PMID- 28006695 OWN - NLM STAT- MEDLINE DCOM- 20170321 LR - 20170321 IS - 1879-1336 (Electronic) IS - 1054-8807 (Linking) VI - 27 DP - 2017 Mar-Apr TI - Role of atrial endothelial cells in the development of atrial fibrosis and fibrillation in response to pressure overload. PG - 18-25 LID - S1054-8807(16)30118-1 [pii] LID - 10.1016/j.carpath.2016.12.001 [doi] AB - BACKGROUND: Monocyte chemoattractant protein-1 (MCP-1)-mediated inflammatory mechanisms have been shown to play a crucial role in atrial fibrosis induced by pressure overload. In the present study, we investigated whether left atrial endothelial cells would quickly respond structurally and functionally to pressure overload to trigger atrial fibrosis and fibrillation. METHODS AND RESULTS: Six-week-old male Sprague-Dawley rats underwent suprarenal abdominal aortic constriction (AAC) or a sham operation. By day 3 after surgery, macrophages were observed to infiltrate into the endocardium. The expression of MCP-1 and E-selectin in atrial endothelium and the expression of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and ED1 in left atrial tissue were enhanced. Atrial endothelial cells were irregularly hypertrophied with the disarrangement of lines of cells by scanning electron microscopy. Various-sized gap formations appeared along the border in atrial endothelial cells, and several macrophages were located just in the endothelial gap. Along with the development of heterogeneous interstitial fibrosis, interatrial conduction time was prolonged and the inducibility of atrial fibrillation by programmed extrastimuli was increased in the AAC rats compared to the sham-operated rats. CONCLUSIONS: Atrial endothelium responds rapidly to pressure overload by expressing adhesion molecules and MCP-1, which induce macrophage infiltration into the atrial tissues. These processes could be an initial step in the development of atrial remodeling for atrial fibrillation. CI - Copyright (c) 2016 Elsevier Inc. All rights reserved. FAU - Kume, Osamu AU - Kume O AD - Department of Cardiology and Clinical Examination, Faculty of Medicine, Oita University, Oita, Japan. FAU - Teshima, Yasushi AU - Teshima Y AD - Department of Cardiology and Clinical Examination, Faculty of Medicine, Oita University, Oita, Japan. Electronic address: teshima@oita-u.ac.jp. FAU - Abe, Ichitaro AU - Abe I AD - Department of Cardiology and Clinical Examination, Faculty of Medicine, Oita University, Oita, Japan. FAU - Ikebe, Yuki AU - Ikebe Y AD - Department of Cardiology and Clinical Examination, Faculty of Medicine, Oita University, Oita, Japan. FAU - Oniki, Takahiro AU - Oniki T AD - Department of Cardiology and Clinical Examination, Faculty of Medicine, Oita University, Oita, Japan. FAU - Kondo, Hidekazu AU - Kondo H AD - Department of Cardiology and Clinical Examination, Faculty of Medicine, Oita University, Oita, Japan. FAU - Saito, Shotaro AU - Saito S AD - Department of Cardiology and Clinical Examination, Faculty of Medicine, Oita University, Oita, Japan. FAU - Fukui, Akira AU - Fukui A AD - Department of Cardiology and Clinical Examination, Faculty of Medicine, Oita University, Oita, Japan. FAU - Yufu, Kunio AU - Yufu K AD - Department of Cardiology and Clinical Examination, Faculty of Medicine, Oita University, Oita, Japan. FAU - Miura, Masahiro AU - Miura M AD - Department of Human Anatomy, Faculty of Medicine, Oita University, Oita, Japan. FAU - Shimada, Tatsuo AU - Shimada T AD - College of Judo Therapy and Acupuncture-Moxibustion, Oita Medical Technology School, Oita, Japan. FAU - Takahashi, Naohiko AU - Takahashi N AD - Department of Cardiology and Clinical Examination, Faculty of Medicine, Oita University, Oita, Japan. LA - eng PT - Journal Article DEP - 20161215 PL - United States TA - Cardiovasc Pathol JT - Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology JID - 9212060 SB - IM MH - Animals MH - Atrial Fibrillation/*pathology MH - Blotting, Western MH - Disease Models, Animal MH - Endothelial Cells/*pathology MH - Enzyme-Linked Immunosorbent Assay MH - Fibrosis/pathology MH - Heart Atria/*pathology MH - Hypertension/complications MH - Immunohistochemistry MH - Isolated Heart Preparation MH - Male MH - Microscopy, Electron, Scanning MH - Rats MH - Rats, Sprague-Dawley OTO - NOTNLM OT - Atrial fibrillation OT - Endothelium OT - Fibrosis OT - Inflammation OT - Pressure overload EDAT- 2016/12/23 06:00 MHDA- 2017/03/23 06:00 CRDT- 2016/12/23 06:00 PHST- 2016/09/07 00:00 [received] PHST- 2016/11/09 00:00 [revised] PHST- 2016/12/06 00:00 [accepted] PHST- 2016/12/23 06:00 [pubmed] PHST- 2017/03/23 06:00 [medline] PHST- 2016/12/23 06:00 [entrez] AID - S1054-8807(16)30118-1 [pii] AID - 10.1016/j.carpath.2016.12.001 [doi] PST - ppublish SO - Cardiovasc Pathol. 2017 Mar-Apr;27:18-25. doi: 10.1016/j.carpath.2016.12.001. Epub 2016 Dec 15.