PMID- 27284347
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 1792-0981 (Print)
IS  - 1792-1015 (Electronic)
IS  - 1792-0981 (Linking)
VI  - 11
IP  - 6
DP  - 2016 Jun
TI  - Effect of AMP-activated protein kinase activation on cardiac fibroblast 
      proliferation induced by coxsackievirus B3.
PG  - 2547-2552
AB  - Excessive fibroblast proliferation and collagen production are the major 
      pathogenic mechanisms in the progression of viral myocarditis, which is most 
      frequently associated with infection by coxsackievirus B3 (CVB3). AMP-activated 
      protein kinase (AMPK) has been confirmed to be involved in the progression of 
      myocardial remodeling. However, it remains unclear whether AMPK has an effect on 
      CVB3-induced cardiac fibroblast proliferation. In the present study, the effects 
      of AMPK on cardiac fibroblast proliferation and collagen secretion induced by 
      CVB3 were investigated. Proliferation of neonatal cardiac fibroblasts was 
      determined by cell counting and detection of newly synthesized DNA in cells, and 
      the proportion of cells in the S phase was measured. Hydroxyproline ELISA was 
      used to detect collagen secretion. Phosphorylation of AMPKalpha-Thr(172) was 
      evaluated by western blotting. It was found that neonatal cardiac fibroblasts 
      were clearly proliferating markedly and secreting collagen at 24 h after CVB3 
      infection, and peaked at 48 h. These effects were inhibited following 
      pretreatment of the fibroblasts with 
      5-aminoimidazole-4-carboxamide-ribonucleoside (AICAR), a specific AMPK activator, 
      for 2 h prior to CVB3 infection. However, if the cells were preincubated with 
      compound C for 30 min, the inhibitive effects of AICAR were reversed. Western 
      blotting results indicated that AMPK alpha-Thr(172) phosphorylation was increased by 
      AICAR and attenuated by Compound C. The results of the present study suggest that 
      CVB3 infection increases cardiac fibroblast proliferation and collagen secretion, 
      and that these phenomena can be inhibited by activated AMPK. These findings 
      contribute to our understanding of AMPK function and the future design of 
      therapeutic approaches for the treatment of cardiac fibrosis caused by chronic 
      viral infection, such as CVB3-induced myocarditis.
FAU - Jiang, Shengyang
AU  - Jiang S
AD  - Department of Cardiology, The Third Affiliated Hospital of Nantong University, 
      Wuxi Institute of Integrated Traditional Chinese and Western Medicine, Wuxi, 
      Jiangsu 214041, P.R. China.
FAU - Tian, Shunli
AU  - Tian S
AD  - Department of Geratology, Tianjin Geriatric Institute, Tianjin Medical University 
      General Hospital, Tianjin 300052, P.R. China.
FAU - Wu, Xueming
AU  - Wu X
AD  - Department of Cardiology, The Third Affiliated Hospital of Nantong University, 
      Wuxi Institute of Integrated Traditional Chinese and Western Medicine, Wuxi, 
      Jiangsu 214041, P.R. China.
FAU - Tao, Yijia
AU  - Tao Y
AD  - Department of Cardiology, The Third Affiliated Hospital of Nantong University, 
      Wuxi Institute of Integrated Traditional Chinese and Western Medicine, Wuxi, 
      Jiangsu 214041, P.R. China.
FAU - Jiang, Donglin
AU  - Jiang D
AD  - Clinical Central Laboratory, The Third Affiliated Hospital of Nantong University, 
      Wuxi Institute of Integrated Traditional Chinese and Western Medicine, Wuxi, 
      Jiangsu 214041, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20160318
PL  - Greece
TA  - Exp Ther Med
JT  - Experimental and therapeutic medicine
JID - 101531947
PMC - PMC4887832
OTO - NOTNLM
OT  - AMP-activated protein kinase
OT  - cardiac fibroblast
OT  - cell proliferation
OT  - collagen
OT  - coxsackievirus
EDAT- 2016/06/11 06:00
MHDA- 2016/06/11 06:01
PMCR- 2016/03/18
CRDT- 2016/06/11 06:00
PHST- 2015/01/28 00:00 [received]
PHST- 2016/03/01 00:00 [accepted]
PHST- 2016/06/11 06:00 [entrez]
PHST- 2016/06/11 06:00 [pubmed]
PHST- 2016/06/11 06:01 [medline]
PHST- 2016/03/18 00:00 [pmc-release]
AID - ETM-0-0-3174 [pii]
AID - 10.3892/etm.2016.3174 [doi]
PST - ppublish
SO  - Exp Ther Med. 2016 Jun;11(6):2547-2552. doi: 10.3892/etm.2016.3174. Epub 2016 Mar 
      18.