Document Detail

Overexpression of interleukin-1β and interferon-γ in type I thoracic aortic dissections and ascending thoracic aortic aneurysms: possible correlation with matrix metalloproteinase-9 expression and apoptosis of aortic media cells.
MedLine Citation:
PMID:  21349736     Owner:  NLM     Status:  Publisher    
Objective: To examine the expression of interleukin-1β and interferon-γ and their possible roles in aortic dissections and aneurysms. Methods: Aortic specimens were obtained from patients with type I thoracic aortic dissection, ascending thoracic aortic aneurysms, and control organ donors. The expression of interleukin-1β, interferon-γ, matrix metalloproteinase-9, and signal transduction factors phospho-p38 and phosphorylated c-jun N-terminal kinase (phospho-JNK) were detected by real time reverse transcription-polymerase chain reaction (real time RT-PCR), Western blot, and immunohistochemistry, respectively. Terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining was performed to detect apoptosis of media cells. The correlation of these factors and apoptosis was also studied. Results: Apoptosis in the media of thoracic aortic dissection and in ascending thoracic aortic aneurysms was dramatically higher than in the control group. The expression of interleukin-1β gradually increased from the control group, thoracic aortic dissection to ascending thoracic aortic aneurysms (p<0.01, respectively). The expression of interferon-γ and matrix metalloproteinase-9 was significantly increased in the media of thoracic aortic dissection and ascending thoracic aortic aneurysms compared with the control group (p<0.01, respectively). There were positive correlations between interleukin-1β versus matrix metalloproteinase-9, interleukin-1β versus phospho-p38 in thoracic aortic dissection (p<0.01, respectively), and interferon-γ versus matrix metalloproteinase-9, interferon-γ versus phospho-JNK, interferon-γ versus apoptosis, and interleukin-1β versus apoptosis in ascending thoracic aortic aneurysms (p=0.02, 0.02, p<0.01, p<0.01). Conclusions: Interleukin-1β and interferon-γ might effect the formation of thoracic aortic dissection and ascending thoracic aortic aneurysms possibly through the up-regulation of matrix metalloproteinase-9 and the apoptosis of media cells in humans.
Lei Zhang; Ming-Fang Liao; Lei Tian; Si-Li Zou; Qing-Sheng Lu; Jun-Min Bao; Yi-Fei Pei; Zai-Ping Jing
Related Documents :
7955246 - Coronary bypass grafting with biological grafts in a canine model.
10901516 - Bilateral internal thoracic artery operations in the elderly.
2626836 - The influence of tissue expanders on grafted vessels.
17616426 - A parametric numerical investigation on haemodynamics in distal coronary anastomoses.
2383126 - A fiber-optic retractor for harvesting the internal mammary artery.
3631116 - Role of thrombolysis in peripheral arterial occlusion.
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-2-22
Journal Detail:
Title:  European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery     Volume:  -     ISSN:  1873-734X     ISO Abbreviation:  -     Publication Date:  2011 Feb 
Date Detail:
Created Date:  2011-2-25     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8804069     Medline TA:  Eur J Cardiothorac Surg     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2010 European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved.
Department of Vascular Surgery, Changhai Hospital, Second Military Medical University, 168 Changhai Road, Shanghai 200433, China.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Hand-held minimised extracorporeal membrane oxygenation: a new bridge to recovery in patients with o...
Next Document:  The lipoproteins of cyanobacterial photosystem II.