PMID- 30877876
OWN - NLM
STAT- MEDLINE
DCOM- 20191212
LR  - 20191217
IS  - 1878-1705 (Electronic)
IS  - 1567-5769 (Linking)
VI  - 71
DP  - 2019 Jun
TI  - LncRNA analysis of lung tissues after hUC-MSCs and FTY720 treatment of 
      lipopolysaccharide-induced acute lung injury in mouse models.
PG  - 68-75
LID - S1567-5769(19)30005-0 [pii]
LID - 10.1016/j.intimp.2019.03.017 [doi]
AB  - Acute lung injury (ALI), a persistent lung inflammatory response syndrome, may 
      evolve into acute respiratory distress syndrome (ARDS). Characterized by rapid 
      onset, critical features, and a complex etiology, ALI remains a challenging 
      critical respiratory disease. Recently, mesenchymal stem cells (MSCs) have 
      provided a new solution for the treatment of ALI. We built a lipopolysaccharide 
      (LPS)-induced ALI model in mice. After treatment with human umbilical cord 
      mesenchymal stem cells (hUC-MSCs), FTY720, or a combination of hUC-MSCs and 
      FTY207, the lung inflammatory response was apparently attenuated. To understand 
      the mechanism underlying MSCs treatment of ALI at the genetic level, significant 
      differentially expressed long non-coding RNAs (lncRNAs) between the treatment and 
      model groups were analyzed using microarray technology. Moreover, genetic gene 
      prediction, gene ontology (GO) analysis, pathway analysis, and transcription 
      factor (TF) prediction were carried out. The results showed that a total of 66 
      lncRNAs were differentially expressed in all three treatment groups, including 8 
      up-regulated and 58 down-regulated lncRNAs. LncRNA A_30_P01029806 and 
      A_30_P01029194, which were down-regulated, were involved in the signaling 
      pathways closely related to ALI. Through further TF analysis, we identified 
      several significant TFs which lay a foundation for revealing the mechanism 
      underlying lncRNAs treatment of ALI. LncRNA A_30_P01029806 and A_30_P01029194 may 
      serve as candidate biomarkers in the diagnosis and treatment of ALI.
CI  - Copyright (c) 2019 Elsevier B.V. All rights reserved.
FAU - Zhang, Xia
AU  - Zhang X
AD  - Institute of Physical Science and Information Technology, Anhui University, Hefei 
      230601, China; Academy of Military Medical Sciences, Beijing 100850, China.
FAU - Liu, Huiying
AU  - Liu H
AD  - Department of Respiratory and Critical Care Diseases, 307 Hospital of PLA, 
      Beijing 100071, China.
FAU - Wang, Shiyu
AU  - Wang S
AD  - Institute of Physical Science and Information Technology, Anhui University, Hefei 
      230601, China; Academy of Military Medical Sciences, Beijing 100850, China.
FAU - Huang, Zihao
AU  - Huang Z
AD  - Institute of Physical Science and Information Technology, Anhui University, Hefei 
      230601, China; Academy of Military Medical Sciences, Beijing 100850, China.
FAU - Wang, Herong
AU  - Wang H
AD  - Academy of Military Medical Sciences, Beijing 100850, China; College of Life 
      Sciences, Jilin University, Changchun 130012, China.
FAU - Niu, Wenkai
AU  - Niu W
AD  - Department of Respiratory and Critical Care Diseases, 307 Hospital of PLA, 
      Beijing 100071, China.
FAU - Qin, Yanhong
AU  - Qin Y
AD  - Department of Respiratory and Critical Care Diseases, 307 Hospital of PLA, 
      Beijing 100071, China.
FAU - Bai, Changqing
AU  - Bai C
AD  - Department of Respiratory and Critical Care Diseases, 307 Hospital of PLA, 
      Beijing 100071, China. Electronic address: mcp1604@sina.com.
FAU - Liu, Gang
AU  - Liu G
AD  - Academy of Military Medical Sciences, Beijing 100850, China. Electronic address: 
      jueliu@sohu.com.
FAU - Chen, Huipeng
AU  - Chen H
AD  - Academy of Military Medical Sciences, Beijing 100850, China.
LA  - eng
PT  - Journal Article
DEP - 20190314
PL  - Netherlands
TA  - Int Immunopharmacol
JT  - International immunopharmacology
JID - 100965259
RN  - 0 (Immunosuppressive Agents)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (RNA, Long Noncoding)
RN  - G926EC510T (Fingolimod Hydrochloride)
SB  - IM
MH  - Acute Lung Injury/*therapy
MH  - Animals
MH  - Combined Modality Therapy
MH  - Disease Models, Animal
MH  - Fingolimod Hydrochloride/*therapeutic use
MH  - Gene Expression Regulation
MH  - Gene Ontology
MH  - Humans
MH  - Immunosuppressive Agents/*therapeutic use
MH  - Lipopolysaccharides/immunology
MH  - Lung/*physiology
MH  - Male
MH  - Mesenchymal Stem Cell Transplantation
MH  - Mesenchymal Stem Cells/*physiology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Pneumonia/immunology/*therapy
MH  - RNA, Long Noncoding/*genetics
MH  - Signal Transduction/genetics
MH  - Umbilical Cord/pathology
OTO - NOTNLM
OT  - Acute lung injury (ALI)
OT  - Long non-coding RNA (lncRNAs)
OT  - Pathway analysis
OT  - Transcription factor
OT  - hUC-MSCs
EDAT- 2019/03/17 06:00
MHDA- 2019/12/18 06:00
CRDT- 2019/03/17 06:00
PHST- 2019/01/03 00:00 [received]
PHST- 2019/02/10 00:00 [revised]
PHST- 2019/03/06 00:00 [accepted]
PHST- 2019/03/17 06:00 [pubmed]
PHST- 2019/12/18 06:00 [medline]
PHST- 2019/03/17 06:00 [entrez]
AID - S1567-5769(19)30005-0 [pii]
AID - 10.1016/j.intimp.2019.03.017 [doi]
PST - ppublish
SO  - Int Immunopharmacol. 2019 Jun;71:68-75. doi: 10.1016/j.intimp.2019.03.017. Epub 
      2019 Mar 14.