Expression of Fas ligand and apoptosis of disc cells in herniated lumbar disc tissue

被引:223
作者
Park, JB
Chang, H
Kim, KW
机构
[1] Catholic Univ Korea, Uijongbu St Marys Hosp, Dept Orthopaed Surg, Kyunggi Do 480130, South Korea
[2] Catholic Univ Korea, St Marys Hosp, Dept Orthopaed Surg, Seoul, South Korea
关键词
apoptosis; autocrine; disc cell; Fas ligand; paracrine;
D O I
10.1097/00007632-200103150-00011
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Study Design. An examination of surgically obtained herniated lumbar disc tissues performed by using immunohistochemical staining and the DNA nick end labeling method. Objective. To investigate the cell type that expresses Fas ligand (FasL) and any evidence of apoptosis of the disc cells in herniated lumbar disc tissues. Summary of Background Data. The Fas/FasL system is involved in delivering a death signal that rapidly commits the cells to apoptosis. In the authors' previous study, the expression of Fas on disc cells was identified in herniated lumbar disc tissue. Methods. Twenty-three herniated lumbar disc tissues (contained disc, n = 9; noncontained disc, n = 14) were examined to investigate the cell type that expresses FasL and any evidence of apoptosis of the disc cells by using immunohistochemical staining and the DNA nick end labeling method, respectively. The percentage of Fast-positive disc cells was calculated and compared with clinical and radiologic data. Results. FasL was expressed in the cytoplasm of the disc cells, and nuclear DNA fragmentation in a few disc cells was identified. A higher degree of FasL expression in disc cells was found in noncontained discs than in contained discs (P < 0.05). The percentage of Fast-positive disc cells significantly increased with the patient's age (P < 0.05), but not with the degree of disc degeneration (P > 0.05). Conclusion. The current results indicate that disc cells, after herniation, undergo apoptotic cell death via autocrine or paracrine FasL mechanisms by the disc cells themselves.
引用
收藏
页码:618 / 621
页数:4
相关论文
共 29 条
[1]
Expression of fas antigen and Fas ligand in the rheumatoid synovial tissue [J].
Asahara, H ;
Hasumuna, T ;
Kobata, T ;
Yagita, H ;
Okumura, K ;
Inoue, H ;
Gay, S ;
Sumida, T ;
Nishioka, K .
CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY, 1996, 81 (01) :27-34
[2]
A ROLE FOR CD95 LIGAND IN PREVENTING GRAFT-REJECTION [J].
BELLGRAU, D ;
GOLD, D ;
SELAWRY, H ;
MOORE, J ;
FRANZUSOFF, A ;
DUKE, RC .
NATURE, 1995, 377 (6550) :630-632
[3]
DETERMINATION OF THE LENGTH OF THE HISTOLOGICAL STAGES OF APOPTOSIS IN NORMAL LIVER AND IN ALTERED HEPATIC FOCI OF RATS [J].
BURSCH, W ;
PAFFE, S ;
PUTZ, B ;
BARTHEL, G ;
SCHULTEHERMANN, R .
CARCINOGENESIS, 1990, 11 (05) :847-853
[4]
COLUMBANO A, 1984, AM J PATHOL, V116, P441
[5]
Involvement of the CD95 (APO-1/Fas) receptor/ligand system in multiple sclerosis brain [J].
Dowling, P ;
Shang, GF ;
Raval, S ;
Menonna, J ;
Cook, S ;
Husar, W .
JOURNAL OF EXPERIMENTAL MEDICINE, 1996, 184 (04) :1513-1518
[6]
FRYMOYER JW, 1991, ADULT SPINE PRINCIPL, P611
[7]
CD95-induced apoptosis in human liver disease [J].
Galle, PR ;
Krammer, PH .
SEMINARS IN LIVER DISEASE, 1998, 18 (02) :141-151
[8]
On the role and significance of Fas (Apo-1/CD95) ligand (FasL) expression in immune privileged tissues and cancer cells using multiple myeloma as a model [J].
Greil, R ;
Egle, A ;
Villunger, A .
LEUKEMIA & LYMPHOMA, 1998, 31 (5-6) :477-+
[9]
FAS LIGAND-INDUCED APOPTOSIS AS A MECHANISM OF IMMUNE PRIVILEGE [J].
GRIFFITH, TS ;
BRUNNER, T ;
FLETCHER, SM ;
GREEN, DR ;
FERGUSON, TA .
SCIENCE, 1995, 270 (5239) :1189-1192
[10]
Analysis of aging and degeneration of the human intervertebral disc - Comparison of surgical specimens with normal controls [J].
Gruber, HE ;
Hanley, EN .
SPINE, 1998, 23 (07) :751-757