Previous studies have identified that the growth factors platelet-derived growth factor, transforming growth factor-␤1, and bFGF can each stimulate the production of VEGF (38,39). Cytokines, such as interleukin-1, can induce VEGF transcripts in VSMC (40); nitric oxide can stimulate VEGF mRNA in the lung (41); and E-series prostaglandins can stimulate VEGF production in osteoblasts (42). Hypoxia is one of the best characterized stimuli for the induction of VEGF production by a variety of tumor cells, as well as VSMC, both in vitro and in vivo (12,13,39).…”

Section: Table IImentioning

confidence: 99%

Vasoactive Peptides Modulate Vascular Endothelial Cell Growth Factor Production and Endothelial Cell Proliferation and Invasion

Pedram¹,

Razandi²,

Hu³

et al. 1997

Journal of Biological Chemistry

176

117

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Induction of vascular endothelial growth factor expression by prostaglandin E2 and E1 in osteoblasts.

Cited by 361 publications

References 49 publications

Activation of PKA and phosphorylation of sodium-dependent vitamin C transporter 2 by prostaglandin E2 promote osteoblast-like differentiation in MC3T3-E1 cells

Activation of PKA and phosphorylation of sodium-dependent vitamin C transporter 2 by prostaglandin E2 promote osteoblast-like differentiation in MC3T3-E1 cells

COX-2/VEGF-Dependent Facilitation of Tumor-Associated Angiogenesis and Tumor Growth in vivo

Vasoactive Peptides Modulate Vascular Endothelial Cell Growth Factor Production and Endothelial Cell Proliferation and Invasion

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