RGD Reference Report - Deficiency of Interleukin-36 Receptor Protected Cardiomyocytes from Ischemia-Reperfusion Injury in Cardiopulmonary Bypass. - Rat Genome Database

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Deficiency of Interleukin-36 Receptor Protected Cardiomyocytes from Ischemia-Reperfusion Injury in Cardiopulmonary Bypass.

Authors: Luo, Cheng  Xie, Xiaoyong  Feng, Xu  Lei, Binfeng  Fang, Chen  Li, Yugui  Cai, Xiongwei  Ling, Guoxing  Zheng, Baoshi 
Citation: Luo C, etal., Med Sci Monit. 2020 Feb 12;26:e918933. doi: 10.12659/MSM.918933.
RGD ID: 126925167
Pubmed: (View Article at PubMed) PMID:32048631
DOI: Full-text: DOI:10.12659/MSM.918933

BACKGROUND Interleukin-36 has been demonstrated to be involved in inflammatory responses. Inflammatory responses due to ischemia-reperfusion injury following cardiopulmonary bypass (CPB) can cause heart dysfunction or damage. MATERIAL AND METHODS The CPB models were constructed in IL-36R-/-, IL-36RN-/-, and wild-type SD rats. Ultrasonic cardiography and ELISA were used to evaluate the cardiac function and measuring myocardial biomarker levels in different groups. TUNEL assay was used to evaluate apoptosis. Western blot assays and RT-PCR were performed to measure the expression of chemokines and secondary inflammatory cytokines in the heart. Oxidative stress in tissue and cultured cells was assessed using a DCFH-DA fluorescence probe and quantification of superoxide dismutase activity. RESULTS Improved systolic function and decreased serum levels of myocardial damage biomarkers were found in IL-36R-/- rats compared to WT rats, while worse cardiac function and cardiomyocyte IR injury were observed in IL-36RN-/- rats compared to WT rats. TUNEL staining and Western blot analyses found that cardiomyocyte apoptosis and inflammation were significantly lower in the hearts of IL-36R-/- rats compared with that of WT rats. Oxidative stress was significantly lower in IL-36R-/- rats compared to WT rats. iNOS expression was significantly reduced, while eNOS expression was increased in the hearts of IL-36R-/- rats. Silencing of IL-36R expression in vitro activated SIRT1/FOXO1/p53 signaling in cardiomyocytes. CONCLUSIONS IL-36R deficiency in cardiomyocytes repressed infiltration of bone marrow-derived inflammatory cells and oxidative stress dependent on SIRT1-FOXO1 signaling, thus protecting cardiomyocytes and improving cardiac function in CPB model rats.



Disease Annotations    

Objects Annotated

Genes (Rattus norvegicus)
Il1rl2  (interleukin 1 receptor-like 2)
Il1rl2tm1(Myh6-cre)Mhzh  (interleukin 1 receptor-like 2; tm1 (Myh6-cre), Mhzh)
Il36rn  (interleukin 36 receptor antagonist)
Il36rntm1(Myh6-cre)Mhzh  (interleukin 36 receptor antagonist; tm1, Mhzh)

Genes (Mus musculus)
Il1rl2  (interleukin 1 receptor-like 2)
Il36rn  (interleukin 36 receptor antagonist)

Genes (Homo sapiens)
IL1RL2  (interleukin 1 receptor like 2)
IL36RN  (interleukin 36 receptor antagonist)


Additional Information