Decay-accelerating factor attenuates remote ischemia–reperfusion-initiated organ damage

Weeks, Christine; Moratz, Chantal; Zacharia, Athina; Stracener, Catherine; Egan, Ryan; Peckham, Russell M.; Moore, Francis D.; Tsokos, George C.

doi:10.1016/j.clim.2007.05.010

Cited by 32 publications

(40 citation statements)

References 77 publications

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“…This synergistic effect of CRP on tissue damage can be prevented by the complement depletion with cobra venom factor [15]. Studies reported that the inhibition of complement activation using membrane complement regulatory proteins, including endogenous [17] and exogenous DAF [18], provided us with an important insight into protection against the potentiating effect of CRP on IR injury.…”

Section: Discussionmentioning

confidence: 96%

“…We selected the therapeutic dose of DAF as 2 mg per mouse in this study as per our previous report [18]. In this study, human DAF concentration in murine serum was not monitored since it has been reported that human DAF has a very short half-life in the circulation, and that the majority of DAF rapidly binds to and deposits on the cell membranes in local and remote tissues 10 min after administration [18].…”

Section: Discussionmentioning

confidence: 99%

“…We have shown that soluble human DAF attenuates local intestinal and remote lung injury in mice subjected to mesenteric IR [18]. Since human and rodent DAFs are not species restricted in their complement-inhibiting activity [19], we hypothesized that IR animals treated with human DAF would down-regulate human CRP-amplified C activity and effectively ameliorate tissue injury induced by mesenteric IR.…”

Section: Introductionmentioning

confidence: 99%

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Decay-Accelerating Factor Attenuates C-Reactive Protein-Potentiated Tissue Injury After Mesenteric Ischemia/Reperfusion

Simovic

et al. 2011

Journal of Surgical Research

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Decay-Accelerating Factor Attenuates C-Reactive Protein-Potentiated Tissue Injury After Mesenteric Ischemia/Reperfusion

Simovic

et al. 2011

Journal of Surgical Research

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“…This procedure was based on a modified method as previous described [21]. Briefly, four to six images from each animal were opened using the Adobe Photoshop software and adjusted until only the fluorescent deposits and no background tissue were visible.…”

Section: Immunofluorescent Quantificationmentioning

confidence: 99%

Blast-induced moderate neurotrauma (BINT) elicits early complement activation and tumor necrosis factor alpha (TNFα) release in a rat brain

Lucca

Chavko

Dubick

et al. 2012

Journal of the Neurological Sciences

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“…Local injury as a consequence of mesenteric IR tissue injury has been well characterized in mouse models by several groups using multiple endpoints (histopathology, neutrophil infiltration, permeability index). It has been shown in the mesenteric IR model that complement inhibitors reduce tissue injury [14][15][16]. Other studies have shown that C3 −/− and C4…”

Section: Isrn Immunologymentioning

confidence: 98%

C3b-Independent Complement Activation in Ischemia/Reperfusion Mesenteric Tissue Injury in Autoimmune Prone (B6.MRL/lpr) Mice

2012

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Complement plays a critical role in the development of tissue injury in systemic lupus erythematosus. The B6.MRL/lpr mouse, an autoimmune prone mouse, exhibits accelerated and intensified tissue injury in the ischemia/reperfusion (IR) model. It has been demonstrated in nonautoimmune mice that inhibition of complement attenuates inflammatory tissue injury in IR models. The role of complement is not as clear in the B6.MRL/lpr strain. B6.MRL/lpr-C3 deficient animals are susceptible to injury, but long-term use of C3 inhibitors in B6.MRL/lpr-C3 competent animals restrained the development of nephritis. To clarify the role of complement in the B6.MRL/lpr strain, initial and midpathway inhibitors were evaluated. C1 inhibition attenuated tissue injury, thrombin deposition, and C5a generation in the B6.MRL/lpr strain. Downstream of C1 inhibition of C3 activation by administration of cobra venom factor suppressed IR injury in immune competent mice, but was not as effective in B6.MRL/lpr mice. C3 levels in both strains were decreased after cobra venom factor treatment; however, C5a generation, thrombin deposition, and tissue injury were observed in the B6.MRL/lpr strain. These studies suggest that in the B6.MRL/lpr autoimmune prone strain C1 activation leads to C3-dependent and C3-independent pathways of complement activation.

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Decay-accelerating factor attenuates remote ischemia–reperfusion-initiated organ damage

Cited by 32 publications

References 77 publications

Decay-Accelerating Factor Attenuates C-Reactive Protein-Potentiated Tissue Injury After Mesenteric Ischemia/Reperfusion

Decay-Accelerating Factor Attenuates C-Reactive Protein-Potentiated Tissue Injury After Mesenteric Ischemia/Reperfusion

Blast-induced moderate neurotrauma (BINT) elicits early complement activation and tumor necrosis factor alpha (TNFα) release in a rat brain

C3b-Independent Complement Activation in Ischemia/Reperfusion Mesenteric Tissue Injury in Autoimmune Prone (B6.MRL/lpr) Mice

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