Sustained Release of Prostaglandin E1 Potentiates the Impaired Therapeutic Angiogenesis by Basic Fibroblast Growth Factor in Diabetic Murine Hindlimb Ischemia

Huang, Yühong; Marui, Akira; Sakaguchi, Hisashi; Esaki, Jiro; Arai, Yoshinori; Hirose, Katsumi; Bir, Shyamal C.; Horiuchi, Hisanori; Maruyama, Takayuki; Ikeda, Tadashi; Tabata, Yasuhiko; Komeda, Masashi

doi:10.1253/circj.cj-07-0960

Cited by 23 publications

(28 citation statements)

References 41 publications

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“…The authors speculate that the repetitive injection maintains a more optimal concentration of S1P in the tissue than the single injection, but no measurement of the S1P concentration was made. In contrast, numerous other studies have shown sustained release of a payload following a single injection of PLGA microparticles 16, 17, 24, 43, 54 .…”

Section: Microparticlesmentioning

confidence: 84%

“…Huang et al injected bFGF (10 μg) in gelatin microparticles (size not stated) and prostaglandin E 1 (PGE 1 ) (0.2 μg) in PLGA microparticles (size not stated) immediately after hindlimb ischemia induction in mice 43 . The addition of encapsulated PGE 1 treatment increased blood vessel density and maturity over that of encapsulated bFGF four weeks after injection.…”

Section: Microparticlesmentioning

confidence: 99%

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Micro- and nanoparticles for treating cardiovascular disease

2015

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Cardiovascular disease, including myocardial infarction (MI) and peripheral artery disease (PAD), afflicts millions of people in Unites States. Current therapies are insufficient to restore blood flow and repair the injured heart or skeletal muscle, respectively, which is subjected to ischemic damage following vessel occlusion. Micro- and nano-particles are being designed as delivery vehicles for growth factors, enzymes and/or small molecules to provide a sustained therapeutic stimulus at the injured tissue. Depending on the formulation, the particles can be injected directly into the heart or skeletal muscle, or accumulate at the site of injury following an intravenous injection. In this article we review existing particle based therapies for treating MI and PAD.

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Section: Microparticlesmentioning

confidence: 84%

Section: Microparticlesmentioning

confidence: 99%

Micro- and nanoparticles for treating cardiovascular disease

2015

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“…Local SR of several growth factors is effective for myocardial ischemia and limb ischemia without systemic side-effects. 7,8,[11][12][13][14][15] In addition, SR of PGE1 potentiated the angiogenesis induced by SR of basic fibroblast growth factor. 12 These treatment strategies improve efficacy without systemic side-effects.…”

Section: Sr System Of Pge1mentioning

confidence: 93%

Local Sustained Release of Prostaglandin E1 Induces Neovascularization in Murine Hindlimb Ischemia

Esaki

Sakaguchi

Marui

et al. 2009

Circ J

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“…The function of FGF-2, which stimulates EC and SMC proliferation, is impaired by STZ-induced DM in the remodelling hindlimb artery [130,131]. In vitro, hyperglycaemia decreased the mitogenic and chemotactic activity of FGF-2 in a time-and dose-dependent manner [132].…”

Section: Growth Factorsmentioning

confidence: 99%

Diabetes impairs arteriogenesis in the peripheral circulation: review of molecular mechanisms

et al. 2010

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Patients suffering from both diabetes and PAD (peripheral arterial disease) are at risk of developing critical limb ischaemia and ulceration, and potentially requiring limb amputation. In addition, diabetes complicates surgical treatment of PAD and impairs arteriogenesis. Arteriogenesis is defined as the remodelling of pre-existing arterioles into conductance vessels to restore the perfusion distal to the occluded artery. Several strategies to promote arteriogenesis in the peripheral circulation have been devised, but the mechanisms through which diabetes impairs arteriogenesis are poorly understood. The present review provides an overview of the current literature on the deteriorating effects of diabetes on the key players in the arteriogenesis process. Diabetes affects arteriogenesis at a number of levels. First, it elevates vasomotor tone and attenuates sensing of shear stress and the response to vasodilatory stimuli, reducing the recruitment and dilatation of collateral arteries. Secondly, diabetes impairs the downstream signalling of monocytes, without decreasing monocyte attraction. In addition, EPC (endothelial progenitor cell) function is attenuated in diabetes. There is ample evidence that growth factor signalling is impaired in diabetic arteriogenesis. Although these defects could be restored in animal experiments, clinical results have been disappointing. Furthermore, the diabetes-induced impairment of eNOS (endothelial NO synthase) strongly affects outward remodelling, as NO signalling plays a key role in several remodelling processes. Finally, in the structural phase of arteriogenesis, diabetes impairs matrix turnover, smooth muscle cell proliferation and fibroblast migration. The review concludes with suggestions for new and more sophisticated therapeutic approaches for the diabetic population.

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Sustained Release of Prostaglandin E1 Potentiates the Impaired Therapeutic Angiogenesis by Basic Fibroblast Growth Factor in Diabetic Murine Hindlimb Ischemia

Cited by 23 publications

References 41 publications

Micro- and nanoparticles for treating cardiovascular disease

Micro- and nanoparticles for treating cardiovascular disease

Local Sustained Release of Prostaglandin E1 Induces Neovascularization in Murine Hindlimb Ischemia

Diabetes impairs arteriogenesis in the peripheral circulation: review of molecular mechanisms

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