Effect of topical application of a stable prostacyclin analogue, SM-10902 on wound healing in diabetic mice

Yamamoto, Takumi; Horikawa, Naotsugu; Komuro, Yoshihiro; Hara, Youichi

doi:10.1016/0014-2999(96)00019-2

Cited by 27 publications

(22 citation statements)

References 25 publications

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“…It has been suggested that prostaglandins are involved in the regulation of both angiogenesis and VP. 25,26 Yamamoto et al 25 recently reported that a stable prostacyclin analogue, SM-10902, accelerated wound healing in a murine model of diabetic skin ulcers. Fujii et al 26 have demonstrated that lipopolysaccharide-induced VP is attenuated by either an NO synthase inhibitor or indomethacin.…”

Section: Discussionmentioning

confidence: 99%

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Vascular Endothelial Growth Factor/Vascular Permeability Factor Enhances Vascular Permeability Via Nitric Oxide and Prostacyclin

et al. 1998

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Background —Vascular endothelial growth factor (VEGF), an endothelial cell mitogen that promotes angiogenesis, was initially identified as a vascular permeability factor (VPF). Abundant evidence suggests that angiogenesis is preceded and/or accompanied by enhanced microvascular permeability. The mechanism by which VEGF/VPF increases vascular permeability (VP), however, has remained enigmatic. Accordingly, we used an in vivo assay of VP (Miles assay) to study the putative mediators of VEGF/VPF-induced permeability. Methods and Results —VEGF/VPF and positive controls (platelet-activating factor [PAF], histamine, and bradykinin) all increased vascular permeability. Prior administration of the tyrosine kinase inhibitors genistein or herbimycin A prevented VEGF/VPF-induced permeability. Placenta growth factor, which binds to Flt -1/VEGF-R1 but not Flk -1/KDR/VEGF-R2 receptor tyrosine kinase, failed to increase permeability. Other growth factors such as basic fibroblast growth factor (FGF), acidic FGF, platelet-derived growth factor-BB, transforming growth factor-β, scatter factor, and granulocyte macrophage-colony stimulating factor (8 to 128 ng) failed to increase permeability. VEGF/VPF-induced permeability was significantly attenuated by the nitric oxide (NO) synthase inhibitors N ω -nitro- l -arginine (10 mg/kg) or N ω -nitro- l -arginine methyl ester (20 mg/kg) and the cyclooxygenase inhibitor indomethacin (5 mg/kg). The inactive enantiomer N ω -nitro- d -arginine methyl ester (20 mg/kg) did not inhibit VEGF/VPF-induced permeability. In vitro studies confirmed that VEGF/VPF stimulates synthesis of NO and prostaglandin metabolites in microvascular endothelial cells. Finally, NO donors and the prostacyclin analogue taprostene administered together but not alone reproduced the increase in permeability observed with VEGF/VPF. Conclusions —These results implicate NO and prostacyclin produced by the interaction of VEGF/VPF with its Flk -1/KDR/VEGF-R2 receptor as mediators of VEGF/VPF-induced vascular permeability. Moreover, this property appears unique to VEGF/VPF among angiogenic cytokines.

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Section: Discussionmentioning

confidence: 99%

“…More recently, prostaglandins have been suggested to contribute to the regulation of VP and angiogenesis. 25,26 Indeed, we demonstrate here that VP induced by VEGF/VPF in vivo results from the synergistic action of both NO and prostacyclin and that this property appears unique to VEGF/VPF among angiogenic cytokines.…”

mentioning

confidence: 97%

Vascular Endothelial Growth Factor/Vascular Permeability Factor Enhances Vascular Permeability Via Nitric Oxide and Prostacyclin

et al. 1998

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“…Although the relationship between NO-mediated signaling events and PGI 2 production in the VEGF signal transduction cascade are not yet known, results of in vivo analysis have suggested that vascular hyperpermeability induced by VEGF results from the synergistic action of both NO and PGI 2 (12). Therefore, the fact that PGI 2 , like NO, has vasodilating effects and has been shown to stimulate vascular hyperpermeability and angiogenesis under some conditions (19,20) suggests that both molecules are likely to be involved in transducing the vascular effects of VEGF.…”

Section: Vascular Endothelial Growth Factor (Vegf)mentioning

confidence: 99%

“…However, influx of external Ca 2ϩ would probably be needed to replenish the intracellular Ca 2ϩ if treatment were continued longer. VEGF-induced PGI 2 Production Is Independent of NOS Activity-PGI 2 , like VEGF, is known to be involved in the regulation of vascular permeability and angiogenesis (19,20). VEGF has been shown to stimulate PGI 2 production in human umbilical vein endothelial cells via activation of flk-1/KDR (18).…”

Section: Vegf Stimulation Of No Formation Requires the Activity Of Tymentioning

confidence: 99%

Vascular Endothelial Growth Factor Signals Endothelial Cell Production of Nitric Oxide and Prostacyclin through Flk-1/KDR Activation of c-Src

He¹,

Venema²,

Gu³

et al. 1999

Journal of Biological Chemistry

445

268

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“…In other studies, a topical PGI2 analog was shown to promote wound healing in diabetic mice by stimulation of angiogenesis and improvement of blood¯ow in neovascularization of the wound. 162,163 TXA2 is implicated as a potential mediator of asthma and induces potent contraction of airway smooth muscles and airway hypersensitivity. 164 Seratrodast, a TXA2 receptor antagonist, and ozagrel, a speci®c inhibitor of TXA2 synthesis, are helpful in the treatment of some patients with bronchial asthma.…”

Section: Lipoxygenase Metabolites and Cancermentioning

confidence: 99%

Arachidonic Acid-Derived Bioactive Lipids: Their Role and the Role for Their Inhibitors in Dermatology

Smith

Skelton

2002

Journal of Cutaneous Medicine and Surgery: Incorporating Medical and Surgical Dermatology

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Newer drug discovery methods, including combinatorial chemistry with molecular modeling, have made it possible to develop inhibitors and analogs with increasing specificity and bioactivity and decreasing toxicity. Although the application of these analogs and inhibitors for cutaneous disease is limited today, either as primary agents or adjuvant therapy, these drugs will have a place in our therapeutic regimes of the future. We present a review of the therapeutic agents now available from manipulation of these bioactive lipids, and their role and future in dermatology.

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Effect of topical application of a stable prostacyclin analogue, SM-10902 on wound healing in diabetic mice

Cited by 27 publications

References 25 publications

Vascular Endothelial Growth Factor/Vascular Permeability Factor Enhances Vascular Permeability Via Nitric Oxide and Prostacyclin

Vascular Endothelial Growth Factor/Vascular Permeability Factor Enhances Vascular Permeability Via Nitric Oxide and Prostacyclin

Vascular Endothelial Growth Factor Signals Endothelial Cell Production of Nitric Oxide and Prostacyclin through Flk-1/KDR Activation of c-Src

Arachidonic Acid-Derived Bioactive Lipids: Their Role and the Role for Their Inhibitors in Dermatology

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