PubTransformer

A site to transform Pubmed publications into these bibliographic reference formats: ADS, BibTeX, EndNote, ISI used by the Web of Knowledge, RIS, MEDLINE, Microsoft's Word 2007 XML.

Cyclooxygenase-2 promotes pulmonary intravascular macrophage accumulation by exacerbating BMP signaling in rat experimental hepatopulmonary syndrome.

Abstract One central factor in hepatopulmonary syndrome (HPS) pathogenesis is intravascular accumulation of activated macrophages in small pulmonary arteries. However, molecular mechanism underlying the macrophage accumulation in HPS is unknown. In this study, we aimed to explore whether elevated COX-2 induces the Bone morphogenic protein-2 (BMP-2)/Crossveinless-2 (CV-2) imbalance and then activation of BMP signaling pathway promotes the macrophage accumulation in Common Bile Duct Ligation (CBDL) rat lung.
PMID
Related Publications

A central role for CD68(+) macrophages in hepatopulmonary syndrome. Reversal by macrophage depletion.

Annexin A1 protein regulates the expression of PMVEC cytoskeletal proteins in CBDL rat serum-induced pulmonary microvascular remodeling.

Bone morphogenic protein-2 regulates the myogenic differentiation of PMVECs in CBDL rat serum-induced pulmonary microvascular remodeling.

The role of receptor tyrosine kinase activation in cholangiocytes and pulmonary vascular endothelium in experimental hepatopulmonary syndrome.

The role of CX₃CL1/CX₃CR1 in pulmonary angiogenesis and intravascular monocyte accumulation in rat experimental hepatopulmonary syndrome.

Authors

Mayor MeshTerms
Keywords

Bone morphogenic protein-2

Crossveinless-2

Cyclooxygenase-2

Hepatopulmonary syndrome

Journal Title biochemical pharmacology
Publication Year Start




PMID- 28642034
OWN - NLM
STAT- In-Process
DA  - 20170623
LR  - 20170704
IS  - 1873-2968 (Electronic)
IS  - 0006-2952 (Linking)
VI  - 138
DP  - 2017 Aug 15
TI  - Cyclooxygenase-2 promotes pulmonary intravascular macrophage accumulation by
      exacerbating BMP signaling in rat experimental hepatopulmonary syndrome.
PG  - 205-215
LID - S0006-2952(17)30440-9 [pii]
LID - 10.1016/j.bcp.2017.06.117 [doi]
AB  - BACKGROUND AND AIMS: One central factor in hepatopulmonary syndrome (HPS)
      pathogenesis is intravascular accumulation of activated macrophages in small
      pulmonary arteries. However, molecular mechanism underlying the macrophage
      accumulation in HPS is unknown. In this study, we aimed to explore whether
      elevated COX-2 induces the Bone morphogenic protein-2 (BMP-2)/Crossveinless-2
      (CV-2) imbalance and then activation of BMP signaling pathway promotes the
      macrophage accumulation in Common Bile Duct Ligation (CBDL) rat lung. METHODS:
      The COX-2/PGE2 signaling activation, the BMP-2/CV-2 imbalance and the activation 
      of Smad1 were evaluated in CBDL rat lung and in cultured pulmonary microvascular 
      endothelial cells (PMVECs) under the HPS serum stimulation. The effects of
      Parecoxib (COX-2 inhibitor), BMP-2 and CV-2 recombinant proteins on 4-week CBDL
      rat lung were determined, respectively. RESULTS: The COX-2/PGE2 signaling pathway
      was activated in CBDL rat lung in vivo and PMVECs in vitro, which was due to the 
      activation of NF-kappaB P65. The inhibition of COX-2 by Parecoxib reduced
      macrophage accumulation, decreased lung angiogenesis and improved HPS. Meanwhile,
      the CBDL rat lung secreted more BMP-2 but less CV-2, and the imbalance between
      BMP-2 and CV-2 exacerbated the BMP signaling activation thus promoting the
      macrophage accumulation and lung angiogenesis. The BMP-2/CV-2 imbalance is
      dependent on the COX-2/PGE2 signaling pathway, and thus the effects of this
      imbalance can be reversed by adminstration of Parecoxib. CONCLUSION: Our findings
      indicate that inhibition of COX-2 by parecoxib can improve the HPS through the
      repression of BMP signaling and macrophage accumulation.
CI  - Copyright (c) 2017 Elsevier Inc. All rights reserved.
FAU - Liu, Chang
AU  - Liu C
AD  - Department of Anesthesia, Southwest Hospital, The Third Military Medical
      University, Chongqing 400038, China.
FAU - Gao, Jing
AU  - Gao J
AD  - Department of Anesthesia, Southwest Hospital, The Third Military Medical
      University, Chongqing 400038, China.
FAU - Chen, Bing
AU  - Chen B
AD  - Department of Anesthesia, Southwest Hospital, The Third Military Medical
      University, Chongqing 400038, China; LBCMCP, Centre de Biologie Integrative
      (CBI), Universite de Toulouse, CNRS, UPS, 31062 Toulouse, France.
FAU - Chen, Lin
AU  - Chen L
AD  - Department of Anesthesia, Southwest Hospital, The Third Military Medical
      University, Chongqing 400038, China.
FAU - Belguise, Karine
AU  - Belguise K
AD  - LBCMCP, Centre de Biologie Integrative (CBI), Universite de Toulouse, CNRS, UPS, 
      31062 Toulouse, France.
FAU - Yu, Weifeng
AU  - Yu W
AD  - Department of Anesthesia, RenJi Hospital, The Shanghai Jiao Tong University
      School of Medicine, Shanghai 200000, China.
FAU - Lu, Kaizhi
AU  - Lu K
AD  - Department of Anesthesia, Southwest Hospital, The Third Military Medical
      University, Chongqing 400038, China.
FAU - Wang, Xiaobo
AU  - Wang X
AD  - Department of Anesthesia, Southwest Hospital, The Third Military Medical
      University, Chongqing 400038, China; LBCMCP, Centre de Biologie Integrative
      (CBI), Universite de Toulouse, CNRS, UPS, 31062 Toulouse, France. Electronic
      address: [email protected]
FAU - Yi, Bin
AU  - Yi B
AD  - Department of Anesthesia, Southwest Hospital, The Third Military Medical
      University, Chongqing 400038, China. Electronic address: [email protected]
LA  - eng
PT  - Journal Article
DEP - 20170619
PL  - England
TA  - Biochem Pharmacol
JT  - Biochemical pharmacology
JID - 0101032
OTO - NOTNLM
OT  - Bone morphogenic protein-2
OT  - Crossveinless-2
OT  - Cyclooxygenase-2
OT  - Hepatopulmonary syndrome
EDAT- 2017/06/24 06:00
MHDA- 2017/06/24 06:00
CRDT- 2017/06/24 06:00
PHST- 2017/03/22 [received]
PHST- 2017/06/08 [accepted]
AID - S0006-2952(17)30440-9 [pii]
AID - 10.1016/j.bcp.2017.06.117 [doi]
PST - ppublish
SO  - Biochem Pharmacol. 2017 Aug 15;138:205-215. doi: 10.1016/j.bcp.2017.06.117. Epub 
      2017 Jun 19.