Cathelicidin aggravates myocardial ischemia/reperfusion injury via activating TLR4 signaling and P2X

Animals Cathelicidins / metabolism Inflammasomes / metabolism Inflammation / pathology Male Mice, Inbred C57BL Mice, Knockout Myocardial Reperfusion Injury / metabolism Myocardium / metabolism NLR Family, Pyrin Domain-Containing 3 Protein / metabolism Neutrophil Infiltration Receptors, Purinergic P2X7 / metabolism Signal Transduction Toll-Like Receptor 4 / metabolism
Cathelicidin Ischemia/reperfusion NLRP3 inflammasome Neutrophils P2X(7)R TLR4

Journal

Journal of molecular and cellular cardiology
ISSN: 1095-8584
Titre abrégé: J Mol Cell Cardiol
Pays: England
ID NLM: 0262322

Informations de publication

Date de publication:
02 2020
Historique:
received: 18 08 2019
revised: 01 12 2019
accepted: 20 12 2019
pubmed: 27 1 2020
medline: 23 1 2021
entrez: 27 1 2020
Statut: ppublish

Résumé

The antimicrobial peptide cathelicidin (Camp) has multifunctional immunomodulatory activities. However, its roles in inflammation-related myocardial ischemia/reperfusion (MI/R) injury remain unclear. In this study, adult male C57BL/6 wild-type (WT) mice were subjected to MI/R injury by left anterior descending coronary artery ligation for 45 min followed by 3 or 24 h of reperfusion. An abundant cardiac expression of cathelicidin was observed during ischemia and reperfusion, which was mainly derived from heart-infiltrating neutrophils. Knockout of Camp in mice reduced MI/R-induced myocardial inflammation, infarct size, and circulating cTnI levels (an indicator of heart damage). CRAMP (the mature form of murine cathelicidin) administration of WT mice immediately before MI/R exerted detrimental effects on the reperfused heart. CRAMP exacerbates MI/R injury via a TLR4 and P2X Our findings reveal that, at the early stage of MI/R, neutrophil-derived cathelicidin plays an injurious role in the heart. Cathelicidin aggravates MI/R injury by over-activating TLR4 signaling and P2X

Identifiants

DOI: 10.1016/j.yjmcc.2019.12.011 PMID: 31982429
pubmed: 31982429
pii: S0022-2828(20)30005-5
doi: 10.1016/j.yjmcc.2019.12.011
pii:
doi:

Substances chimiques

Cathelicidins 0
Inflammasomes 0
NLR Family, Pyrin Domain-Containing 3 Protein 0
Receptors, Purinergic P2X7 0
Toll-Like Receptor 4 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

75-86

Subventions

Organisme : NIDDK NIH HHS
ID : R01 DK100697
Pays : United States

Informations de copyright

Copyright © 2020 Elsevier Ltd. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest None declared.

Auteurs

Yan Wu (Y)

Department of Metabolism and Endocrinology, the Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China; National Clinical Research Center for Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, Metabolic Syndrome Research Center, the Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.

Yacheng Zhang (Y)

Department of Metabolism and Endocrinology, the Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China; National Clinical Research Center for Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, Metabolic Syndrome Research Center, the Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.

Jie Zhang (J)

Department of Metabolism and Endocrinology, the Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China; National Clinical Research Center for Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, Metabolic Syndrome Research Center, the Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.

Tingting Zhai (T)

Department of Metabolism and Endocrinology, the Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China; National Clinical Research Center for Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, Metabolic Syndrome Research Center, the Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.

Jingping Hu (J)

Department of Metabolism and Endocrinology, the Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China; National Clinical Research Center for Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, Metabolic Syndrome Research Center, the Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.

Hairong Luo (H)

Department of Metabolism and Endocrinology, the Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China; National Clinical Research Center for Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, Metabolic Syndrome Research Center, the Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.

Haiyan Zhou (H)

Department of Metabolism and Endocrinology, the Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China; National Clinical Research Center for Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, Metabolic Syndrome Research Center, the Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.

Qinghai Zhang (Q)

Department of Metabolism and Endocrinology, the Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China; National Clinical Research Center for Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, Metabolic Syndrome Research Center, the Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.

Zhiguang Zhou (Z)

Department of Metabolism and Endocrinology, the Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China; National Clinical Research Center for Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, Metabolic Syndrome Research Center, the Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China. Electronic address: zhouzhiguang@csu.edu.cn.

Feng Liu (F)

Department of Metabolism and Endocrinology, the Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China; National Clinical Research Center for Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, Metabolic Syndrome Research Center, the Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China; Department of Pharmacology, University of Texas at San Antonio, San Antonio, TX 78229, USA. Electronic address: liuf@uthscsa.edu.

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Classifications MeSH

questionsmedicales.fr › Eucaryotes › Animaux › Cathelicidin aggravates myocardial...
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines membranaires › Perforines › Peptides antimicrobiens cationiques › Cathélicidines › Cathelicidin aggravates myocardial...
questionsmedicales.fr › Structures macromoléculaires › Complexes multiprotéiques › Inflammasomes › Cathelicidin aggravates myocardial...
questionsmedicales.fr › États, signes et symptômes pathologiques › Processus pathologiques › Inflammation › Cathelicidin aggravates myocardial...
questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Rodentia › Muridae › Murinae › Souris › Lignées consanguines de souris › Souris de lignée C57BL › Cathelicidin aggravates myocardial...
questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Rodentia › Muridae › Murinae › Souris › Souris transgéniques › Souris knockout › Cathelicidin aggravates myocardial...
questionsmedicales.fr › États, signes et symptômes pathologiques › Processus pathologiques › Complications postopératoires › Lésion d'ischémie-reperfusion › Lésion de reperfusion myocardique › Cathelicidin aggravates myocardial...
questionsmedicales.fr › Tissus › Muscles › Muscle strié › Myocarde › Cathelicidin aggravates myocardial...
questionsmedicales.fr › Acides aminés, peptides et protéines › Peptides › Protéines NLR › Protéine-3 de la famille des NLR contenant un domaine pyrine › Cathelicidin aggravates myocardial...
questionsmedicales.fr › Phénomènes du système immunitaire › Infiltration par les neutrophiles › Cathelicidin aggravates myocardial...
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines membranaires › Récepteurs de surface cellulaire › Récepteurs aux neuromédiateurs › Récepteurs purinergiques › Récepteurs purinergiques P2 › Récepteurs purinergiques P2X › Récepteurs purinergiques P2X7 › Cathelicidin aggravates myocardial...
questionsmedicales.fr › Phénomènes physiologiques cellulaires › Transduction du signal › Cathelicidin aggravates myocardial...
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines membranaires › Récepteurs de surface cellulaire › Récepteurs immunologiques › Récepteurs de reconnaissance de motifs moléculaires › Récepteurs de type Toll › Récepteur de type Toll-4 › Cathelicidin aggravates myocardial...