PMID- 9048591
OWN - NLM
STAT- MEDLINE
DCOM- 19970407
LR  - 20131121
IS  - 0013-7227 (Print)
IS  - 0013-7227 (Linking)
VI  - 138
IP  - 3
DP  - 1997 Mar
TI  - Low concentrations of ethanol inhibits prolactin-induced mitogenesis and cytokine 
      expression in cultured astrocytes.
PG  - 922-8
AB  - Whereas the immunosuppressive effects of chronic alcohol use have been well 
      documented, little is known about the effect of ethanol on the neuroimmune 
      response. We previously demonstrated that PRL is a potent mitogen and induces the 
      expression of several inflammatory cytokines, including tumor necrosis 
      factor-alpha (TNF alpha) in cultured rat astrocytes. The aim of this study was to 
      examine the effects of ethanol on PRL-induced mitogenesis and TNF alpha 
      expression in cultured rat astrocytes. We found that low concentrations of 
      ethanol blocked PRL-induced increases in [3H]thymidine incorporation and TNF 
      alpha levels. In contrast, ethanol had no effect on platelet-derived growth 
      factor- or fibroblast growth factor-induced increases in [3H]thymidine 
      incorporation. Radioligand binding analysis revealed that ethanol did not effect 
      PRL receptor binding. We also examined the effect of prenatal alcohol exposure 
      (PAE) on PRL-induced mitogenesis and cytokine expression. PAE during the last 5 
      days of gestation blunted the PRL-induced increase in [3H]thymidine incorporation 
      and TNF alpha levels in cells grown in the absence of ethanol in the culture 
      medium. Addition of ethanol to primary PAE astrocyte cultures resulted in a 
      modest increase in basal [3H]thymidine incorporation, but completely blocked the 
      PRL-induced increase in [3H]thymidine incorporation and TNF alpha levels. In 
      contrast, platelet-derived growth factor- and serum (10%)-induced increases in 
      [3H]thymidine incorporation remained intact. Together, these data indicate that 
      ethanol blocks PRL-induced mitogenesis and the expression of TNF alpha in 
      cultured rat astrocytes and are consistent with the possible inhibition of the 
      astrocytic response by ethanol in vivo.
FAU - DeVito, W J
AU  - DeVito WJ
AD  - Division of Endocrinology, University of Massachusetts Medical Center, Worcester 
      01655, USA.
FAU - Stone, S
AU  - Stone S
FAU - Mori, K
AU  - Mori K
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Endocrinology
JT  - Endocrinology
JID - 0375040
RN  - 0 (Cytokines)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 3K9958V90M (Ethanol)
RN  - 9002-62-4 (Prolactin)
RN  - VC2W18DGKR (Thymidine)
SB  - IM
MH  - Animals
MH  - Astrocytes/cytology/*drug effects/*metabolism
MH  - Cells, Cultured
MH  - Cytokines/*metabolism
MH  - Ethanol/*pharmacology
MH  - Female
MH  - Mitosis/*drug effects
MH  - Osmolar Concentration
MH  - Pregnancy
MH  - Prenatal Exposure Delayed Effects
MH  - Prolactin/*antagonists & inhibitors/*pharmacology
MH  - Rats
MH  - Thymidine/metabolism
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 1997/03/01 00:00
MHDA- 1997/03/01 00:01
CRDT- 1997/03/01 00:00
PHST- 1997/03/01 00:00 [pubmed]
PHST- 1997/03/01 00:01 [medline]
PHST- 1997/03/01 00:00 [entrez]
AID - 10.1210/endo.138.3.4964 [doi]
PST - ppublish
SO  - Endocrinology. 1997 Mar;138(3):922-8. doi: 10.1210/endo.138.3.4964.