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Vol. 72, No. 3, 2005
Issue release date: April 2005
Section title: Original Paper
Pathobiology 2005;72:146–151
(DOI:10.1159/000084118)

Alteration of Gene Expression in Intervertebral Disc Degeneration of Passive Cigarette- Smoking Rats: Separate Quantitation in Separated Nucleus pulposus and Annulus fibrosus

Ogawa T. · Matsuzaki H. · Uei H. · Nakajima S. · Tokuhashi Y. · Esumi M.
Departments of aOrthopedic Surgery and bPathology, Nihon University School of Medicine, Tokyo, Japan

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: 8/4/2004
Accepted: 10/22/2004
Published online: 4/21/2005

Number of Print Pages: 6
Number of Figures: 3
Number of Tables: 0

ISSN: 1015-2008 (Print)
eISSN: 1423-0291 (Online)

For additional information: http://www.karger.com/PAT

Abstract

Objective: We constructed a passive cigarette-smoking model with rats to investigate the molecular mechanism of intervertebral disc degeneration, and foundby gene expression analysis that passive cigarette smoking stimulated the stress-responsive signal pathway and inhibited the apoptotic pathway. In this study, to clarify that these changes were derived from either nucleus pulposus (NP) or annulus fibrosus (AF), we separately collected NP and AF and quantitatively analyzed gene expression. Methods: Total RNA was extracted from NP and AF of the lumbar intervertebral discs from rats which were kept in a smoking box for 4 and 8 weeks. Gene expression was measured by real-time PCR of cDNA synthesized from the total RNA. Results: Stress-responsive protein, heat shock protein 70, was expressed similarly in NP and AF, and wasupregulated to the same degree after 8 weeks of passive cigarette smoking. The protein tyrosine phosphatase gene was expressed more strongly in AF than in NP, and wasupregulated after 8 weeks of smoking in both tissueparts. The type II collagen and aggrecan genes were predominantly expressed in AF and NP, respectively. Conclusion: These results indicate that passive cigarette smoking stimulates both NP and AF, and induces the stress-responsible genes such as heat shock protein 70 and protein tyrosine phosphatase in both.


  

Author Contacts

Dr. Mariko Esumi, PhD
Department of Pathology, Nihon University School of Medicine
30-1, Ooyaguchikami-machi, Itabashi-ku
Tokyo 173-8610 (Japan)
Tel. +81 3 3972 8111, Fax +81 3 3972 8830, E-Mail mesumi@med.nihon-u.ac.jp

  

Article Information

Received: August 23, 2004
Accepted: October 22, 2004
Number of Print Pages : 6
Number of Figures : 3, Number of Tables : 0, Number of References : 18

  

Publication Details

Pathobiology

Vol. 72, No. 3, Year 2005 (Cover Date: April 2005)

Journal Editor: Borisch, B. (Geneva)
ISSN: 1015–2008 (print), 1423–0291 (Online)

For additional information: http://www.karger.com/pat


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: 8/4/2004
Accepted: 10/22/2004
Published online: 4/21/2005

Number of Print Pages: 6
Number of Figures: 3
Number of Tables: 0

ISSN: 1015-2008 (Print)
eISSN: 1423-0291 (Online)

For additional information: http://www.karger.com/PAT


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