PMID- 33459958 OWN - NLM STAT- MEDLINE DCOM- 20210525 LR - 20210525 IS - 1573-4978 (Electronic) IS - 0301-4851 (Linking) VI - 48 IP - 1 DP - 2021 Jan TI - Resolvin D1 and E1 promote resolution of inflammation in rat cardiac fibroblast in vitro. PG - 57-66 LID - 10.1007/s11033-020-06133-8 [doi] AB - Cardiac fibroblasts (CFs) have a key role in the inflammatory response after cardiac injury and are necessary for wound healing. Resolvins are potent agonists that control the duration and magnitude of inflammation. They decrease mediators of pro-inflammatory expression, reduce neutrophil migration to inflammation sites, promote the removal of microbes and apoptotic cells, and reduce exudate. However, whether resolvins can prevent pro-inflammatory-dependent effects in CFs is unknown. Thus, the present work was addressed to study whether resolvin D1 and E1 (RvD1 and RvE1) can prevent pro-inflammatory effects on CFs after lipopolysaccharide (LPS) challenge. For this, CFs were stimulated with LPS, in the presence or absence of RvD1 or RvE1, to analyze its effects on intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion protein 1 (VCAM-1), monocyte adhesion and the cytokine levels of tumor necrosis factor alpha (TNF-alpha), interleukin-6(IL-6), interleukin-1beta (IL-1beta), monocyte chemoattractant protein-1 (MCP-1) and interleukin-10 (IL-10). Our results showed that CFs are expressing ALX/FPR2 and ChemR23, RvD1 and RvE1 receptors, respectively. RvD1 and RvE1 prevent the increase of ICAM-1 and VCAM-1 protein levels and the adhesion of spleen mononuclear cells to CFs induced by LPS. Finally, RvD1, but not RvE1, prevents the LPS-induced increase of IL-6, MCP-1, TNF-alpha, and IL-10. In conclusion, our findings provide evidence that in CFs, RvD1 and RvE1 might actively participate in the prevention of inflammatory response triggered by LPS. FAU - Salas-Hernandez, Aimee AU - Salas-Hernandez A AD - Department of Chemical Pharmacology and Toxicology, Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santos Dumont 964, Independencia, Santiago, Chile. AD - Department of Pharmacology, Toxicology and Pharmacodependence, Pharmacy Faculty, University of Costa Rica, San Jose, Costa Rica. FAU - Espinoza-Perez, Claudio AU - Espinoza-Perez C AD - Department of Chemical Pharmacology and Toxicology, Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santos Dumont 964, Independencia, Santiago, Chile. FAU - Vivar, Raul AU - Vivar R AD - Pharmacology Program, Biomedical Sciences Institute, University of Chile, Independencia 1027, Independencia, Santiago, Chile. FAU - Espitia-Corredor, Jenaro AU - Espitia-Corredor J AD - Department of Chemical Pharmacology and Toxicology, Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santos Dumont 964, Independencia, Santiago, Chile. FAU - Lillo, Jose AU - Lillo J AD - Department of Chemical Pharmacology and Toxicology, Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santos Dumont 964, Independencia, Santiago, Chile. FAU - Parra-Flores, Pablo AU - Parra-Flores P AD - Department of Chemical Pharmacology and Toxicology, Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santos Dumont 964, Independencia, Santiago, Chile. FAU - Sanchez-Ferrer, Carlos F AU - Sanchez-Ferrer CF AD - Department of Pharmacology, Faculty of Medicine, Universidad Autonoma de Madrid and Instituto de Investigacion Sanitaria Hospital Universitario La Paz (IdiPAZ), Madrid, Spain. FAU - Peiro, Concepcion AU - Peiro C AD - Department of Pharmacology, Faculty of Medicine, Universidad Autonoma de Madrid and Instituto de Investigacion Sanitaria Hospital Universitario La Paz (IdiPAZ), Madrid, Spain. FAU - Diaz-Araya, Guillermo AU - Diaz-Araya G AUID- ORCID: 0000-0001-7960-8104 AD - Department of Chemical Pharmacology and Toxicology, Faculty of Chemical and Pharmaceutical Sciences, University of Chile, Santos Dumont 964, Independencia, Santiago, Chile. gadiaz@ciq.uchile.cl. AD - Advanced Center for Chronic Diseases (ACCDiS), Faculty of Chemical and Pharmaceutical Sciences and Faculty of Medicine, University of Chile, Santos Dumont 964, Independencia, Santiago, Chile. gadiaz@ciq.uchile.cl. LA - eng GR - 1170425/fondecyt/ GR - OAICE-CAB-03-031-2015/Universidad de Costa Rica/ PT - Journal Article DEP - 20210118 PL - Netherlands TA - Mol Biol Rep JT - Molecular biology reports JID - 0403234 RN - 0 (Cytokines) RN - 0 (IL1B protein, human) RN - 0 (Interleukin-1beta) RN - 0 (Lipopolysaccharides) RN - 0 (Tumor Necrosis Factor-alpha) RN - 0 (Vascular Cell Adhesion Molecule-1) RN - 0 (resolvin D1) RN - 25167-62-8 (Docosahexaenoic Acids) RN - AAN7QOV9EA (Eicosapentaenoic Acid) RN - GND3JH08JA (5S,12R,18R-trihydroxy-6Z,8E,10E,14Z,16E-eicosapentaenoic acid) SB - IM MH - Animals MH - Cell Movement/drug effects MH - Cytokines/genetics MH - Docosahexaenoic Acids/*pharmacology MH - Eicosapentaenoic Acid/*analogs & derivatives/pharmacology MH - Fibroblasts/drug effects MH - Gene Expression Regulation/drug effects MH - Heart Injuries/chemically induced/*drug therapy/pathology MH - Humans MH - Inflammation/chemically induced/*drug therapy/pathology MH - Interleukin-1beta/genetics MH - Lipopolysaccharides/toxicity MH - Neutrophils/drug effects MH - Rats MH - Tumor Necrosis Factor-alpha/genetics MH - Vascular Cell Adhesion Molecule-1/genetics MH - Wound Healing/drug effects OTO - NOTNLM OT - Cardiac fibroblasts OT - Cytokines OT - Resolvin D1 OT - Resolvin E1 EDAT- 2021/01/19 06:00 MHDA- 2021/05/26 06:00 CRDT- 2021/01/18 12:17 PHST- 2020/09/19 00:00 [received] PHST- 2020/12/24 00:00 [accepted] PHST- 2021/01/19 06:00 [pubmed] PHST- 2021/05/26 06:00 [medline] PHST- 2021/01/18 12:17 [entrez] AID - 10.1007/s11033-020-06133-8 [pii] AID - 10.1007/s11033-020-06133-8 [doi] PST - ppublish SO - Mol Biol Rep. 2021 Jan;48(1):57-66. doi: 10.1007/s11033-020-06133-8. Epub 2021 Jan 18.