Effects of angiogenic growth factors on endothelium-derived prostacyclin production by ovine uterine and placental arteries

Krishnamurthy, Parul; Bird, Ian M.; Sheppard, C; Magness, Ronald R.

doi:10.1016/s0090-6980(98)00066-5

Cited by 20 publications

(8 citation statements)

References 39 publications

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“…The HGF expression is upregulated by prostacyclin agonists 64) . VEGF and bFGF increase endothelium-derived PGI2 production 65) . Bone marrow-derived EPCs circulate in the body and support neoangiogenesis via the production of neoangiogenic factors 66) .…”

Section: Effects Of Pgi2 and Pgi3 On Neoangiogenesismentioning

confidence: 99%

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Eicosapentaenoic Acid (EPA) Reduces Cardiovascular Events: Relationship with the EPA/Arachidonic Acid Ratio

Ohnishi

Saitō

2013

JAT

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The clinical efficacy of fish oil and high-purity eicosapentaenoic acid ethyl ester (hp-EPA-E) for treating cardiovascular disease (CVD) has been reported. Fish oil contains saturated and monounsaturated fatty acids that have pharmacological effects opposite to those of ω3 fatty acids (ω3). Moreover, ω3, such as EPA and docosahexaenoic acid (DHA), do not necessarily have the same metabolic and biological actions. This has obscured the clinical efficacy of ω3. Recently, the Japan EPA Lipid Intervention Study (JELIS) of hp-EPA-E established the clinical efficacy of EPA for CVD, and higher levels of blood EPA, not DHA, were found to be associated with a lower incidence of major coronary events. A significant reduction in the risk of coronary events was observed when the ratio of EPA to arachidonic acid (AA) (EPA/AA) was ＞0.75. Furthermore, the ratio of prostaglandin (

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Section: Effects Of Pgi2 and Pgi3 On Neoangiogenesismentioning

confidence: 99%

“…65 . When 14 C-EPA is incubated with platelets, 14 C-EPA is incorporated at 67.0%, 13.1%, 13.9% and 2.9% into PC, PE, PI and PS, respectively.…”

Section: Subclasses Of Platelet Phospholipidsmentioning

confidence: 99%

Eicosapentaenoic Acid (EPA) Reduces Cardiovascular Events: Relationship with the EPA/Arachidonic Acid Ratio

Ohnishi

Saitō

2013

JAT

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“…Eicosanoid production as well as prostanoids and PGI 2 could also play a role in regulating placental vascular tone and maintaining placental blood flow and nutrient transfer to the fetus. In addition, PGI 2 production by the uterine artery increases 2-to 3-fold in pregnant compared with nonpregnant ewes, probably because of up-regulation of COX1 and PGIS in response to shear stress forces and hormone-dependent mechanisms (Krishnamurthy et al, 1999;Magness et al, 2000). Normotensive pregnant women are refractory to infused vasoactive agents such as angiotensin II, partly as a result of increased synthesis of the vasodilators PGI 2 and PGE 2 (Keith et al, 1993;Krishnamurthy et al, 1999;Magness et al, 2000).…”

Section: Prostacyclin Metabolism In Pregnancyassociated Vascular mentioning

confidence: 99%

Molecular Mechanisms Regulating the Vascular Prostacyclin Pathways and Their Adaptation during Pregnancy and in the Newborn

2012

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“…Consistent with the conclusion that PGE 2 mediates VEGF and bFGF up-regulation of CXCR4, VEGF-and bFGF-induced tubular formation in SDF-1␣ containing Matrigel was blocked with aspirin (10 M) by about 50%, and piroxicam (0.2 M) or NS-398 (0.1 M) by about 70% ( Figure 5I). Thus, not only do VEGF and bFGF generate PGE 2 , [12][13][14][15][16][17] resulting in the subsequent up-regulation of CXCR4 expression on HMECs, but the effects of VEGF and bFGF on tubular formation are to a considerable extent mediated by induction of PGE 2 , in a mechanism that is dependent on CXCR4.…”

Section: Blocking Cxcr4 Inhibits Pge 2 -Induced Tubular Formation By mentioning

confidence: 99%

“…11 In addition to inducing CXCR4, there is copious evidence in the literature that VEGF and bFGF are inducers of cyclooxygenase (COX) with subsequent induction of prostaglandin synthesis in endothelial cells. [12][13][14][15][16][17] Prostaglandin E 2 (PGE 2 ) is the major COX product of human microvascular endothelial cells (HMECs). [18][19][20][21] Prostaglandins participate in angiogenesis [22][23][24][25][26][27][28][29][30] by several mechanisms, such as promoting endothelial cell tubular formation.…”

Section: Introductionmentioning

confidence: 99%

Angiogenic effects of prostaglandin E2 are mediated by up-regulation of CXCR4 on human microvascular endothelial cells

Salcedo

Zhang

Young

et al. 2003

Blood

165

114

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Stimulation of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) increases the expression of CXCR4 on endothelial cells, rendering these cells more responsive to stromalderived factor 1 (SDF-1), an angiogenic CXC chemokine and unique ligand for CXCR4. Here, we show that prostaglandin E 2 (PGE 2 ) mediates the effects of bFGF and VEGF in up-regulating CXCR4 expression on human microvascular endothelial cells (HMECs). Forskolin or 3-isobutyl-1-methyl xanthine (IBMX), 2 inducers of adenylate cyclase, markedly enhanced, whereas cyclooxygenase (COX) inhibitors including aspirin, piroxicam, and NS398 markedly inhibited CXCR4 expression on HMECs. Furthermore, the ability of PGE 2 to augment in vitro tubular formation in SDF-1␣ containing matrigel was inhibited completely by blocking CXCR4. Treatment of bFGF-or VEGF-stimulated HMECs with COX inhibitors blocked tubular formation by about 50% to 70%. Prostaglandin-induced human endothelial cell organization and subsequent vascularization can be inhibited to a greater extent by a neutralizing antibody to human CXCR4 in severe combined immunodeficient mice. Additionally, VEGF-and bFGFinduced angiogenesis in vivo was also inhibited by about 50% by NS-398 or piroxicam, and this inhibitory effect was accompanied by decreased expression of CXCR4 on murine endothelial cells. IntroductionChemokines induce angiogenesis directly by binding their cognate receptors on endothelial cells or indirectly by promoting inflammatory cell infiltrates, which deliver other angiogenic stimuli. A number of proinflammatory chemokines including interleukin 8 (IL-8), growth-regulated oncogene ␣ (GRO-␣), stromal cell-derived factor 1 (SDF-1), monocyte chemotactic protein 1 (MCP-1), eotaxin 1, and I-309 have been shown to act as direct inducers of angiogenesis. [1][2][3] SDF-1 acts as a chemoattractant for leukocytes, 4 hematopoietic progenitor cells, 5 and endothelial cells. 6-8 SDF-1-deficient mice are grossly normal but die shortly after birth, lack B-cell lymphopoiesis during embryonic development, have defective bone marrow myelopoiesis, have a ventricular septal defect, 9 and have impaired vascularization of the gastrointestinal tract. 10 We previously reported that angiogenic factors, namely, basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF), can enhance the expression of CXCR4, but not other chemokine receptors on endothelial cells rendering endothelial cells more responsive to SDF-1. Conversely, SDF-1 enhances the production of VEGF and bFGF in a positive feedback loop, therefore, linking classical angiogenic factors to chemokine-induced angiogenesis. 11 In addition to inducing CXCR4, there is copious evidence in the literature that VEGF and bFGF are inducers of cyclooxygenase (COX) with subsequent induction of prostaglandin synthesis in endothelial cells. 12-17 Prostaglandin E 2 (PGE 2 ) is the major COX product of human microvascular endothelial cells (HMECs). [18][19][20][21] Prostaglandins participate in angiogenesis [22...

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Effects of angiogenic growth factors on endothelium-derived prostacyclin production by ovine uterine and placental arteries

Cited by 20 publications

References 39 publications

Eicosapentaenoic Acid (EPA) Reduces Cardiovascular Events: Relationship with the EPA/Arachidonic Acid Ratio

Eicosapentaenoic Acid (EPA) Reduces Cardiovascular Events: Relationship with the EPA/Arachidonic Acid Ratio

Molecular Mechanisms Regulating the Vascular Prostacyclin Pathways and Their Adaptation during Pregnancy and in the Newborn

Angiogenic effects of prostaglandin E2 are mediated by up-regulation of CXCR4 on human microvascular endothelial cells

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