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dc.contributor.authorDeVito, William J.
dc.contributor.authorStone, Scott
dc.contributor.authorMori, Kouki
dc.date2022-08-11T08:10:02.000
dc.date.accessioned2022-08-23T16:52:54Z
dc.date.available2022-08-23T16:52:54Z
dc.date.issued1997-03-01
dc.date.submitted2008-07-09
dc.identifier.citation<p>Endocrinology. 1997 Mar;138(3):922-8.</p>
dc.identifier.issn0013-7227 (Print)
dc.identifier.pmid9048591
dc.identifier.urihttp://hdl.handle.net/20.500.14038/42152
dc.description.abstractWhereas 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.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=9048591&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.1210/en.138.3.922
dc.subjectAnimals
dc.subjectAstrocytes
dc.subjectCells, Cultured
dc.subjectCytokines
dc.subjectEthanol
dc.subjectFemale
dc.subjectMitosis
dc.subjectOsmolar Concentration
dc.subjectPregnancy
dc.subjectPrenatal Exposure Delayed Effects
dc.subjectProlactin
dc.subjectRats
dc.subjectThymidine
dc.subjectTumor Necrosis Factor-alpha
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleLow concentrations of ethanol inhibits prolactin-induced mitogenesis and cytokine expression in cultured astrocytes
dc.typeArticle
dc.source.journaltitleEndocrinology
dc.source.volume138
dc.source.issue3
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/525
dc.identifier.contextkey545007
html.description.abstract<p>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.</p>
dc.identifier.submissionpathoapubs/525
dc.contributor.departmentDivision of Endocrinology
dc.source.pages922-8


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