Growth hormone protects human lymphocytes from irradiation-induced cell death

被引:27
作者
Lempereur, L
Brambilla, D
Scoto, GM
D'Alcamo, M
Goffin, V
Crosta, L
Palmucci, T
Rampello, L
Bernardini, R
Cantarella, G
机构
[1] Univ Catania, Dept Expt & Clin Pharmacol, I-95124 Catania, Italy
[2] Univ Catania, Dept Pharmaceut Sci, I-95124 Catania, Italy
[3] CHU Necker, INSERM, U344 Endocrinol Mol, Fac Med, F-75015 Paris, France
[4] Univ Palermo, Dept Oncol, I-90133 Palermo, Italy
[5] Univ Catania, Dept Radiol, I-95124 Catania, Italy
[6] Univ Catania, Dept Neurol, I-95124 Catania, Italy
关键词
browth hormone; immune response; tumor radiotherapy; apoptosis; protection; receptor antagonists;
D O I
10.1038/sj.bjp.0705173
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
1 Undesired effects of cancer radiotherapy mainly affect the hematopoietic system. Growth hormone (GH) participates in both hematopoiesis and modulation of the immune response. We report both r-hGH cell death prevention and restoration of secretory capacities of irradiated human peripheral blood lymphocytes (PBL) in vitro. 2 r-hGH induced cell survival and increased proliferation of irradiated cells. Western blot analysis indicated that these effects of GH were paralleled by increased expression of the antiapoptotic protein Bcl-2. 3 r-hGH restored mitogen-stimulated release of IL-2 by PBL. Preincubation of irradiated lymphocytes with the growth hormone receptor (GHR) antagonists B2036 and G120K abrogated r-hGH-dependent IL-2 release. 4 These results demonstrate that r-hGH protects irradiated PBL from death in a specific, receptor-mediated manner. Such effect of r-hGH on PBL involves activation of the antiapoptotic gene bcl-2 and prevention of cell death, associated with preserved functional cell capacity. Finally, potential use of GH as an immunopotentiating agent could be envisioned during radiation therapy of cancer.
引用
收藏
页码:1411 / 1416
页数:6
相关论文
共 44 条
[1]  
Anderson R E, 1976, Adv Immunol, V24, P215, DOI 10.1016/S0065-2776(08)60331-4
[2]   IDENTIFICATION OF JAK2 AS A GROWTH-HORMONE RECEPTOR-ASSOCIATED TYROSINE KINASE [J].
ARGETSINGER, LS ;
CAMPBELL, GS ;
YANG, XN ;
WITTHUHN, BA ;
SILVENNOINEN, O ;
IHLE, JN ;
CARTERSU, C .
CELL, 1993, 74 (02) :237-244
[3]   RADIOPROTECTIVE EFFECTS OF THE ASSOCIATION THYMOPENTIN INTERLEUKIN-1-ALPHA IN THE C57BL/6 MOUSE [J].
BARBERA, N ;
PALMUCCI, T ;
CHIARENZA, A ;
BARTOLONI, G ;
CORDARO, S ;
GRECO, S ;
SCAPAGNINI, U ;
BERNARDINI, R .
PHARMACOLOGY & TOXICOLOGY, 1993, 72 (4-5) :256-261
[5]   GROWTH-HORMONE AND BODY-COMPOSITION [J].
BENGTSSON, BA ;
BRUMMER, RJ ;
BOSAEUS, I .
HORMONE RESEARCH, 1990, 33 :19-24
[6]  
Boreham DR, 2000, RADIAT RES, V153, P579, DOI 10.1667/0033-7587(2000)153[0579:DREFAA]2.0.CO
[7]  
2
[8]  
BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1016/0003-2697(76)90527-3
[9]  
CHEN WY, 1994, J BIOL CHEM, V269, P15892
[10]   FUNCTIONAL ANTAGONISM BETWEEN ENDOGENOUS MOUSE GROWTH-HORMONE (GH) AND A GH ANALOG RESULTS IN DWARF TRANSGENIC MICE [J].
CHEN, WY ;
WHITE, ME ;
WAGNER, TE ;
KOPCHICK, JJ .
ENDOCRINOLOGY, 1991, 129 (03) :1402-1408