Low concentrations of ethanol inhibits prolactin-induced mitogenesis and cytokine expression in cultured astrocytes
dc.contributor.author | DeVito, William J. | |
dc.contributor.author | Stone, Scott | |
dc.contributor.author | Mori, Kouki | |
dc.date | 2022-08-11T08:10:02.000 | |
dc.date.accessioned | 2022-08-23T16:52:54Z | |
dc.date.available | 2022-08-23T16:52:54Z | |
dc.date.issued | 1997-03-01 | |
dc.date.submitted | 2008-07-09 | |
dc.identifier.citation | <p>Endocrinology. 1997 Mar;138(3):922-8.</p> | |
dc.identifier.issn | 0013-7227 (Print) | |
dc.identifier.pmid | 9048591 | |
dc.identifier.uri | http://hdl.handle.net/20.500.14038/42152 | |
dc.description.abstract | 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. | |
dc.language.iso | en_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.url | https://doi.org/10.1210/en.138.3.922 | |
dc.subject | Animals | |
dc.subject | Astrocytes | |
dc.subject | Cells, Cultured | |
dc.subject | Cytokines | |
dc.subject | Ethanol | |
dc.subject | Female | |
dc.subject | Mitosis | |
dc.subject | Osmolar Concentration | |
dc.subject | Pregnancy | |
dc.subject | Prenatal Exposure Delayed Effects | |
dc.subject | Prolactin | |
dc.subject | Rats | |
dc.subject | Thymidine | |
dc.subject | Tumor Necrosis Factor-alpha | |
dc.subject | Life Sciences | |
dc.subject | Medicine and Health Sciences | |
dc.title | Low concentrations of ethanol inhibits prolactin-induced mitogenesis and cytokine expression in cultured astrocytes | |
dc.type | Journal Article | |
dc.source.journaltitle | Endocrinology | |
dc.source.volume | 138 | |
dc.source.issue | 3 | |
dc.identifier.legacycoverpage | https://escholarship.umassmed.edu/oapubs/525 | |
dc.identifier.contextkey | 545007 | |
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.submissionpath | oapubs/525 | |
dc.contributor.department | Division of Endocrinology | |
dc.source.pages | 922-8 |