Cobra Venom Factor-induced complement depletion protects against lung ischemia reperfusion injury through alleviating blood-air barrier damage

Chang, Haihua; Wang, Wei; Huang, Kun; Liao, Yuanli; Lin, Fei

doi:10.1038/s41598-018-28724-z

Cited by 20 publications

(19 citation statements)

References 33 publications

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“…The complement system plays an important role in activating the innate immune system, but uncontrolled activation can result in tissue injury in LIRI. 110 , 111 Complement system activation enhances the inflammatory response by generating anaphylatoxins (ie, C3a and C5a), which results in increased vascular permeability. 112 Membrane attack complex formations (C5b-9) have also been implicated in ALI.…”

Section: Pathophysiology and Therapeutic Strategiesmentioning

confidence: 99%

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Ischemia-reperfusion Injury in the Transplanted Lung: A Literature Review

Talaie

DiChiacchio

Prasad

et al. 2021

Transplantation Direct

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Lung ischemia-reperfusion injury (LIRI) and primary graft dysfunction are leading causes of morbidity and mortality among lung transplant recipients. Although extensive research endeavors have been undertaken, few preventative and therapeutic treatments have emerged for clinical use. Novel strategies are still needed to improve outcomes after lung transplantation. In this review, we discuss the underlying mechanisms of transplanted LIRI, potential modifiable targets, current practices, and areas of ongoing investigation to reduce LIRI and primary graft dysfunction in lung transplant recipients.

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Section: Pathophysiology and Therapeutic Strategiesmentioning

confidence: 99%

“…In a rat model of LIRI, pretreatment with cobra venom factor, a functional analogue of C3, resulted in complement depletion and subsequently reduced proinflammatory factors as well as neutrophil infiltration. 110 …”

Section: Pathophysiology and Therapeutic Strategiesmentioning

confidence: 99%

Ischemia-reperfusion Injury in the Transplanted Lung: A Literature Review

Talaie

DiChiacchio

Prasad

et al. 2021

Transplantation Direct

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“…Purified recombinant human C3 protein (HuC3, 20 ng/ml, MBS230377, MyBioSource, San Diego, CA) was added to or left out of the culturing medium. Exogenous C3 was depleted with cobra venom factor (CVF; Heng Fei biological technology, Shanghai, China), as previously described [20]. Complement receptor 1 (CR1/CD35, MBS717740, MyBioSource) was used to block C3 activation as previously confirmed [21], with JAK2 blocker (AG490, 25 μM, InvivoGen, Hongkong) used to inhibit STAT3 signaling pathway [22].…”

Section: Cell Lines and Cell Culturementioning

confidence: 99%

Complement C3 overexpression activates JAK2/STAT3 pathway and correlates with gastric cancer progression

Yuan¹,

Ye²,

Liu

et al. 2020

J Exp Clin Cancer Res

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Background: Localized C3 deposition is a well-known factor of inflammation. However, its role in oncoprogression of gastric cancer (GC) remains obscured. This study aims to explore the prognostic value of C3 deposition and to elucidate the mechanism of C3-related oncoprogression for GC. Methods: From August to December 2013, 106 GC patients were prospectively included. The regional expression of C3 and other effectors in gastric tissues were detected by WB, IHC, qRT-PCR and other tests. The correlation of localized C3 deposition and oncologic outcomes was determined by 5-year survival significance. Human GC and normal epithelial cell lines were employed to detect a relationship between C3 and STAT3 signaling pathway in vitro experiments. Results: C3 and C3a expression were markedly enhanced in GC tissues at both mRNA and protein levels compared with those in paired nontumorous tissues. According to IHC C3 score, 65 (61.3%) and 41 (38.7%) patients had high and low C3 deposition, respectively. C3 deposition was negatively correlated with plasma levels of C3 and C3a (both P < 0.001) and positively correlated with pathological T and TNM stages (both P < 0.001). High C3 deposition was identified as an independent prognostic factor of poor 5-year overall survival (P = 0.045). In vitro C3 administration remarkably enhanced p-JAK2/p-STAT3 expression in GC cell lines but caused a reduction of such activation when pre-incubated with a C3 blocker. Importantly, C3 failed to activate such signaling in cells pretreated with a JAK2 inhibitor.Conclusions: Localized C3 deposition in the tumor microenvironment is a relevant immune signature for predicting prognosis of GC. It may aberrantly activate JAK2/STAT3 pathway allowing oncoprogression.

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“…We identified MASP1 and MASP2 that are of alternative pathways of complement activation, involved in the activation of factor D [ 63 ], complement factor I, complement C1r subcomponent and complement component C7, which possibly participate in the tissue damage in a host bitten by B. jararaca and may aid in the venom poisoning . The excessive complement activation and immune activation could exacerbate the severity of the tissue injury [ 64 ].…”

Section: Discussionmentioning

confidence: 99%

In-depth transcriptome reveals the potential biotechnological application of Bothrops jararaca venom gland

Pereira

Messias

Sorroche

et al. 2020

J. Venom. Anim. Toxins incl. Trop. Dis

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Background: Lack of complete genomic data of Bothrops jararaca impedes molecular biology research focusing on biotechnological applications of venom gland components. Identification of full-length coding regions of genes is crucial for the correct molecular cloning design. Methods: RNA was extracted from the venom gland of one adult female specimen of Bothrops jararaca . Deep sequencing of the mRNA library was performed using Illumina NextSeq 500 platform. De novo assembly of B. jararaca transcriptome was done using Trinity. Annotation was performed using Blast2GO. All predicted proteins after clustering step were blasted against non-redundant protein database of NCBI using BLASTP. Metabolic pathways present in the transcriptome were annotated using the KAAS-KEGG Automatic Annotation Server. Toxins were identified in the B. jararaca predicted proteome using BLASTP against all protein sequences obtained from Animal Toxin Annotation Project from Uniprot KB/Swiss-Pro database. Figures and data visualization were performed using ggplot2 package in R language environment. Results: We described the in-depth transcriptome analysis of B. jararaca venom gland, in which 76,765 de novo assembled isoforms, 96,044 transcribed genes and 41,196 unique proteins were identified. The most abundant transcript was the zinc metalloproteinase-disintegrin-like jararhagin. Moreover, we identified 78 distinct functional classes of proteins, including toxins, inhibitors and tumor suppressors. Other venom proteins identified were the hemolytic lethal factors stonustoxin and verrucotoxin. Conclusion: It is believed that the application of deep sequencing to the analysis of snake venom transcriptomes may represent invaluable insight on their biotechnological potential focusing on candidate molecules.

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Cobra Venom Factor-induced complement depletion protects against lung ischemia reperfusion injury through alleviating blood-air barrier damage

Cited by 20 publications

References 33 publications

Ischemia-reperfusion Injury in the Transplanted Lung: A Literature Review

Ischemia-reperfusion Injury in the Transplanted Lung: A Literature Review

Complement C3 overexpression activates JAK2/STAT3 pathway and correlates with gastric cancer progression

In-depth transcriptome reveals the potential biotechnological application of Bothrops jararaca venom gland

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