Plasma C1q/tumor necrosis factor-related protein-3 concentrations are associated with diabetic peripheral neuropathy

Lin, Ke; Liu, Yang; Xiong, Yi; Feng, Keduo; Wang, Zeng; Deng, Bo

doi:10.1136/bmjdrc-2021-002746

Cited by 2 publications

(1 citation statement)

References 41 publications

(44 reference statements)

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“…To induce sepsis, mice were injected with 30 mg/kg LPS. Results showed that CTRP6 was downregulated in lungs peripheral neuropathy, 19 while CTRP6 deficiency enhanced complement activation and contributed to development of inflammatory diseases. 14 This study found that CTRP6 exhibited anti-inflammatory effect to protect against sepsisassociated lung injury and inhibited neutrophil extracellular traps formation.…”

Section: Ctrp6 Ameliorated Septic Lung Injurymentioning

confidence: 99%

CTRP6 suppresses neutrophil extracellular traps formation to ameliorate sepsis-induced lung injury through inactivation of ERK pathway

Xuan²,

Wu³

et al. 2022

Allergol Immunopathol

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Background: Septic lung injury is associated with excessive neutrophil activation, while neu-trophil extracellular traps formation contributes to inflammatory lung injury in sepsis. C1q/ tumor necrosis factor–related protein-6 (CTRP6) is a paralog of adiponectin and exerts anti-inflammatory and antioxidant properties. The role of CTRP6 in sepsis-associated inflammatory lung injury was investigated in this study. Methods: Mice were injected with lipopolysaccharides (LPS) intraperitoneally to establish the mouse sepsis model. They were first tail-vein injected with adenovirus-mediated overexpression CTRP6 (Ad-CTRP6) and then subjected to the LPS injection. Pathological changes in lungs were detected by hematoxylin and eosin staining. Inflammation cytokine levels in bronchoalveolar lavage fluid were assessed by qRT-PCR and ELISA. Flow cytometry was used to detect the number of neutrophils in bronchoalveolar lavage fluid, and immunofluorescence was performed to assess neutrophil extracellular traps. Results: Lipopolysaccharides induced pulmonary congestion, interstitial edema, and alveolar wall thickening in the lungs, as well as upregulated lung histology score and wet/dry weight ratio. CTRP6 was reduced in lung tissues of septic mice. Injection with Ad-CTRP6 ameliorated extensive histopathological changes in LPS-induced mice and decreased lung histology score and wet/dry weight ratio. Overexpression of CTRP6 reduced the levels of TNF-α, IL-6, and IL-1β in septic mice. Injection with Ad-CTRP6 also decreased the number of neutrophils and down-regulated Cit-H3 and myeloperoxidase polymers in septic mice. Protein expression of p-ERK in septic mice was reduced by overexpression of CTRP6. Conclusion: CTRP6 attenuated septic lung injury, exerted anti-inflammatory effect, and sup-pressed neutrophil extracellular traps formation against sepsis through inactivation of extra-cellular signal-regulated kinase signaling.

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Section: Ctrp6 Ameliorated Septic Lung Injurymentioning

confidence: 99%

CTRP6 suppresses neutrophil extracellular traps formation to ameliorate sepsis-induced lung injury through inactivation of ERK pathway

Xuan²,

Wu³

et al. 2022

Allergol Immunopathol

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Exploring causal correlations between plasma proteins and peripheral neuropathy: a Mendelian randomization

Song,

Chen,

et al. 2024

Front. Neurol.

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BackgroundPeripheral neuropathy (PN) is a common neurological disorder, and circulating plasma proteins with causal genetic evidence are a major source of therapeutic targets. This study identifies several potential plasma proteins that are causally related to PN risk, providing new insights into protein-mediated pathogenesis of PN and potential targets for novel therapies.MethodsTo identify potential therapeutic targets for PN, we employed two-sample Mendelian randomization (MR) to identify plasma proteins associated with six common PN. First, we screened for proteins related to PN using genome-wide association studies (GWAS), obtaining genetic data on plasma proteomes from 35,559 Icelanders. Summary data for six common PN, including Carpal Tunnel Syndrome (CTS), Trigeminal Neuralgia (TN), Alcoholic Neuropathy (AIP), Drug-induced Neuropathy (DIP), Diabetic Neuropathy (DP), and Guillain-Barré syndrome (GBS), were obtained from the FinnGen database. Two-sample MR and colocalization analyses were then conducted to further identify protein-PN pairs with presumed causal relationships. Enrichment analysis of positive proteins revealed potential biological processes and pathways. Based on drug-gene interaction analysis, we ultimately identified causal proteins associated with PN that could serve as potential drug targets for treating PN.ResultsThrough MR analysis, we identified eight proteins (UBC12, SEM4C, IL23R, Prothrombin, CBS, Microglobulin, MATN4, COLEC12) with causal relationships to PN. We found that UBC12 is a protective factor for DP and CTS, while the remaining proteins are risk factors. Further colocalization analysis showed a posterior probability of hypothesis 4 (PPH4) less than 0.75, indicating no positive colocalization results were found. From the pathway enrichment analysis, we discovered that the proteins were mainly concentrated in pathways related to defense response to bacterium, receptor signaling pathway via STAT, cell killing, negative regulation of cytokine production, and leukocyte mediated immunity. Finally, in Drug-Gene Interaction database (DGIdb), we identified three protein-coding genes (IL23R, F2, CBS) as potential drug targets for PN.ConclusionMendelian randomization studies confirm the causal relationship between genetically predicted PN-related risk and genetically predicted plasma protein abundance. Plasma proteins, as biomarkers associated with PN, can provide potential drug targets for etiological intervention research in PN.

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Plasma C1q/tumor necrosis factor-related protein-3 concentrations are associated with diabetic peripheral neuropathy

Cited by 2 publications

References 41 publications

CTRP6 suppresses neutrophil extracellular traps formation to ameliorate sepsis-induced lung injury through inactivation of ERK pathway

CTRP6 suppresses neutrophil extracellular traps formation to ameliorate sepsis-induced lung injury through inactivation of ERK pathway

Exploring causal correlations between plasma proteins and peripheral neuropathy: a Mendelian randomization

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