PMID- 19150247
OWN - NLM
STAT- MEDLINE
DCOM- 20100108
LR  - 20091102
IS  - 1879-1336 (Electronic)
IS  - 1054-8807 (Linking)
VI  - 18
IP  - 6
DP  - 2009 Nov-Dec
TI  - The effects of NK4 on viral myocarditis mice.
PG  - 323-31
LID - 10.1016/j.carpath.2008.10.008 [doi]
AB  - NK4 may be a promising agent to inhibit tumor invasion and metastasis. To observe 
      the effects of NK4 on the cardiovascular system with pathological injury and to 
      discuss the mechanism, we established an experimental model of viral myocarditis 
      (VCM) by coxsackievirus B3 infection in Balb/c mice on Day 0 and administered NK4 
      twice daily to the VCM and control mice from Day 20 to Day 45. We then evaluated 
      the cardiac function by means of ultrasonic inspection. Hepatocyte growth factor, 
      TNF (tumor necrosis factor)-alpha, and angiotensin II levels in the myocardial 
      tissue were measured with enzyme-linked immunosorbent assay. Myocardium 
      histopathology was examined with hematoxylin and eosin stain. Collagen deposition 
      of the myocardium was detected through Masson staining. Microvessel staining with 
      the RECA antibody and apoptosis detection with terminal deoxynucleotidyl 
      transferase-mediated dUTP-biotin end labeling were performed in the myocardium. 
      The changes in MMP3 (matrix metalloproteinase 3), MMP9, TIMP1 (tissue inhibitor 
      of metalloproteinase 1), and TGF (transforming growth factor)-beta1 expression in 
      the myocardium were measured by reverse-transcriptase polymerase chain reaction. 
      We found that NK4 intervention increased TGF-beta and angiotensin II expression, 
      suppressed MMPs, improved the activities of TIMPs, and then promoted collagen 
      deposition in the myocardium. NK4 intervention also decreased the microvessels' 
      density and increased the apoptotic cell count in the myocardia of VCM mice. 
      However, we did not observe the obvious changes in the myocardia of control mice 
      after NK4 intervention. These data suggest that NK4 made negative impacts on the 
      restoration of cardiac function and the recovery from VCM in the experimental 
      mice.
FAU - Shen, Difei
AU  - Shen D
AD  - Department of Cardiology, Renmin Hospital, Wuhan University, Wuhan, P.R. China.
FAU - Tang, Qizhu
AU  - Tang Q
FAU - Huang, Zhengrong
AU  - Huang Z
FAU - Chen, Ying
AU  - Chen Y
FAU - Xiong, Ran
AU  - Xiong R
FAU - Wu, Hui
AU  - Wu H
FAU - Huang, Ji
AU  - Huang J
FAU - Feng, Siting
AU  - Feng S
FAU - Yan, Ling
AU  - Yan L
FAU - Bian, Zhouyan
AU  - Bian Z
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090115
PL  - United States
TA  - Cardiovasc Pathol
JT  - Cardiovascular pathology : the official journal of the Society for Cardiovascular 
      Pathology
JID - 9212060
RN  - 0 (Angiogenesis Inhibitors)
RN  - 0 (Cytokines)
RN  - 67256-21-7 (Hepatocyte Growth Factor)
RN  - EC 3.4.24.- (Matrix Metalloproteinases)
SB  - IM
MH  - Angiogenesis Inhibitors/*pharmacology
MH  - Animals
MH  - Apoptosis/drug effects
MH  - Coxsackievirus Infections/drug therapy/pathology
MH  - Cytokines/biosynthesis
MH  - Echocardiography
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Hepatocyte Growth Factor/metabolism
MH  - In Situ Nick-End Labeling
MH  - Male
MH  - Matrix Metalloproteinases/drug effects/metabolism
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Myocarditis/*drug therapy/*pathology
MH  - Myocardium/pathology
MH  - Reverse Transcriptase Polymerase Chain Reaction
EDAT- 2009/01/20 09:00
MHDA- 2010/01/09 06:00
CRDT- 2009/01/20 09:00
PHST- 2007/12/16 00:00 [received]
PHST- 2008/08/11 00:00 [revised]
PHST- 2008/10/21 00:00 [accepted]
PHST- 2009/01/20 09:00 [entrez]
PHST- 2009/01/20 09:00 [pubmed]
PHST- 2010/01/09 06:00 [medline]
AID - S1054-8807(08)00153-1 [pii]
AID - 10.1016/j.carpath.2008.10.008 [doi]
PST - ppublish
SO  - Cardiovasc Pathol. 2009 Nov-Dec;18(6):323-31. doi: 10.1016/j.carpath.2008.10.008. 
      Epub 2009 Jan 15.