The use of nerve growth factor in herpetic keratitis: a case report

Cellini, Mauro; Leonetti, Pietro; Campos, Emilio C.

doi:10.1186/1752-1947-1-124

Cited by 7 publications

(3 citation statements)

References 9 publications

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“…In all these cases, even if it was not specifically assessed, it is possible that NGF-induced neoangiogenesis may have contributed to the healing action of the NT. NGF additionally proved its ability to treat neurotrophic (25, 143) and herpetic corneal ulcer (171).…”

Section: Neurotrophin-based Therapeutic Perspectivesmentioning

confidence: 99%

Cardiovascular Actions of Neurotrophins

Caporali¹,

Emanueli²

2009

Physiological Reviews

176

180

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Neurotrophins were christened in consideration of their actions on the nervous system and, for a long time, they were the exclusive interest of neuroscientists. However, more recently, this family of proteins has been shown to possess essential cardiovascular functions. During cardiovascular development, neurotrophins and their receptors are essential factors in the formation of the heart and critical regulator of vascular development. Postnatally, neurotrophins control the survival of endothelial cells, vascular smooth muscle cells, and cardiomyocytes and regulate angiogenesis and vasculogenesis, by autocrine and paracrine mechanisms. Recent studies suggest the capacity of neurotrophins, via their tropomyosin-kinase receptors, to promote therapeutic neovascularization in animal models of hindlimb ischemia. Conversely, the neurotrophin low-affinity p75NTRreceptor induces apoptosis of endothelial cells and vascular smooth muscle cells and impairs angiogenesis. Finally, nerve growth factor looks particularly promising in treating microvascular complications of diabetes or reducing cardiomyocyte apoptosis in the infarcted heart. These seminal discoveries have fuelled basic and translational research and thus opened a new field of investigation in cardiovascular medicine and therapeutics. Here, we review recent progress on the molecular signaling and roles played by neurotrophins in cardiovascular development, function, and pathology, and we discuss therapeutic potential of strategies based on neurotrophin manipulation.

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Section: Neurotrophin-based Therapeutic Perspectivesmentioning

confidence: 99%

Cardiovascular Actions of Neurotrophins

Caporali¹,

Emanueli²

2009

Physiological Reviews

176

180

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“…Consistent with the findings reported here, TrkA −/− mice display decreased innervation of corneal stroma and epithelium and decreased corneal sensitivity [53] , and clinical studies have shown that topical NGF treatment generally increased corneal sensitivity [54] , [55] . In other clinical studies, topical administration of NGF eye drops has been perceived as generally favorable by observations of decreased healing time and increased epithelial closure in refractive disease [56] – [62] , presumably by stimulating epithelial migration [32] . The findings presented here suggest that NGF serves as part of a signaling hierarchy that regulates neurolymphatic remodeling in the cornea, and that clinical strategies to block NGF function may facilitate wound recovery by modulating these processes.…”

Section: Discussionmentioning

confidence: 99%

Nerve Growth Factor Regulates Neurolymphatic Remodeling during Corneal Inflammation and Resolution

et al. 2014

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The cellular and physiologic mechanisms that regulate the resolution of inflammation remain poorly defined despite their widespread importance in improving inflammatory disease outcomes. We studied the resolution of two cardinal signs of inflammation–pain and swelling–by investigating molecular mechanisms that regulate neural and lymphatic vessel remodeling during the resolution of corneal inflammation. A mouse model of corneal inflammation and wound recovery was developed to study this process in vivo. Administration of nerve growth factor (NGF) increased pain sensation and inhibited neural remodeling and lymphatic vessel regression processes during wound recovery. A complementary in vivo approach, the corneal micropocket assay, revealed that NGF-laden pellets stimulated lymphangiogenesis and increased protein levels of VEGF-C. Adult human dermal lymphatic endothelial cells did not express canonical NGF receptors TrkA and p75NTR or activate downstream MAPK- or Akt-pathway effectors in the presence of NGF, although NGF treatment increased their migratory and tubulogenesis capacities in vitro. Blockade of the VEGF-R2/R3 signaling pathway ablated NGF-mediated lymphangiogenesis in vivo. These findings suggest a hierarchical relationship with NGF functioning upstream of the VEGF family members, particularly VEGF-C, to stimulate lymphangiogenesis. Taken together, these studies show that NGF stimulates lymphangiogenesis and that NGF may act as a pathogenic factor that negatively regulates the normal neural and lymphatic vascular remodeling events that accompany wound recovery.

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“…On the other hand, application of NGF resulted in dramatic shrinkage or disappearance of lesions in chronic vasculitic ulcers and allergic encephalomyelitis, and accelerated wound healing, which suggested an anti-inflammatory role for NGF as well [41][42][43][44]. In studies which investigated NGF's interaction with anti-inflammatory cytokines, a strong interaction between NGF and IL-10 was found.…”

Section: Ngf and Inflammationmentioning

confidence: 94%