Chun Liang

Shanghai Changzheng Hospital

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Zhiqing He

Shanghai Changzheng Hospital

Zonggui Wu

Second Military Medical University

Ru Ding

Chengdu University of Traditional Chinese Medicine

Feng Wu

China Medical University

Jian Zhao

Chinese PLA General Hospital

Yangxin Li

Soochow University

Yanda Zhang

Lamont-Doherty Earth Observatory

Yusheng Ren

East China University of Science and Technology

Xiangbin Pan

Chinese Academy of Medical Sciences & Peking Union Medical College

Xianliang Dai

Second Military Medical University

Cooperative Institutions

Second Military Medical University

Shanghai Changzheng Hospital

Shanghai Jiao Tong University

Soochow University

Chinese Academy of Medical Sciences & Peking Union Medical College

Fudan University

Sun Yat-sen University

First Affiliated Hospital of Soochow University

Chinese Academy of Sciences

Huazhong University of Science and Technology

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Mechanisms in hypertension and target organ damage: Is the role of the thymus key? (Review)

International Journal of Molecular Medicine (2018)

Xianliang Dai Li Hua Yihong Chen Jiamei Wang Jingyi Li

A variety of cells and cytokines have been shown to be involved in the whole process of hypertension. Data from experimental and clinical studies on hypertension have confirmed the key roles of immune cells and inflammation in the process. Dysfunction of the thymus, which modulates the development and maturation of lymphocytes, has been shown to be associated with the severity of hypertension. Furthermore, gradual atrophy, functional decline or loss of the thymus has been revealed to be associated with aging. The restoration or enhancement of thymus function via upregulation in the expression of thymus transcription factors forkhead box N1 or thymus transplantation may provide an option to halt or reverse the pathological process of hypertension. Therefore, the thymus may be key in hypertension and associated target organ damage, and may provide a novel treatment strategy for the clinical management of patients with hypertension in addition to different commercial drugs. The purpose of this review is to summarize and discuss the advances in our understanding of the impact of thymus function on hypertension from data from animal and human studies, and the potential mechanisms.

10.3892/ijmm.2018.3605

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Citations (16)

Vitamin E ameliorates ox-LDL-induced foam cells formation through modulating the activities of oxidative stress-induced NF-κB pathway

Molecular and Cellular Biochemistry (2011)

Zhigang Huang Chun Liang Shu-fang Han Zonggui Wu

Foam cell

U937 cell

10.1007/s11010-011-1153-2

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Citations (31)

Stem Cell-Derived Exosomes Prevent Aging-Induced Cardiac Dysfunction through a Novel Exosome/lncRNA MALAT1/NF-κB/TNF-α Signaling Pathway

Oxidative Medicine and Cellular Longevity (2019)

Bao Zhu Lulu Zhang Chun Liang Bin Liu Xiangbin Pan

Aging is a risk factor for cardiovascular disease, and there is no effective therapeutic approach to alleviate this condition. NF-κB and TNF-α have been implicated in the activation of the aging process, but the signaling molecules responsible for the inactivation of NF-κB and TNF-α remain unknown. Exosomes have been reported to improve heart functions by releasing miRNA. Recent studies suggest that lncRNAs are more tissue-specific and developmental stage-specific compared to miRNA. However, the role of lncRNA in exosome-mediated cardiac repair has not been explored. In the present study, we focused on metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), which is an lncRNA associated with cell senescence. We discovered that human umbilical cord mesenchymal stem cell- (UMSC-) derived exosomes prevent aging-induced cardiac dysfunction. Silencer RNA against lncRNA MALAT1 blocked the beneficial effects of exosomes. In summary, we discovered that UMSC-derived exosomes prevent aging-induced cardiac dysfunction by releasing novel lncRNA MALAT1, which in turn inhibits the NF-κB/TNF-α signaling pathway. These findings will lead to the development of therapies that delay aging and progression of age-related diseases.

MALAT1

Exosome

10.1155/2019/9739258

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Citations (99)

Effects of Intracoronary Pro-urokinase or Tirofiban on Coronary Flow During Primary Percutaneous Coronary Intervention for Acute Myocardial Infarction: A Multi-Center, Placebo-Controlled, Single-Blind, Randomized Clinical Trial

Frontiers in Cardiovascular Medicine (2021)

Dong Huang Juying Qian Zongjun Liu Yawei Xu Xianxian Zhao

Background: To determine whether intracoronary pro-urokinase or tirofiban improves myocardial reperfusion during primary percutaneous coronary intervention (PCI) for acute ST-segment elevation myocardial infarction (STEMI). Methods: The study included patients with acute STEMI presenting within 12 h of symptoms at 11 hospitals in China between November 2015 and July 2017. Patients were randomized to receive selective intracoronary infusion of recombinant pro-urokinase (20 mg), tirofiban (10 μg/kg), or saline (20 mL) proximal to the infarct-related lesion over a 3-min period before stent implantation during primary PCI. The primary outcome was final corrected thrombolysis in myocardial infarction (TIMI) frame count (CTFC) after PCI. Results: This study included 345 patients. Initial angiography identified a high-grade thrombus (TIMI 4–5) in 80% of patients. Final CTFC after PCI was significantly lower in the pro-urokinase ( P < 0.001) and tirofiban ( P < 0.001) groups than in the saline group and similar between the pro-urokinase and tirofiban groups ( P > 0.05). The pro-urokinase ( P = 0.008) and tirofiban groups ( P = 0.022) had more complete ST-segment resolution at 2 h and lower peak creatine kinase-MB levels after PCI than the saline group ( P = 0.006 and P = 0.023). The 30-day incidence of major adverse cardiac events was 4.5% in the pro-urokinase group, 3.4% in the tirofiban group, and 2.6% in the saline group. The incidence of in-hospital TIMI major bleeding events was low and comparable between groups. Conclusions: Adjunctive intracoronary pro-urokinase or tirofiban given before stent implantation during primary PCI improves myocardial reperfusion without increasing the incidence of major bleeding events.

Tirofiban

TIMI

10.3389/fcvm.2021.710994

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Citations (16)

The Disposition and Management Strategy of Decommissioning Offshore Oil Platform in Chengdao, China

Energy Procedia (2011)

Jiang Luqing Zheng Xilai Chun Liang Feng Yue Junjie Zhang

The case study of disposition and management of decommissioning offshore oil platform hasn't reported completely in China so far. In this paper, the disposition and management strategy of decommissioning platforms was proposed and discussed for Chengdao offshore oilfield of China. By partial removal and reefing platform, the decommissioning oil platforms will be converted into artificial reefs with integrated functions such as resource enrichment, zoology recovery and entertainment. This strategy will provide valuable experiences for reasonable disposition of decommissioning offshore oil platform in China.

Nuclear decommissioning

Disposition

10.1016/j.egypro.2011.03.091

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Citations (3)

Correction: Network pharmacology for the identification of phytochemicals in traditional Chinese medicine for COVID-19 that may regulate interleukin-6

Bioscience Reports (2021)

Wenhao Niu Feng Wu Wen-Yue Cao Zonggui Wu Yu-Chieh Chao

The authors of the original article “Network pharmacology for the identification of phytochemicals in traditional Chinese medicine for COVID-19 that may regulate interleukin-6” (Biosci Rep (2021) 41(1), https://doi.org/10.1042/BSR20202583) would like to correct the authorship of their article. The co-corresponding author Fei Peng had been removed from the main authorship line at proof by the author erroneously, though Fei Peng was still listed as a correspondence.The correct authorship list is therefore as follows:Wen-hao Niu1, Feng Wu2, Wen-yue Cao3, Zong-gui Wu1, Yu-Chieh Chao4, Fei Peng5 and Chun Liang11Department of Cardiology, Shanghai Changzheng Hospital, Naval Medical University, Shanghai 200001, China; 2Department of Cardiology, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Affiliated hospital of Shanghai University of Traditional Chinese Medicine, Shanghai 200080, China; 3Department of Ultrasound, Shanghai Chest Hospital, Shanghai Jiaotong University, Shanghai 200030, China; 4Department of Anesthesiology, Shanghai Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200120, China; 5Department of Nursing, Shanghai Changzheng Hospital, Naval Medical University, Shanghai 200001, China.The live manuscript was corrected 23 February 2021.

Identification

10.1042/bsr-20202583_cor

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Homocysteine upregulates angiotensin Ⅱ receptor type 1 (AT1R) expression via activating ERK1/2 signaling pathway in rat vascular smooth muscle cells

Academic Journal of Second Military Medical University (2014)

Heng Jiang Manli Yu Yong Wei Ping Ouyang Chun Liang

10.3724/sp.j.1008.2014.00968

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GW24-e2104 Epinephrine enhanced LPS-induced pro-inflammatory cytokines release by BMMCs: a cross-talking between catecholamine, circadian rhythm and inflammation

Heart (2013)

Huang Xiao Chun Liang Zhao Xinna Zhiqing He Zonggui Wu

Objectives

Occurring of acute coronary syndromes (ACSs) displayed circadian rhythms as well as the levels of catecholamines and pro-inflammatory cytokines in vivo. Such circadian rhythms were proved to exist also in mast cells which secreted plenty of pro-inflammatory cytokines and accumulated in the shoulder region of human coronary atherosclerosis plaques. Rev-erb α, a circadian rhythm modulating molecular, has been shown to modulate the release of pro-inflammatory cytokines in vitro and in vivo. Interestingly, an enhancing effect of epinephrine on pro-inflammatory cytokine release has been observed recently in human gingival fibroblasts. We hypothesised that there might be an cross-talking between catecholamine and circadian rhythm which could modulate production of pro-inflammatory cytokines in mast cells. We investigated whether epinephrine affects pro-inflammatory cytokines released from mast cells and whether rev-erb α modulates pro-inflammatory cytokines production in mast cells.

Methods

Cultured murine bone marrow derived mast cells (BMMCs) were stimulated by lipopolysaccharide (LPS) with or without epinephrine at different concentrations from 10^-6 M to 10^-4 M for 2 hours. Then, SB203580(p38MAPK inhibitor), PD98059 (ERK1/2 MAPK inhibitor), PDTC (NF-κB inhibitor), SR8278 and GSK 4112 (rev-erb α antagonist and agonist) were added into cultures according to the protocol, respectively. Rev-erb α siRNA was transfected in to BMMCs by an nucleofector II device to confirm the role of rev-erb α in modulating pro-inflammatory cytokines production in BMMCs. IL-6, TNF-α and MCP-1 levels in medium were determined by ELISA. And, NF-κB p65, MAPK p38 and ERK1/2 phosphorylation and rev-erb α protein were assessed by western blot. BMMCs viability was assessed by WST-1 kit.

Results

The production of IL-6, TNF-α and MCP-1 from LPS challenged BMMCs was significantly enhanced at the epinephrine concentration of 10^-4M. Epinephrine increased phosphorylated p38 MAPK and phosphorylated p65 NF-κB expression, and LPS plus epinephrine could further increase the expression of phosphorylated p38, ERK1/2 and p65. SB203580, PD98059 and PDTC inhibited such enhancing effect of epinephrine on IL-6, TNF-α and MCP-1 from LPS challenged BMMCs. LPS increased rev-erb α protein expression in BMMCs, and epinephrine could exert further increasing effect on rev-erb α protein expression in LPS challenged BMMCs. Both GSK4112 and SR8278 significantly inhibited IL-6 production in LPS-challenged BMMCs. But a decreased cell viability was detected in GSK4112 activated BMMCs by WST-1 kit. And epinephrine had no significant enhancing effect on LPS-induced IL-6 release from SR8278 cultured BMMCs. Suppressive siRNA inhibited rev-erb α mRNA expression efficiently, and a decreased IL-6 releasing was observed in siRNA transfected BMMCs, compared to scramble control siRNA transfected BMMCs. No significant enhancing effect of epinephrine on IL-6 production was observed in siRNA transfected BMMCs.

Conclusions

Epinephrine could further increase the production of pro-inflammatory cytokines from LPS-challenged BMMCs. MAPK and NF-κB pathway activations were involved in such effects of epinephrine on pro-inflammatory cytokines production. Rev-erb α activation negatively regulated LPS-induced pro-inflammatory cytokines release from BMMCs. The enhancing effect of epinephrine on pro-inflammatory cytokines was rev-erb α dependent.

Proinflammatory cytokine

10.1136/heartjnl-2013-304613.204

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GW26-e2436 Eliminating Sputum and Removing Stasis Formulation improves Atherosclerotic Plaque via regulating Mast Cell function and related mechanism

Journal of the American College of Cardiology (2015)

Lei Duan Changzhe Chen Xianliang Dai Chun Liang

10.1016/j.jacc.2015.06.329

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Cytokine Signaling in Skeletal Muscle Wasting

Trends in Endocrinology and Metabolism (2016)