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单位：西安交通大学第二附属医院

研究方向：急诊医学

社会任职
西安交通大学第二附属医院急诊科/急诊ICU副主任医师、副教授。曾于2011年赴台湾阳明大学医学院、台北荣民总医院交流访问。从事急诊医学临床工作十余年，近年来，致力于急性胰腺炎、心脏损伤、心肺复苏、急性中毒、急危重症救治技术相关研究，对各种急危重症疾病的救治有丰富经验，擅长重症急性胰腺炎、心脏损伤、MODS等的救治。主持科研项目11项，参与多项；以第一作者或通讯作者发表SCI论文19篇、中文核心期刊收录论文32篇。以第2完成人获陕西高等学校科学技术研究优秀成果奖二等奖1项。获国家发明专利授权1项。出版专著11部，其中主编专著4部、副主编专著3部（人民卫生出版社1部）；主编科普著作2部；参编规划教材2部，其中主编1部。

个人介绍
中华医学会急诊分会临床研究学组委员，中国医师协会急诊分会急诊信息化建设与智慧医疗专委会委员，中国医教协会急诊专委会委员，中国医教协会县域医共体急救医学工作委员会常委，中国药学会应急与保障专委会委员，海医会急诊分会青委会委员，陕西省医学会院前急救分会委员，陕西省临床医学工程学会急诊急救工程专委会常务副主委兼秘书长，陕西省研究型医院学会青委会常委，陕西省医学传播学会急诊急救专委会副主委，陕西省医促会急救与复苏专委会副主委。教育部同等学力研究生考试命题专家。中国医学传播学教学联盟副秘书长。中国科普作家协会医学科普创作专委会委员。《World Journal of Emergency Medicine》编委；《中华急诊医学杂志》通讯编委；《中国全科医学》青年编委；《中国急救医学》编委；《现代生物医学进展》常务编委；《中南大学学报（医学版）》、《临床与病理杂志》中青年编委；《实用心脑肺血管病杂志》编委；《实用医学杂志》、《心肺血管病杂志》、《临床医学研究与实践》青年编委；《疑难病杂志》通讯编委

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1. Interfering hsa_circ_0073748 alleviates caerulein-induced ductal cell injury in acute pancreatitis by inhibiting miR-132-3p/TRAF3/NF-κB pathway

[学者论文] RS评分：0

作者： Song Ren, Longfei Pan, Linqing Yang, Zequn Niu, Liming Wang, Yanxia Gao, Jie Liu, Zhong Liu, Honghong Pei

《Cell Cycle》2022年 21卷 2期

摘要：Circular RNA hsa_circ_0073748 (circ_0073748) is upregulated in patients with acute pancreatitis (AP), a clinically common sudden inflammatory response. MicroRNA (miR)-132-3p is a stressinduced factor with high conservation between species. Herein, expression and role of circ_0073748 and miR-132-3p in caerulein-induced pancreatitis were studied. Expression levels of circ_0073748, miR-132-3p, TNF receptor associated factor 3 (TRAF3), Bcl-2 and Bcl-2-associated X protein (Bax) were examined by reverse transcription-quantitative PCR and Western blotting. Cell proliferation was measured by MTS and EdU assays. Flow cytometry and assay kits detected apoptosis, inflammatory, and oxidative responses. Western blotting detected nuclear factor (NF)-κB signaling pathway. Circ_0073748 was upregulated and miR-132-3p was downregulated in AP patients’ plasma and human pancreatic ductal HPDE6-C7 cells with caerulein induction. Interfering circ_0073748 and reinforcing miR-132-3p improved cell viability, EdU incorporation, and superoxide dismutase (SOD) activity of caerulein-treated HPDE6-C7 cells but suppressed malonaldehyde (MDA), IL-6 and TNF-α levels and apoptosis rate. Moreover, TRAF3 downregulation was allied with circ_0073748 silencing and miR-132-3p overexpression in caerulein-induced HPDE6-C7 cells. Mechanically, circ_0073748 was identified as a sponge for miR-132-3p to modulate TRAF3 expression, thus establishing a competitive endogenous RNA (ceRNA) regulation model. Notably, circ_0073748 blockage could suppress expressions of phosphorylated P65 (p-P65) and p-IκB in caerulein-induced HPDE6-C7 cells by promoting miR-132-3p and inhibiting TRAF3. Silencing circ_0073748 and upregulating miR-132-3p could alleviate caerulein-induced HPDE6-C7 injury and inactivate canonical NF-κB signal by inhibiting TRAF3. Circ_0073748/miR-132-3p/TRAF3 ceRNA pathway might be one underlying mechanism and therapeutic target of caeruleininduced AP.

关键词：circ_0073748m, miR-132-3p, TRAF3, acute pancreatitis, NF-κB pathway

浏览量: 310 下载: 0 发表时间：2021/12/1 0:00:00

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2. MALAT1 shuttled by extracellular vesicles promotes M1 polarization of macrophages to induce acute pancreatitis via miR-181a-5p/HMGB1 axis

[学者论文] RS评分：0

作者： Jie Liu, Zequn Niu, Rui Zhang, Zhuo Peng, Liming Wang, Zhong Liu, Yanxia Gao, Honghong Pei, Longfei Pan

《Journal of Cellular and Molecular Medicine》2021年 25卷 19期

摘要：Acute pancreatitis (AP) is a serious condition carrying a mortality of 25–40%.Extracellular vesicles (EVs) have reported to exert potential functions in cell-to-cell communication in diseases such as pancreatitis. Thus, we aimed at investigating the mechanisms by which EV-encapsulated metastasis-associated lung adenocarcinoma transcript-1 (MALAT1) might mediate the M1 polarization of macrophages in AP. Expression patterns of MALAT1, microRNA-181a-5p (miR-181a-5p) and high-mobility group box 1 protein (HMGB1) in serum of AP patients were determined.EVs were isolated from serum and pancreatic cells. The binding affinity among miR-181a-5p, MALAT1 and HMGB1 was identified. AP cells were co-cultured with EVs from caerulein-treated MPC-83 cells to determine the levels of M1/2 polarization markers and TLR4, NF-κB and IKBa. Finally, AP mouse models were established to study the effects of EV-encapsulated MALAT1 on the M1 polarization of macrophages in AP in vivo. MALAT1 was transferred into MPC-83 cells via EVs, which promoted M1 polarization of macrophages in AP. MALAT1 competitively bound to miR-181a-5p, which targeted HMGB1. Moreover, MALAT1 activated the TLR4 signalling pathway by regulating HMGB1. EV-encapsulated MALAT1 competitively bound to miR-181a-5p to upregulate the levels of IL-6 and TNF-α by regulating HMGB1 via activation of the TLR4 signalling pathway, thereby inducing M1 polarization of macrophages in AP. In vivo experimental results also confirmed that MALAT1 shuttled by EVs promoted M1 polarization of macrophages in AP via the miR-181a-5p/HMGB1/TLR4 axis. Overall, EV-loaded MALAT1 facilitated M1 polarization of macrophages in AP via miR-181a-5p/HMGB1/TLR4, highlighting a potential target for treating AP.

关键词：acute pancreatitis, extracellular vesicles, high-mobility group box 1 protein, long non-coding RNA, M1 polarization of macrophages, metastasis-associated lung adenocarcinoma transcript-1,microRNA-181a-5p

浏览量: 316 下载: 0 发表时间：2021/8/27 0:00:00

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3. miR-29a-3p transferred by mesenchymal stem cells-derived extracellular vesicles protects against myocardial injury after severe acute pancreatitis

[学者论文] RS评分：0

作者： Song Ren, Longfei Pan, Linqing Yang, Zequn Niu, Liming Wang, Hui Feng, Miao Yuan

《Life Sciences》2021年 272卷期

摘要：Aims: Acute pancreatitis (AP) is an inflammatory disease of the pancreas that may affect local tissues or remote organ systems, while severe acute pancreatitis (SAP) is a life-threatening disorder associated with multiple organ failure. In this investigation, we set about to determine whether microRNA-29a-3p (miR-29a-3p) carried by mesenchymal stem cell (MSCs)-derived extracellular vesicles (EVs) affects the myocardial injury during SAP. Main methods: EVs were isolated from MSCs of rat bone marrow by differential centrifugation. An SAP rat model was developed and treated with MSCs-EVs and/or alteration of miR-29a-3p and HMGB1 expression, followed by assessment of the rats’ cardiac function and inflammation. Next, cardiomyocytes H9C2 were co-cultured with MSC-EVs and internalization of EVs was evaluated, followed by evaluation of whether EVs could transmit miR- 29a-3p cargos into H9C2 cells and affect their biological functions. Key findings: EVs derived from MSCs were observed to protect against SAP-induced myocardial injury. In SAPinduced rats, miR-29a-3p was under-expressed in myocardial tissues. In addition, we also confirmed that miR- 29a-3p could be transferred into the H9C2 cardiomyocytes by MSC-derived EVs, which downregulated the expression of inflammatory markers and improve cardiac function to attenuate myocardial injury. Furthermore, miR-29a-3p inhibited the expression of HMGB1 to downregulate TLR4 expression and further inactivate the Akt signaling pathway. Significance: These findings support the cardioprotective action of miR-29a-3p transmitted by MSCs-derived EVs in SAP-induced myocardial injury via downregulation of the HMGB1/TLR4/Akt axis, highlighting a promising target for the EV-based therapy for SAP.

关键词：Mesenchymal stem cells, Extracellular vesicles, microRNA-29a-3p, High mobility group box 1 protein, Toll-like receptor 4, Protein kinase B, Severe acute pancreatitis, Myocardial injury

浏览量: 281 下载: 0 发表时间：2021/2/1 0:00:00

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1. Interfering hsa_circ_0073748 alleviates caerulein-induced ductal cell injury in acute pancreatitis by inhibiting miR-132-3p/TRAF3/NF-κB pathway

2. MALAT1 shuttled by extracellular vesicles promotes M1 polarization of macrophages to induce acute pancreatitis via miR-181a-5p/HMGB1 axis

3. miR-29a-3p transferred by mesenchymal stem cells-derived extracellular vesicles protects against myocardial injury after severe acute pancreatitis