PMID- 31726502
OWN - NLM
STAT- MEDLINE
DCOM- 20191126
LR  - 20201209
IS  - 1001-9391 (Print)
IS  - 1001-9391 (Linking)
VI  - 37
IP  - 10
DP  - 2019 Oct 20
TI  - [Activation of lung endothelial cells by extracellular histone in mice with acute 
      respiratory distress syndrome].
PG  - 732-736
LID - 10.3760/cma.j.issn.1001-9391.2019.10.004 [doi]
AB  - Objective: To observe the changes of extracellular histones and pulmonary 
      microvascular endothelial cells, and study the activating role of extracellular 
      histones to pulmonary microvascular endothelial cells in the pathogenesis of 
      acute respiratory distress syndrome (ARDS) . Methods: The correlation of the 
      severity of acute lung injury with extracellular histones and pulmonary 
      endothelial damage was studied through mice model, and acute lung injury was 
      produced by aspiration of different concentrations of hydrochloric acid 
      (0.01、0.1、0.3 and 0.5 mol/L, 2 ml/kg). Tumor necrosis factor-alpha (TNF-alpha), soluble 
      thrombomodulin (sTM) and lung pathological change were measured. The 
      pro-inflammatory role of extracellular histones was tested by injecting calf 
      thymus histones (CTH) or specific anti-H4 antibody through tail vein. The direct 
      activating role of extracellular histones to pulmonary microvascular endothelial 
      cells was studied through pulmonary endothelial model. Results: The extracellular 
      histones in plasma were increased obviously 6h after aspiration of different 
      concentrations of hydrochloric acid in mice. A positive correlation was seen 
      between extracellular histones and concentrations of aspirated hydrochloric acid 
      (r=0.9180, P<0.05). The sTM in plasma also showed a positive correlation with 
      concentrations of aspirated hydrochloric acid (r=0.8701, P<0.05). Merely 
      administering CTH could not only increase TNF-alpha and sTM in plasma but also cause 
      obvious lung injury, while specific anti-H4 antibody could relieve the 
      inflammation and lung damage caused by CTH. Extracellular histones could directly 
      damage pulmonary endothelial cells to release sTM in pulmonary endothelial model 
      in vitro, while anti-H4 antibody could protect the endothelial cells. Conclusion: 
      Extracellular histones are the key endogenic inflammatory mediators during the 
      pathogenesis of ARDS caused by aspiration of hydrochloric acid, which could 
      promote inflammation by directly activating pulmonary endothelial cells.
FAU - Zhang, Y L
AU  - Zhang YL
AD  - Research Center of Occupational Medicine, Peking University Third Hospital, 
      Beijing 100191, China.
FAU - Zhao, J
AU  - Zhao J
AD  - Institute of Pharmacology and Toxicology, Academy of Military Medical Science, 
      Beijing 100850, China.
FAU - Guan, L
AU  - Guan L
AD  - Research Center of Occupational Medicine, Peking University Third Hospital, 
      Beijing 100191, China.
FAU - Zheng, Y M
AU  - Zheng YM
AD  - Research Center of Occupational Medicine, Peking University Third Hospital, 
      Beijing 100191, China.
FAU - Chen, M
AU  - Chen M
AD  - Research Center of Occupational Medicine, Peking University Third Hospital, 
      Beijing 100191, China.
FAU - Guo, L X
AU  - Guo LX
AD  - Research Center of Occupational Medicine, Peking University Third Hospital, 
      Beijing 100191, China.
FAU - Guan, X X
AU  - Guan XX
AD  - Research Center of Occupational Medicine, Peking University Third Hospital, 
      Beijing 100191, China.
FAU - Mao, L J
AU  - Mao LJ
AD  - Research Center of Occupational Medicine, Peking University Third Hospital, 
      Beijing 100191, China.
FAU - Li, S Q
AU  - Li SQ
AD  - Research Center of Occupational Medicine, Peking University Third Hospital, 
      Beijing 100191, China.
FAU - Zhao, J Y
AU  - Zhao JY
AD  - Research Center of Occupational Medicine, Peking University Third Hospital, 
      Beijing 100191, China.
LA  - chi
GR  - 81773374/National Natural Science Foundation of China/
GR  - 7182179/Natural Science Foundation of Beijing Municipality/
GR  - Y75513-05/Start-up Fund for Excellent Returnee of Peking University Third 
      Hospital/
PT  - Journal Article
PL  - China
TA  - Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi
JT  - Zhonghua lao dong wei sheng zhi ye bing za zhi = Zhonghua laodong weisheng 
      zhiyebing zazhi = Chinese journal of industrial hygiene and occupational diseases
JID - 8410840
RN  - 0 (Histones)
RN  - 0 (Thrombomodulin)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - QTT17582CB (Hydrochloric Acid)
SB  - IM
MH  - Acute Lung Injury/chemically induced/*pathology
MH  - Animals
MH  - Endothelial Cells/*cytology/pathology
MH  - Histones/*blood
MH  - Hydrochloric Acid
MH  - Inflammation
MH  - Lung
MH  - Mice
MH  - Respiratory Distress Syndrome/chemically induced/*pathology
MH  - Thrombomodulin/blood
MH  - Tumor Necrosis Factor-alpha/blood
OTO - NOTNLM
OT  - Acute respiratory distress syndrome
OT  - Endothelial cells
OT  - Extracellular histones
OT  - Inflammation
OT  - Mice
EDAT- 2019/11/15 06:00
MHDA- 2019/11/27 06:00
CRDT- 2019/11/15 06:00
PHST- 2019/11/15 06:00 [entrez]
PHST- 2019/11/15 06:00 [pubmed]
PHST- 2019/11/27 06:00 [medline]
AID - 10.3760/cma.j.issn.1001-9391.2019.10.004 [doi]
PST - ppublish
SO  - Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2019 Oct 20;37(10):732-736. doi: 
      10.3760/cma.j.issn.1001-9391.2019.10.004.