PMID- 28450497
OWN - NLM
STAT- MEDLINE
DCOM- 20180313
LR  - 20181113
IS  - 1573-4935 (Electronic)
IS  - 0144-8463 (Print)
IS  - 0144-8463 (Linking)
VI  - 37
IP  - 3
DP  - 2017 Jun 30
TI  - Integrating 3-omics data analyze rat lung tissue of COPD states and medical 
      intervention by delineation of molecular and pathway alterations.
LID - BSR20170042 [pii]
LID - 10.1042/BSR20170042 [doi]
AB  - Chronic obstructive pulmonary disease (COPD) is a serious health problem. 
      However, the molecular pathogenesis of COPD remains unknown. Here, we explored 
      the molecular effects of cigarette smoke and bacterial infection in lung tissues 
      of COPD rats. We also investigated therapeutic effects of aminophylline (APL) on 
      the COPD rats and integrated transcriptome, proteome, and metabolome data for a 
      global view of molecular mechanisms of COPD progression. Using molecular function 
      and pathway analyses, the genes and proteins regulated in COPD and APL-treated 
      rats were mainly attributed to oxidoreductase, antioxidant activity, energy and 
      fatty acid metabolism. Furthermore, we identified hub proteins such as Gapdh 
      (glyceraldehyde-3-phosphate dehydrogenase), Pkm (pyruvate kinase isozymes M1/M2), 
      and Sod1 (superoxide dismutase 1), included in energy metabolism and oxidative 
      stress. Then, we identified the significantly regulated metabolic pathways in 
      lung tissues of COPD- and APL-treated rats, such as arachidonic acid, linoleic 
      acid, and alpha-linolenic acid metabolism, which belong to the lipid metabolism. In 
      particular, we picked the arachidonic acid metabolism for a more detailed pathway 
      analysis of transcripts, proteins, and metabolites. We could observe an increase 
      in metabolites and genes involved in arachidonic acid metabolism in COPD rats and 
      the decrease in these in APL-treated rats, suggesting that inflammatory responses 
      were up-regulated in COPD rats and down-regulated in APL-treated rats. In 
      conclusion, these system-wide results suggested that COPD progression and its 
      treatment might be associated with oxidative stress, lipid and energy metabolism 
      disturbance. Additionally, we demonstrated the power of integrated omics for the 
      elucidation of genes, proteins, and metabolites' changes and disorders that were 
      associated with COPD.
CI  - (c) 2017 The Author(s).
FAU - Li, Jiansheng
AU  - Li J
AD  - Henan Key Laboratory of Chinese Medicine for Respiratory Disease, Henan 
      University of Chinese Medicine, Zhengzhou, Henan 450046, China li_js8@163.com.
AD  - Collaborative Innovation Center for Respiratory Disease Diagnosis and Treatment 
      and Chinese Medicine Development of Henan Province, Henan University of Chinese 
      Medicine, Zhengzhou, Henan 450046, China.
FAU - Zhao, Peng
AU  - Zhao P
AD  - Henan Key Laboratory of Chinese Medicine for Respiratory Disease, Henan 
      University of Chinese Medicine, Zhengzhou, Henan 450046, China.
AD  - Collaborative Innovation Center for Respiratory Disease Diagnosis and Treatment 
      and Chinese Medicine Development of Henan Province, Henan University of Chinese 
      Medicine, Zhengzhou, Henan 450046, China.
FAU - Yang, Liping
AU  - Yang L
AD  - Henan Key Laboratory of Chinese Medicine for Respiratory Disease, Henan 
      University of Chinese Medicine, Zhengzhou, Henan 450046, China.
AD  - Collaborative Innovation Center for Respiratory Disease Diagnosis and Treatment 
      and Chinese Medicine Development of Henan Province, Henan University of Chinese 
      Medicine, Zhengzhou, Henan 450046, China.
FAU - Li, Ya
AU  - Li Y
AD  - Henan Key Laboratory of Chinese Medicine for Respiratory Disease, Henan 
      University of Chinese Medicine, Zhengzhou, Henan 450046, China.
AD  - Collaborative Innovation Center for Respiratory Disease Diagnosis and Treatment 
      and Chinese Medicine Development of Henan Province, Henan University of Chinese 
      Medicine, Zhengzhou, Henan 450046, China.
FAU - Tian, Yange
AU  - Tian Y
AD  - Henan Key Laboratory of Chinese Medicine for Respiratory Disease, Henan 
      University of Chinese Medicine, Zhengzhou, Henan 450046, China.
AD  - Collaborative Innovation Center for Respiratory Disease Diagnosis and Treatment 
      and Chinese Medicine Development of Henan Province, Henan University of Chinese 
      Medicine, Zhengzhou, Henan 450046, China.
FAU - Li, Suyun
AU  - Li S
AD  - Collaborative Innovation Center for Respiratory Disease Diagnosis and Treatment 
      and Chinese Medicine Development of Henan Province, Henan University of Chinese 
      Medicine, Zhengzhou, Henan 450046, China.
AD  - Department of Respiratory Diseases, The First Affiliated Hospital of Henan 
      University of Chinese Medicine, Zhengzhou 450000, China.
FAU - Bai, Yunping
AU  - Bai Y
AD  - Henan Key Laboratory of Chinese Medicine for Respiratory Disease, Henan 
      University of Chinese Medicine, Zhengzhou, Henan 450046, China.
AD  - Collaborative Innovation Center for Respiratory Disease Diagnosis and Treatment 
      and Chinese Medicine Development of Henan Province, Henan University of Chinese 
      Medicine, Zhengzhou, Henan 450046, China.
LA  - eng
PT  - Journal Article
DEP - 20170621
PL  - England
TA  - Biosci Rep
JT  - Bioscience reports
JID - 8102797
RN  - 0 (Bronchodilator Agents)
RN  - 0 (Proteome)
RN  - 27Y3KJK423 (Aminophylline)
SB  - IM
MH  - Aminophylline/therapeutic use
MH  - Animals
MH  - Bacterial Infections/complications
MH  - Bronchodilator Agents/therapeutic use
MH  - Disease Models, Animal
MH  - Down-Regulation
MH  - Female
MH  - Inflammation/drug therapy/genetics/metabolism/pathology
MH  - Lipid Metabolism/drug effects
MH  - Lung/*metabolism/pathology
MH  - Male
MH  - *Metabolome
MH  - Oxidative Stress/drug effects
MH  - *Proteome
MH  - Pulmonary Disease, Chronic Obstructive/drug 
      therapy/genetics/*metabolism/pathology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Smoking/adverse effects
MH  - *Transcriptome
MH  - Up-Regulation
PMC - PMC5479022
OTO - NOTNLM
OT  - chronic obstructive pulmonary disease
OT  - metabolomics
OT  - molecular pathogenesis
OT  - proteomics
OT  - transcriptomics
COIS- The authors declare that there are no competing interests associated with the 
      manuscript.
EDAT- 2017/04/30 06:00
MHDA- 2018/03/14 06:00
PMCR- 2017/06/21
CRDT- 2017/04/29 06:00
PHST- 2017/01/11 00:00 [received]
PHST- 2017/04/25 00:00 [revised]
PHST- 2017/04/27 00:00 [accepted]
PHST- 2017/04/30 06:00 [pubmed]
PHST- 2018/03/14 06:00 [medline]
PHST- 2017/04/29 06:00 [entrez]
PHST- 2017/06/21 00:00 [pmc-release]
AID - BSR20170042 [pii]
AID - 10.1042/BSR20170042 [doi]
PST - epublish
SO  - Biosci Rep. 2017 Jun 21;37(3):BSR20170042. doi: 10.1042/BSR20170042. Print 2017 
      Jun 30.