Radioprotective effect of heat shock protein 25 on submandibular glands of rats

被引:47
作者
Lee, Hae-June
Lee, Yoon-Jin
Kwon, Hee-Chung
Bae, Sangwoo
Kim, Sung-Ho
Min, Jung-Joon
Cho, Chul-Koo
Lee, Yun-Sil
机构
[1] Korea Inst Radiol & Med Sci, Lab Radiat Effect, Seoul 139706, South Korea
[2] Korea Inst Radiol & Med Sci, Lab Mol Canc, Seoul 139706, South Korea
[3] Korea Inst Radiol & Med Sci, Dept Radiat Oncol, Seoul 139706, South Korea
[4] Chonnam Natl Univ, Dept Nucl Med, Kwangju, South Korea
[5] Chonnam Natl Univ, Coll Vet Med, Kwangju, South Korea
关键词
D O I
10.2353/ajpath.2006.060327
中图分类号
R36 [病理学];
学科分类号
100104 [病理学与病理生理学];
摘要
Irradiation (IR) is a fundamental treatment modality for head and neck malignancies. However, a significant drawback of IR treatment is irreversible damage of salivary gland in the ER field. in the present study, we investigated whether heat shock protein (HSP) 25 could be used as a radioprotective molecule for radiation-induced salivary gland damage in rats. HSP25 as well as inducible HSP70 (HSP70i) that were delivered to the salivary gland via an adenoviral vector significantly ameliorated radiation-induced salivary fluid loss. Radiation-induced apoptosis, caspase-3 activation, and poly(ADP-ribose) polymerase cleavage in acinar cells, granular convoluted cells, and intercalated ductal cells were also inhibited by HSP25 or HSP70i transfer. The alteration of salivary contents, including amylase, protein, Ca+, Cl-, and Na+, was also attenuated by HSP25 transfer. Histological analysis revealed almost no radiation-induced damage in salivary gland when HSP25 was transferred. Aquaporin 5 expression in salivary gland was inhibited by radiation; and HSP25 transfer to salivary gland prevented this alteration. The protective effect of HSP70i on radiationinduced salivary gland damage was less or delayed than that of HSP25. These results indicate that HSP25 is a good candidate molecule to protect salivary gland from the toxicity of IR.
引用
收藏
页码:1601 / 1611
页数:11
相关论文
共 50 条
[1]
MORPHOLOGIC AND HISTOCHEMICAL-STUDIES ON THE DIFFERING RADIOSENSITIVITY OF DUCTULAR AND ACINAR-CELLS OF THE RAT SUBMANDIBULAR-GLAND [J].
ABOK, K ;
BRUNK, U ;
JUNG, B ;
ERICSSON, J .
VIRCHOWS ARCHIV B-CELL PATHOLOGY INCLUDING MOLECULAR PATHOLOGY, 1984, 45 (04) :443-460
[2]
AQUAPORIN WATER CHANNELS - UNANSWERED QUESTIONS AND UNRESOLVED CONTROVERSIES [J].
AGRE, P ;
BROWN, D ;
NIELSEN, S .
CURRENT OPINION IN CELL BIOLOGY, 1995, 7 (04) :472-483
[3]
Over-expression of heat shock protein 70 protects neuronal cells against both thermal and ischaemic stress but with different efficiencies [J].
Amin, V ;
Cumming, DV ;
Latchman, DS .
NEUROSCIENCE LETTERS, 1996, 206 (01) :45-48
[4]
THE DEGREE OF PROTECTION PROVIDED TO NEURONAL CELLS BY A PRECONDITIONING STRESS CORRELATES WITH THE AMOUNT OF HEAT-SHOCK-PROTEIN-70 IT INDUCES AND NOT WITH THE SIMILARITY OF THE SUBSEQUENT STRESS [J].
AMIN, V ;
CUMMING, DVE ;
COFFIN, RS ;
LATCHMAN, DS .
NEUROSCIENCE LETTERS, 1995, 200 (02) :85-88
[5]
BECKER TC, 1994, METHOD CELL BIOL, V43, P161
[6]
Stress (heat shock) proteins - Molecular chaperones in cardiovascular biology and disease [J].
Benjamin, IJ ;
McMillan, DR .
CIRCULATION RESEARCH, 1998, 83 (02) :117-132
[7]
Does amifostine have a role in chemoradiation treatment? [J].
Brizel, DM .
LANCET ONCOLOGY, 2003, 4 (06) :378-381
[8]
Phase III randomized trial of amifostine as a radioprotector in head and neck cancer [J].
Brizel, DM ;
Wasserman, TH ;
Henke, M ;
Strnad, V ;
Rudat, V ;
Monnier, A ;
Eschwege, F ;
Zhang, J ;
Russell, L ;
Oster, W ;
Sauer, R .
JOURNAL OF CLINICAL ONCOLOGY, 2000, 18 (19) :3339-3345
[9]
Downregulation of ERK2 is essential for the inhibition of radiation-induced cell death in HSP25 overexpressed L929 cells [J].
Cho, HN ;
Lee, YJ ;
Cho, CK ;
Lee, SJ ;
Lee, YS .
CELL DEATH AND DIFFERENTIATION, 2002, 9 (04) :448-456
[10]
Cook D. I., 1994, P1061