PMID- 27853364
OWN - NLM
STAT- MEDLINE
DCOM- 20170807
LR  - 20181113
IS  - 1178-2005 (Electronic)
IS  - 1176-9106 (Print)
IS  - 1176-9106 (Linking)
VI  - 11
DP  - 2016
TI  - Curcumin modulates the effect of histone modification on the expression of 
      chemokines by type II alveolar epithelial cells in a rat COPD model.
PG  - 2765-2773
AB  - BACKGROUND: Studies have suggested that histone modification has a positive 
      impact on various aspects associated with the progression of COPD. Histone 
      deacetylase 2 (HDAC2) suppresses proinflammatory gene expression through 
      deacetylation of core histones. OBJECTIVE: To investigate the effect of histone 
      modification on the expression of chemokines in type II alveolar epithelial cells 
      (AEC II) in a rat COPD model and regulation of HDAC2 expression by curcumin in 
      comparison with corticosteroid. MATERIALS AND METHODS: The rat COPD model was 
      established by cigarette smoke exposure and confirmed by histology and 
      pathophysioloy. AEC II were isolated and cultured in vitro from the COPD models 
      and control animals. The cells were treated with curcumin, corticosteroid, or 
      trichostatin A, and messenger RNA (mRNA) expression of interleukin-8 (IL-8), 
      monocyte chemoattractant protein-1 (MCP-1), and macrophage inflammatory 
      protein-2alpha (MIP-2alpha) was assessed by quantitative real-time polymerase chain 
      reaction (RT-PCR). The expression of HDAC2 was measured by Western blot. 
      Chromatin immunoprecipitation was used to detect H3/H4 acetylation and H3K9 
      methylation in the promoter region of three kinds of chemokine genes (IL-8, 
      MCP-1, and MIP-2alpha). RESULTS: Compared to the control group, the mRNAs of MCP-1, 
      IL-8, and MIP-2alpha were upregulated 4.48-fold, 3.14-fold, and 2.83-fold, 
      respectively, in the AEC II from COPD model. The protein expression of HDAC2 in 
      the AEC II from COPD model was significantly lower than from the control group 
      (P<0.05). The decreased expression of HDAC2 was negatively correlated with the 
      increased expression of IL-8, MCP-1, and MIP-2alpha mRNAs (all P<0.05). The level of 
      H3/H4 acetylation was higher but H3K9 methylation in the promoter region of 
      chemokine genes was lower in the cells from COPD model than from the control 
      group (all P<0.05). Curcumin downregulated the expression of MCP-1, IL-8, and 
      MIP-2alpha, and the expression was further enhanced in the presence of 
      corticosteroid. Moreover, curcumin restored HDAC2 expression, decreased the 
      levels of H3/H4 acetylation, and increased H3K9 methylation in the promoter 
      region of chemokine in the presence or absence of dexamethasone (all P<0.05). 
      CONCLUSION: Curcumin may suppress chemokines and restore corticosteroid 
      resistance in COPD through modulating HDAC2 expression and its effect on histone 
      modification.
FAU - Gan, Lixing
AU  - Gan L
AD  - Department of Respiratory Medicine, Shanghai Ninth People's Hospital, Shanghai 
      Jiao Tong University School of Medicine, Shanghai.
FAU - Li, Chengye
AU  - Li C
AD  - Department of Respiratory Medicine, The First Affiliated Hospital of Wenzhou 
      Medical University, Wenzhou.
FAU - Wang, Jian
AU  - Wang J
AD  - Department of Respiratory Medicine, Shanghai Ninth People's Hospital, Shanghai 
      Jiao Tong University School of Medicine, Shanghai.
FAU - Guo, Xuejun
AU  - Guo X
AD  - Department of Respiratory Medicine, Xin Hua Hospital Affiliated to Shanghai Jiao 
      Tong University School of Medicine, Shanghai, People's Republic of China.
LA  - eng
PT  - Comparative Study
PT  - Journal Article
DEP - 20161107
PL  - New Zealand
TA  - Int J Chron Obstruct Pulmon Dis
JT  - International journal of chronic obstructive pulmonary disease
JID - 101273481
RN  - 0 (Adrenal Cortex Hormones)
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Ccl2 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CXCL2)
RN  - 0 (Chemokines)
RN  - 0 (Cxcl2 protein, rat)
RN  - 0 (Histones)
RN  - 0 (Interleukin-8)
RN  - 0 (RNA, Messenger)
RN  - 0 (Smoke)
RN  - EC 3.5.1.98 (Hdac2 protein, rat)
RN  - EC 3.5.1.98 (Histone Deacetylase 2)
RN  - IT942ZTH98 (Curcumin)
SB  - IM
MH  - Acetylation
MH  - Adrenal Cortex Hormones/pharmacology
MH  - Alveolar Epithelial Cells/*drug effects/metabolism
MH  - Animals
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Cells, Cultured
MH  - Chemokine CCL2/genetics/metabolism
MH  - Chemokine CXCL2/genetics/metabolism
MH  - Chemokines/genetics/*metabolism
MH  - Curcumin/*pharmacology
MH  - Disease Models, Animal
MH  - Down-Regulation
MH  - Histone Deacetylase 2/metabolism
MH  - Histones/*metabolism
MH  - Interleukin-8/genetics/metabolism
MH  - Male
MH  - Methylation
MH  - Promoter Regions, Genetic
MH  - Pulmonary Disease, Chronic Obstructive/*drug therapy/etiology/genetics/metabolism
MH  - RNA, Messenger/genetics/metabolism
MH  - Rats, Sprague-Dawley
MH  - Smoke/adverse effects
MH  - Smoking/adverse effects
PMC - PMC5106221
OTO - NOTNLM
OT  - chronic obstructive pulmonary disease
OT  - corticosteroid
OT  - curcumin
OT  - histone deacetylase
OT  - type II alveolar epithelial cell
COIS- The authors report no conflicts of interest in this work.
EDAT- 2016/11/18 06:00
MHDA- 2017/08/08 06:00
PMCR- 2016/11/07
CRDT- 2016/11/18 06:00
PHST- 2016/11/18 06:00 [entrez]
PHST- 2016/11/18 06:00 [pubmed]
PHST- 2017/08/08 06:00 [medline]
PHST- 2016/11/07 00:00 [pmc-release]
AID - copd-11-2765 [pii]
AID - 10.2147/COPD.S113978 [doi]
PST - epublish
SO  - Int J Chron Obstruct Pulmon Dis. 2016 Nov 7;11:2765-2773. doi: 
      10.2147/COPD.S113978. eCollection 2016.