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Effect of Sepsis on Circulating CTRP3 Levels
Author(s) -
Musick Adam,
Shipley Madison M,
Tu Fei,
Li Chuanfu,
Yakubenko Valentin,
Peterson Jonathan
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.752.9
Subject(s) - sepsis , adipokine , adipose tissue , lipopolysaccharide , flow cytometry , endogeny , tumor necrosis factor alpha , immunology , biology , medicine , insulin , insulin resistance
Adipose tissue is an active endocrine organ which secrets several pro‐ and anti‐ inflammatory mediators, collectively called adipokines. Our previous work has identified a novel anti‐inflammatory adipokine called C1q TNF Related Protein 3 (CTRP3). Localized overexpression of CTRP3 protects myocardial tissue from lipopolysaccharide (LPS)‐induced sepsis, indicating a potential protective role of CTRP3. However, endogenous regulation of CTRP3 in response to a sepsis event has not been explored. Therefore, the purpose of this project was to explore the potential role of CTRP3 in sepsis by determining the effects of a sepsis event on circulating CTRP3 levels. METHODS Gonadal adipose tissue and serum were collected 8 hours after induction of the cecal‐puncture and ligation (CLP) model of sepsis or sham control mice. The circulating levels of CTRP3 were quantified by immunoblot analysis. The transcription levels of CTRP3 in adipose tissue were measured by Real‐Time PCR. In addition, to explore a potential mechanism for a protective role of CTRP3, thioglycollate‐induced peritoneal macrophages were isolated and binding of recombinant CTRP3 protein was determined by imaging flow cytometry. RESULTS CLP‐induced sepsis reduced circulating CTRP3 levels by ~90%, compared to sham treated mice. However, there was no difference in the CTRP3 mRNA level. Further, imaging flow cytometry demonstrated that CTRP3 binds directly to isolated macrophages. CONCLUSION The observed reduction in circulating CTRP3 protein levels combined with the absence of changes to the CTRP3 transcription level, indicate that during sepsis CTRP3 is actively removed from the blood. Combine these data support future research to determine if circulating CTRP3 levels are a biomarker indicative of sepsis prognosis. In addition, as CTRP3 binds to and inhibits macrophage activation future research should also determine if restoring circulating CTRP3 levels could reduce the cytokine storm associated with a sepsis event. Support or Funding Information NIH NIDDK R15DK105496 This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .