DOPAMINE-INDUCED LYMPHOMA CELL-DEATH BY INHIBITION OF HORMONE-RELEASE

被引:8
作者
BRAESCHANDERSEN, S
PAULIE, S
STAMENKOVIC, I
机构
[1] HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA
[2] UNIV STOCKHOLM, DEPT IMMUNOL, S-10691 STOCKHOLM, SWEDEN
关键词
D O I
10.1111/j.1365-3083.1992.tb03223.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Dopamine inhibits prolactin release from pituitary cells and seems to affect the release of several other hormones as well. We report here that dopamine may have similar effects on human B lymphoma cells leading to inhibition of production or release of endogenous factors required for cell viability and proliferation. Thus. addition of dopamine to serum-free cultures of Burkitt lymphoma cells (Raji, Namalwa, Daudi and Jijoye) resulted in rapid and extensive cell death while a myeloma cell line, SKO, appeared to be refractory to this treatment. The addition of FCS or supernatant from serum-free cultures of Raji or T24 bladder carcinoma cells could, to a variable degree, counteract the effect of dopamine, suggesting that dopamine acts by inhibiting the production of essential autocrine factors. When two of the hormones known to be under dopamine control, i.e. prolactin (PRL) and thyrotropin (TSH), were tested, they were able to prevent dopamine-induced cell death if combined with heparin. We further observed that the reducing agent 2-mercaptoethanol (2-ME), which is known to inhibit the binding of TSH to its receptor, displayed similar effects to those of dopamine and was strongly inhibitory for Burkitt lymphoma but not for myeloma cells. As expected from its blocking activity at the receptor level, the effect of 2-ME could not be reversed by adding exogenous factors. Contrary to its effect on B lymphoma cells. 2-ME is essential for growth of the murine T-cell lymphoma line CTLL. However, we show here that dopamine can fully compensate for 2-ME, suggesting that TSH or another factor under dopamine control is intimately involved in the regulation of T-cell growth. This study lends further support to the notion of an active interplay between the neuroendocrine and immune systems and emphasizes PRL and TSH as important regulators of lymphoid cell function. It also shows that these hormones may contribute to the autonomous growth pattern of B lymphoma cells and suggests a potential role for dopamine in the treatment of B-cell tumours.
引用
收藏
页码:547 / 553
页数:7
相关论文
共 21 条
[1]   INCREASED DOPAMINERGIC ACTIVITY INHIBITS BASAL AND METOCLOPRAMIDE-STIMULATED PROLACTIN AND THYROTROPIN SECRETION [J].
AGNER, T ;
HAGEN, C ;
ANDERSEN, AN ;
DJURSING, H .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1986, 62 (04) :778-782
[2]   AN EPSTEIN-BARR VIRUS-NEGATIVE BURKITT-LYMPHOMA CELL-LINE (SFRAMOS) SECRETES A PROLACTIN-LIKE PROTEIN DURING CONTINUOUS GROWTH IN SERUM-FREE MEDIUM [J].
BAGLIA, LA ;
CRUZ, D ;
SHAW, JE .
ENDOCRINOLOGY, 1991, 128 (05) :2266-2272
[3]  
BELLINGER DL, 1990, ANN NY ACAD SCI, V594, P17
[4]  
BROOKS KH, 1990, J MOL CELL IMMUNOL, V4, P327
[5]   REQUIREMENT OF NUCLEAR PROLACTIN FOR INTERLEUKIN-2 - STIMULATED PROLIFERATION OF LYMPHOCYTES-T [J].
CLEVENGER, CV ;
ALTMANN, SW ;
PRYSTOWSKY, MB .
SCIENCE, 1991, 253 (5015) :77-79
[6]   A HUMAN-B-LYMPHOBLASTOID CELL-LINE PRODUCES PROLACTIN [J].
DIMATTIA, GE ;
GELLERSEN, B ;
BOHNET, HG ;
FRIESEN, HG .
ENDOCRINOLOGY, 1988, 122 (06) :2508-2517
[7]  
ESCALERA GM, 1988, ENDOCRINOLOGY, V47, P38
[8]   EVIDENCE THAT THE PORCINE THYROTROPIN (TSH) RECEPTOR CONTAINS AN ESSENTIAL DISULFIDE BRIDGE [J].
GINSBERG, J ;
SMITH, BR ;
HALL, R .
MOLECULAR AND CELLULAR ENDOCRINOLOGY, 1982, 26 (1-2) :95-102
[9]  
GORDON J, 1991, ADV CANCER RES, V56, P313
[10]   HYPERPROLACTINEMIA IN ACUTE MYELOID-LEUKEMIA AND INDICATION OF ECTOPIC EXPRESSION OF HUMAN PROLACTIN IN BLAST CELLS OF A PATIENT OF SUBTYPE-M4 [J].
HATFILL, SJ ;
KIRBY, R ;
HANLEY, M ;
RYBICKI, E ;
BOHM, L .
LEUKEMIA RESEARCH, 1990, 14 (01) :57-62