PMID- 27069537
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20160412
LR  - 20201001
IS  - 1943-8141 (Print)
IS  - 1943-8141 (Electronic)
IS  - 1943-8141 (Linking)
VI  - 8
IP  - 1
DP  - 2016
TI  - Angiotensin II induces apoptosis of human pulmonary microvascular endothelial 
      cells in acute aortic dissection complicated with lung injury patients through 
      modulating the expression of monocyte chemoattractant protein-1.
PG  - 28-36
AB  - Patients with acute aortic dissection (AAD) usually showed acute lung injury 
      (ALI). However, its pathogenesis is still not well defined. Apoptosis of 
      pulmonary microvascular endothelial cells (PMVECs) is closely related to the 
      alveolus-capillary barrier injury and the increased vascular permeability. In 
      this study, we aim to investigate the human PMVECs (hPMVECs) apoptosis induced by 
      angiotensin II (AngII) and monocyte chemoattractant protein-1 (MCP-1) and their 
      potential interaction in the pathogenesis of AAD complicated with ALI. 
      Fifty-eight newly diagnosed AAD, 12 matched healthy individuals were included. 
      Pulmonary tissues of AAD complicated with lung injury were obtained from 2 
      cadavers to determine the levels of AngII type 1 receptor (AT1-R) and MCP-1. 
      Serum AngII was measured using commercial ELISA kit. H&E staining and 
      immunohistostaining were performed to determine the expression of AT1-R and 
      MCP-1. For the in vitro experiment, hPMVECs were divided into control, AngII 
      group, AngII+Bindarit group and Bindarit group, respectively. Flow cytometry was 
      performed to analyze the apoptosis in each group. Reverse 
      transcription-polymerase chain reaction was performed to determine the mRNA 
      expression of MCP-1. Western blot analysis was performed to evaluate the 
      expression of MCP-1 and apoptosis related protein. Apoptosis of hPMVECs was 
      observed in the lung tissues in the cadavers with AAD complicated with ALI. 
      Besides, the expression of AT1-R and MCP-1 was remarkably elevated. Compared with 
      normal individuals and the non-lung injury AAD patients, the expression of serum 
      AngII was remarkably elevated in AAD patients complicated with ALI. In vitro 
      experiments showed AngII contributed to the apoptosis and elevation of MCP1 in 
      hPMVECs. Besides, it involved in the down-regulation of Bcl-2 protein, and 
      up-regulation of Bax and Caspase-3. Such phenomenon was completely reversed after 
      administration of MCP-1 inhibitor (Bindarit). The production of MCP-1 and 
      cellular apoptosis induced by AngII in hPMVECs are closely related to the 
      pathogenesis of AAD complicated with ALI. The association between MCP-1 and AngII 
      is crucial in the apoptosis of hPMVECs.
FAU - Wu, Zhiyong
AU  - Wu Z
AD  - Department of Cardiovascular Surgery, Wuhan University Renmin Hospital Wuhan, 
      China.
FAU - Dai, Feifeng
AU  - Dai F
AD  - Department of Cardiovascular Surgery, Wuhan University Renmin Hospital Wuhan, 
      China.
FAU - Ren, Wei
AU  - Ren W
AD  - Department of Cardiovascular Surgery, Wuhan University Renmin Hospital Wuhan, 
      China.
FAU - Liu, Huagang
AU  - Liu H
AD  - Department of Cardiovascular Surgery, Wuhan University Renmin Hospital Wuhan, 
      China.
FAU - Li, Bowen
AU  - Li B
AD  - Department of Cardiovascular Surgery, Wuhan University Renmin Hospital Wuhan, 
      China.
FAU - Chang, Jinxing
AU  - Chang J
AD  - Department of Cardiovascular Surgery, Wuhan University Renmin Hospital Wuhan, 
      China.
LA  - eng
PT  - Journal Article
DEP - 20160115
PL  - United States
TA  - Am J Transl Res
JT  - American journal of translational research
JID - 101493030
PMC - PMC4759413
OTO - NOTNLM
OT  - Aortic dissection
OT  - MCP-1
OT  - angiotensin II
OT  - apoptosis
OT  - lung injury
EDAT- 2016/04/14 06:00
MHDA- 2016/04/14 06:01
PMCR- 2016/01/15
CRDT- 2016/04/13 06:00
PHST- 2015/11/22 00:00 [received]
PHST- 2016/01/02 00:00 [accepted]
PHST- 2016/04/13 06:00 [entrez]
PHST- 2016/04/14 06:00 [pubmed]
PHST- 2016/04/14 06:01 [medline]
PHST- 2016/01/15 00:00 [pmc-release]
PST - epublish
SO  - Am J Transl Res. 2016 Jan 15;8(1):28-36. eCollection 2016.