Role of complement and complement membrane attack complex in laser-induced choroidal neovascularization

Bora, Puran S.; Sohn, Jong Hee; Cruz, J.M.; Jha, Purushottam; Nishihori, H.; Wang, Y.; Kaliappan, S.; Kaplan, Henry J.; Bora, Nalini S.

doi:10.1016/j.ajo.2005.03.011

Cited by 44 publications

(119 citation statements)

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“…In addition, VEGF levels were lower in treated knockout mice compared with treated wild type mice (Nozaki et al, 2006). In other mouse models complement factors C3 and B were found essential for the formation of laser-induced CNV (Bora et al, 2006;Bora et al, 2005). In these studies, the end-product of complement activation, the membrane attack complex (MAC), was found to be essential for the development of CNV after laser injury and was temporally associated with VEGF production (Bora et al, 2005).…”

Section: Stimuli For Neovascular Amd and Vegf Expressionmentioning

confidence: 88%

“…Complement can lead to increased VEGF release from RPE and from recruited macrophages (Nozaki et al, 2006), and lead to MAC formation (Bora et al, 2005), which is also temporally associated with CNV and VEGF immunoreactivity in laser-induced CNV models (Fig. 18B).…”

Section: Stimuli For Neovascular Amd and Vegf Expressionmentioning

confidence: 93%

“…In other mouse models complement factors C3 and B were found essential for the formation of laser-induced CNV (Bora et al, 2006;Bora et al, 2005). In these studies, the end-product of complement activation, the membrane attack complex (MAC), was found to be essential for the development of CNV after laser injury and was temporally associated with VEGF production (Bora et al, 2005). Inhibition of the alternative pathway with small interfering RNA (siRNA) directed against factor B resulted in decreased levels of VEGF, MAC, and CNV, whereas siRNA directed against C1q, a factor involved in the classical pathway, did not affect CNV.…”

Section: Stimuli For Neovascular Amd and Vegf Expressionmentioning

confidence: 99%

“…VEGF is found in RPE in surgically excised human AMD specimens of CNV (Lopez et al, 1996;Frank et al, 1996;Grossniklaus et al, 2002). VEGF has been localized to CNV in rodent models of laserinduced CNV (Bora et al, 2005;Yi et al, 1997) and genetically modified mouse models of CNV (Ambati et al, 2003). The overexpression of VEGF in RPE caused intrachoroidal neovascularization in one model (Schwesinger et al, 2001).…”

Section: Vegf In Pathologic Neovascularization: Models Of Neovascularmentioning

confidence: 99%

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Vascular endothelial growth factor in eye disease

Penn

Madan

Caldwell

et al. 2008

Progress in Retinal and Eye Research

612

527

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Collectively, angiogenic ocular conditions represent the leading cause of irreversible vision loss in developed countries. In the U.S., for example, retinopathy of prematurity, diabetic retinopathy and age-related macular degeneration are the principal causes of blindness in the infant, working age and elderly populations, respectively. Evidence suggests that vascular endothelial growth factor (VEGF), a 40 kDa dimeric glycoprotein, promotes angiogenesis in each of these conditions, making it a highly significant therapeutic target. However, VEGF is pleiotropic, affecting a broad spectrum of endothelial, neuronal and glial behaviors, and confounding the validity of anti-VEGF strategies, particularly under chronic disease conditions. In fact, among other functions VEGF can influence cell proliferation, cell migration, proteolysis, cell survival and vessel permeability in a wide variety of biological contexts. This article will describe the roles played by VEGF in the pathogenesis of retinopathy of prematurity, diabetic retinopathy and age-related macular degeneration. The potential disadvantages of inhibiting VEGF will be discussed, as will the rationales for targeting other VEGF-related modulators of angiogenesis.

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Section: Stimuli For Neovascular Amd and Vegf Expressionmentioning

confidence: 88%

Section: Stimuli For Neovascular Amd and Vegf Expressionmentioning

confidence: 93%

Section: Stimuli For Neovascular Amd and Vegf Expressionmentioning

confidence: 99%

Section: Vegf In Pathologic Neovascularization: Models Of Neovascularmentioning

confidence: 99%

See 2 more Smart Citations

Vascular endothelial growth factor in eye disease

Penn

Madan

Caldwell

et al. 2008

Progress in Retinal and Eye Research

612

527

View full text Add to dashboard Cite

show abstract

“…35 The CNV was inhibited by complement depletion using cobra venom factor and did not develop in C3(À/À) mice. It was also noted that elevated levels of angiogenic factors in mice with laser-induced CNV were marked reduced after complement depletion.…”

Section: Complement Activation and Angiogenesismentioning

confidence: 97%

The complement system and age-related macular degeneration

Sivaprasad

Chong

2006

Eye

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Purpose Age-related macular degeneration (AMD) is the leading cause of blindness in the developed world. There are increasing evidences to suggest the complement system may play a significant role on the pathogenesis of AMD. In this review, we summarise the current research in this area. Methods Review of literature. Results The complement system is a complex system with several activation pathways. Complement factor H (CFH) polymorphisms has been associated with increase risk of AMD. CFH is an inhibitor protein; the polymorphisms might cause uncontrolled activation by initiation events. Conclusion Further studies on the molecular basis of the complement-mediated pathogenesis of AMD may offer novel therapy to AMD Eye (2006) 20, 867-872.

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Estimation of Systemic Complement C3 Activity in Age-Related Macular Degeneration

Sivaprasad

Adewoyin²,

Bailey³

et al. 2007

Arch Ophthalmol

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Objectives: To determine the role of systemic complement activation in the pathogenesis of age-related macular degeneration and to examine whether serum C3a des Arg reflects systemic complement activation, independent of individual complement component levels.Methods: Plasma complement C3a des Arg levels and a single nucleotide polymorphism at position 402 of the complement factor H gene (CFH) were determined in 3 groups of subjects: 42 subjects with early age-related maculopathy, 42 subjects with neovascular (wet) agerelated macular degeneration, and a control group of 38 subjects with no clinical evidence of age-related changes at the macula. Results:The median (range) of plasma complement C3a des Arg levels in the age-related maculopathy and neovascular age-related macular degeneration groups were 52.6 (2.8-198.1) ng/mL and 60.9 (3.1-173.1) ng/mL, re-spectively. The levels were significantly raised compared with the control group (n=38), which had a median (range) plasma complement C3a des Arg level of 40.3 (6.1-81.7) ng/mL (analysis of variance, P=.02). The concentration of plasma C3a des Arg did not differ significantly between those with different CFH genotypes (P =.07). Conclusion:Systemic activation of the complement system may contribute to the pathogenesis of age-related macular degeneration independent of CFH polymorphism. Clinical Relevance:The results of this study may be relevant to aiming new treatment strategies toward reducing systemic low-grade inflammation.

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Role of complement and complement membrane attack complex in laser-induced choroidal neovascularization

Cited by 44 publications

References 0 publications

Vascular endothelial growth factor in eye disease

Vascular endothelial growth factor in eye disease

The complement system and age-related macular degeneration

Estimation of Systemic Complement C3 Activity in Age-Related Macular Degeneration

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