A Comparison of Two Controlled-Release Delivery Systems for the Delivery of Amiloride to Control Angiogenesis

Knoll, Andrew K.; Schmidt, Steven; Chapman, Michelle; Wiley, David M.; Bulgrin, Jeffrey P.; Blank, James L.; Kirchner, Loren M.

doi:10.1006/mvre.1999.2149

Cited by 25 publications

(13 citation statements)

References 15 publications

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“…2C and D) may be sufficient to explain improvements in locomotor recovery, other processes relevant to functional recovery after SCI that could also be affected by amiloride cannot be ruled out. For example, it is conceivable that amiloride may also modulate angiogenesis after SCI (Alliegro et al, 1993;Knoll et al, 1999;MiterniqueGrosse et al, 2006), and altering angiogenesis can critically affect functional recovery after SCI, as is elegantly shown by Han and associates (2010).…”

Section: Fig 2 (A)mentioning

confidence: 97%

Amiloride Improves Locomotor Recovery after Spinal Cord Injury

Durham-Lee

Mokkapati²,

Johnson³

et al. 2011

Journal of Neurotrauma

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Amiloride is a drug approved by the United States Food and Drug Administration, which has shown neuroprotective effects in different neuropathological conditions, including brain injury or brain ischemia, but has not been tested in spinal cord injury (SCI). We tested amiloride's therapeutic potential in a clinically relevant rat model of contusion SCI inflicted at the thoracic segment T10. Rats receiving daily administration of amiloride from 24 h to 35 days after SCI exhibited a significant improvement in hindlimb locomotor ability at 21, 28, and 35 days after injury, when compared to vehicle-treated SCI rats. Rats receiving amiloride treatment also exhibited a significant increase in myelin oligodendrocyte glycoprotein (MOG) levels 35 days after SCI at the site of injury (T10) when compared to vehicle-treated controls, which indicated a partial reverse in the decrease of MOG observed with injury. Our data indicate that higher levels of MOG correlate with improved locomotor recovery after SCI, and that this may explain the beneficial effects of amiloride after SCI. Given that amiloride treatment after SCI caused a significant preservation of myelin levels, and improved locomotor recovery, it should be considered as a possible therapeutic intervention after SCI.

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Section: Fig 2 (A)mentioning

confidence: 97%

Amiloride Improves Locomotor Recovery after Spinal Cord Injury

Durham-Lee

Mokkapati²,

Johnson³

et al. 2011

Journal of Neurotrauma

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“…Alginate beads (5 mL) containing vehicle or 11.5 pmoles of FGF8b with or without PTX3 (46 pmoles) or K5-OS (3.0 mg) were prepared as described (25) and placed on top of the chicken embryo chorioallantoic membrane (CAM) of fertilized White Leghorn chicken eggs at day 11 of incubation (6-8 eggs per experimental group). In a second set of experiments, mock_S115 cells or hPTX3_S115 cells were delivered onto the CAM (20,000 cells per embryo) after a 24 hour-incubation in the absence or in the presence of 10 nmol/L DHT (26).…”

Section: Chick Embryo Chorioallantoic Membrane Assaymentioning

confidence: 99%

Long Pentraxin-3 Inhibits FGF8b-Dependent Angiogenesis and Growth of Steroid Hormone–Regulated Tumors

Leali

Alessi

Coltrini

et al. 2011

Molecular Cancer Therapeutics

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Fibroblast growth factor-8b (FGF8b) exerts nonredundant autocrine/paracrine functions in steroid hormone-regulated tumors. Previous observations had shown that the soluble pattern recognition receptor long pentraxin-3 (PTX3) is a natural selective antagonist for a restricted number of FGF family members, inhibiting FGF2 but not FGF1 and FGF4 activity. Here, we assessed the capacity of PTX3 to antagonize FGF8b and to inhibit the vascularization and growth of steroid hormone-regulated tumors. Surface plasmon resonance analysis shows that PTX3 binds FGF8b with high affinity (K d ¼ 30-90 nmol/L). As a consequence, PTX3 prevents the binding of FGF8b to its receptors, inhibits FGF8b-driven ERK1/2 activation, cell proliferation, and chemotaxis in endothelial cells, and suppresses FGF8b-induced neovascularization in vivo. Also, PTX3 inhibits dihydrotestosterone (DHT)-and FGF8b-driven proliferation of androgen-regulated Shionogi 115 (S115) mouse breast tumor cells. Furthermore, DHT-treated, PTX3 overexpressing hPTX3_S115 cell transfectants show a reduced proliferation rate in vitro and a limited angiogenic activity in the chick embryo chorioallantoic membrane and murine s.c. Matrigel plug assays. Accordingly, hPTX3_S115 cells show a dramatic decrease of their tumorigenic activity when grafted in immunodeficient male mice. These results identify PTX3 as a novel FGF8b antagonist endowed with antiangiogenic and antineoplastic activity with possible implications for the therapy of hormonal tumors. Mol Cancer Ther; 10(9); 1600-10. Ó2011 AACR.

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“…Alginate beads (5 l) containing vehicle, 300 ng of HMGB1 with or without 100 ng of neutralizing anti-RAGE Ab were prepared as previously described (19) and placed on top of the CAM of fertilized White Leghorn chicken eggs at day 11 of incubation. After 72 h, blood vessels converging toward the implant were counted at ϫ50 magnification.…”

Section: Chicken Embryo Chorioallantoic Membrane (Cam) Assaymentioning

confidence: 99%

Cutting Edge: Extracellular High Mobility Group Box-1 Protein Is a Proangiogenic Cytokine

Mitola

Belleri

Urbinati

et al. 2006

The Journal of Immunology

201

193

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The chromosomal high mobility group box-1 (HMGB1) protein acts as a proinflammatory cytokine when released in the extracellular environment by necrotic and inflammatory cells. In the present study, we show that HMGB1 exerts proangiogenic effects by inducing MAPK ERK1/2 activation, cell proliferation, and chemotaxis in endothelial cells of different origin. Accordingly, HMGB1 stimulates membrane ruffling and repair of a mechanically wounded endothelial cell monolayer and causes endothelial cell sprouting in a three-dimensional fibrin gel. In keeping with its in vitro properties, HMGB1 stimulates neovascularization when applied in vivo on the top of the chicken embryo chorioallantoic membrane whose blood vessels express the HMGB1 receptor for advanced glycation end products (RAGE). Accordingly, RAGE blockade by neutralizing Abs inhibits HMGB1-induced neovascularization in vivo and endothelial cell proliferation and membrane ruffling in vitro. Taken together, the data identify HMGB1/RAGE interaction as a potent proangiogenic stimulus.

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A Comparison of Two Controlled-Release Delivery Systems for the Delivery of Amiloride to Control Angiogenesis

Cited by 25 publications

References 15 publications

Amiloride Improves Locomotor Recovery after Spinal Cord Injury

Amiloride Improves Locomotor Recovery after Spinal Cord Injury

Long Pentraxin-3 Inhibits FGF8b-Dependent Angiogenesis and Growth of Steroid Hormone–Regulated Tumors

Cutting Edge: Extracellular High Mobility Group Box-1 Protein Is a Proangiogenic Cytokine

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