{ "labelLang" : "hun", "responseDate" : "2024-03-28 17:06", "content" : { "otype" : "JournalArticle", "mtid" : 31595203, "status" : "VALIDATED", "published" : true, "comment" : "State Key Laboratory for Bioactive Substances and Functions of Natural Medicines, Beijing Key Laboratory of New Drug Mechanisms and Pharmacological Evaluation Study, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing, China \n Department of Cardiology, State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing, China \n Center of Translational Mongolian Medicine, Inner Mongolia Hospital of International Mongolian Medicine, Hohhot, Inner Mongolia, China \n Department of Clinical Pharmacy, Institute of Pharmacy, Inner Mongolia Medical University, Hohhot, Inner Mongolia, China \n Beijing Institute of Genomics, Chinese Academy of SciencesBeijing, China \n Export Date: 8 September 2020 \n CODEN: ATHSB \n Correspondence Address: Zhu, H.; State Key Laboratory for Bioactive Substances and Functions of Natural Medicines, Beijing Key Laboratory of New Drug Mechanisms and Pharmacological Evaluation Study, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, State Key Laboratory of Cardiovascular Disease, Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, No.2A, Nanwei Road, Xicheng District, China; email: zhuhaibo@imm.ac.cn \n Funding details: 2018ZX09711001-003-011 \n Funding details: CIFMS 2016-I2M-1-009 \n Funding details: National Natural Science Foundation of China, NSFC, 91539126, 201920200807 \n Funding text 1: This work was supported by funding support from CAMS Innovation Fund for Medical Sciences [ CIFMS 2016-I2M-1-009 ], The Drug Innovation Major Project [grant number 2018ZX09711001-003-011 ], The National Natural Sciences Foundation of China (NSFC) [grant number 91539126 ], and Disciplines construction project for multi-omics pharmacology [grant number 201920200807 ].\nFunding Agency and Grant Number: CAMS Innovation Fund for Medical Sciences [CIFMS 2016-I2M-1-009]; Drug Innovation Major Project [2018ZX09711001-003-011]; National Natural Sciences Foundation of China (NSFC)National Natural Science Foundation of China (NSFC) [91539126]; Disciplines construction project for multiomics pharmacology [201920200807]\n Funding text: This work was supported by funding support from CAMS Innovation Fund for Medical Sciences [CIFMS 2016-I2M-1-009], The Drug Innovation Major Project [grant number 2018ZX09711001-003-011], The National Natural Sciences Foundation of China (NSFC) [grant number 91539126], and Disciplines construction project for multiomics pharmacology [grant number 201920200807].", "unhandledTickets" : 0, "deleted" : false, 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The present study was designed to characterise a new transmembrane protein—NFAT activating protein with ITAM motif 1 (NFAM1)—on monocytes and uncover the potential effects and underlying mechanisms in coronary artery disease. Methods: Monocytes from a population of four controls, five stable coronary artery disease patients and five acute coronary syndrome patients were isolated for RNA sequencing. A potential monocyte biomarker molecule was discovered and then validated with a group of 79 controls, 70 stable coronary artery disease patients and 183 acute coronary syndrome patients. A stable cell line was generated as an in vitro model to determine chemotaxis migration and chemokine receptor expression. Results: NFAM1 was identified through RNA sequencing analysis. The validation results confirmed that NFAM1 expression on monocytes was significantly increased by coronary artery disease status. A higher expression level of NFAM1 on classical and intermediate monocytes was observed compared with that on nonclassical monocytes. As shown in the in vitro cell model, knockdown of NFAM1 significantly attenuated chemotactic migration of monocytes by downregulating chemokine receptor expression and the p38 MAPK signalling pathway. Multivariable regression analysis of a group of 16 individuals suggested that NFAM1 was positively correlated with CCR2 expression. 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