Neovastat inhibits airway inflammation and hyperresponsiveness in a murine model of asthma

Lee, S.; Kim, S.; Kwon, Soon Suk; Jung, Sung-No

doi:10.1016/j.jaci.2004.12.305

Cited by 10 publications

(11 citation statements)

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“…The administration of endostatin/Fc to OVA-sensitized mice inhibited AHR; pulmonary allergic inflammation; the production of OVA-specific IgE; and expression of CD31, mRNA, and markers of lung inflammation (59). In addition, a naturally occurring multifunctional antiangiogenic agent (neovastat, shark collagen) inhibited airway inflammation and AHR in a murine model of AAD (60). Both these studies produced results that show the protective effects of the antiangiogenic inhibitors endostatin and neovastat using murine models of AAD in which angiogenesis did not occur.…”

Section: Discussionmentioning

confidence: 99%

Reduction of Tumstatin in Asthmatic Airways Contributes to Angiogenesis, Inflammation, and Hyperresponsiveness

Burgess¹,

Boustany²,

Moir³

et al. 2010

Am J Respir Crit Care Med

110

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Section: Discussionmentioning

confidence: 99%

Reduction of Tumstatin in Asthmatic Airways Contributes to Angiogenesis, Inflammation, and Hyperresponsiveness

Burgess¹,

Boustany²,

Moir³

et al. 2010

Am J Respir Crit Care Med

110

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“…In this study, VEGF is also increased in the BAL of asthmatics as compared with healthy controls, supporting the concept of an angiogenic environment in the asthmatic lung. In the BALB/c murine model of asthma, the treatment of animals with antiangiogenic agents results in reduced inflammation (73,74), decreased airway hyperresponsiveness, and the reduction of OVA-specific IgE (74). Definitive evidence of a role for angiogenesis, and likely VEGF, in asthma pathogenesis is provided by a transgenic mouse model with lung-targeted, regulatable VEGF expression.…”

Section: Discussionmentioning

confidence: 99%

Th1- and Th2-Dependent Endothelial Progenitor Cell Recruitment and Angiogenic Switch in Asthma

Asosingh

Swaidani

Aronica

et al. 2007

The Journal of Immunology

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Increased numbers of submucosal vessels are a consistent pathologic component of asthmatic airway remodeling. However, the relationship between new vessel formation and asthmatic inflammatory response is unknown. We hypothesized that angiogenesis is a primary event during the initiation of airway inflammation and is linked to the recruitment of bone marrow-derived endothelial progenitor cells (EPC). To test this hypothesis, circulating EPC and EPC-derived endothelial cell colony formation of individuals with asthma or allergic rhinitis and health controls was evaluated. Circulating EPC were increased in asthma, highly proliferative, and exhibited enhanced incorporation into endothelial cell tubes as compared with controls. In an acute allergen challenge murine asthma model, EPC mobilization occurred within hours of challenge and mobilized EPC were selectively recruited into the challenged lungs of sensitized animals, but not into other organs. EPC recruitment was Th1 and Th2 dependent and was temporally associated with an increased microvessel density that was noted within 48 h of allergen challenge, indicating an early switch to an angiogenic lung environment. A chronic allergen challenge model provided evidence that EPC recruitment to the lung persisted and was associated with increasing microvessel density over time. Thus, a Th1- and Th2-dependent angiogenic switch with EPC mobilization, recruitment, and increased lung vessel formation occurs early but becomes a sustained and cumulative component of the allergen-induced asthmatic response.

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“…There are few recent reports that focus on its MMP inhibition (initial data suggest that this is the result of TIMP-type proteins [227] in the Neovastat mixture). Lee et al [228] have shown recently that Neovastat was effective in the standard ovalbumin-induced airway inflammation mouse model of asthma, and that this efficacy correlated with reduced MMP-9 activity in the lung lavage fluid.…”

Section: Endogenous Mmp Inhibitorsmentioning

confidence: 98%

Recent advances in MMP inhibitor design

Fisher

Mobashery

2006

Cancer Metastasis Rev

239

205

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The search for an MMP inhibitor with anticancer efficacy is a nearly three-decade endeavor. This inhibitor is yet to be found. The reasons for this failure include shortcomings in the chemistry of these compounds (including broad MMP sub-type selectivity, metabolic lability, and toxicity) as well as the emerging, and arguably extraordinary, complexity of MMP cell (and cancer) biology. Together these suggest that the successful anticancer inhibitor must possess MMP selectivity against the MMP subtype whose involvement is critical, yet highly temporally (with respect to metastatic progression) and mechanistically (with respect to matrix degradation) regulated. This review summarizes the progression of chemical structure and mechanistic thinking toward these objectives, with emphasis on the disappointment, the perseverance, and the resilient optimism that such an inhibitor is there to be discovered.

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Neovastat inhibits airway inflammation and hyperresponsiveness in a murine model of asthma

Cited by 10 publications

References 0 publications

Reduction of Tumstatin in Asthmatic Airways Contributes to Angiogenesis, Inflammation, and Hyperresponsiveness

Reduction of Tumstatin in Asthmatic Airways Contributes to Angiogenesis, Inflammation, and Hyperresponsiveness

Th1- and Th2-Dependent Endothelial Progenitor Cell Recruitment and Angiogenic Switch in Asthma

Recent advances in MMP inhibitor design

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