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Article: Lactation increases prolactin receptor expression in spleen and thymus of rats

TitleLactation increases prolactin receptor expression in spleen and thymus of rats
Authors
KeywordsLactation
Prolactin receptor binding
Prolactin receptor gene expression
Issue Date1998
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescie
Citation
Life Sciences, 1998, v. 63 n. 2, p. 111-119 How to Cite?
AbstractProlactin receptors (PRL-R) are widely expressed on cells of the immune system. During lactation, the increase in serum PRL levels may modify the gene expression of these receptors. Specific PRL binding sites and the expressions of both PRL-R-L and PRL-R-S forms in thymus and spleen of nulliparous control, 10-day postpartum lactating, and 10-day postpartum nonlactating rats were studied. A semi-quantitative RT-PCR technique was used to detect the PRL-R gene transcript in the tissues. Our results showed that specific PRL binding sites and PRL-R-L mRNA and PRL-R-S mRNA were present in the lymphoid tissues with the PRL-R-L mRNA predominant. Lactation markedly increased specific binding sites and PRL-R-L mRNA in both spleen and thymus and only PRL-R-S in spleen. No differences between nulliparous control and postpartum nonlactating rats were observed in any of the parameters measured. The parallel increase in specific PRL binding sites and PRL-R-L mRNA suggests that lactation up-regulates PRL-R expression in lymphoid tissues and may be beneficial to the maternal immune system.
Persistent Identifierhttp://hdl.handle.net/10722/224110
ISSN
2021 Impact Factor: 6.780
2020 SCImago Journal Rankings: 1.131
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorFeng, JC-
dc.contributor.authorLoh, TT-
dc.contributor.authorSheng, HP-
dc.date.accessioned2016-03-24T01:30:55Z-
dc.date.available2016-03-24T01:30:55Z-
dc.date.issued1998-
dc.identifier.citationLife Sciences, 1998, v. 63 n. 2, p. 111-119-
dc.identifier.issn0024-3205-
dc.identifier.urihttp://hdl.handle.net/10722/224110-
dc.description.abstractProlactin receptors (PRL-R) are widely expressed on cells of the immune system. During lactation, the increase in serum PRL levels may modify the gene expression of these receptors. Specific PRL binding sites and the expressions of both PRL-R-L and PRL-R-S forms in thymus and spleen of nulliparous control, 10-day postpartum lactating, and 10-day postpartum nonlactating rats were studied. A semi-quantitative RT-PCR technique was used to detect the PRL-R gene transcript in the tissues. Our results showed that specific PRL binding sites and PRL-R-L mRNA and PRL-R-S mRNA were present in the lymphoid tissues with the PRL-R-L mRNA predominant. Lactation markedly increased specific binding sites and PRL-R-L mRNA in both spleen and thymus and only PRL-R-S in spleen. No differences between nulliparous control and postpartum nonlactating rats were observed in any of the parameters measured. The parallel increase in specific PRL binding sites and PRL-R-L mRNA suggests that lactation up-regulates PRL-R expression in lymphoid tissues and may be beneficial to the maternal immune system.-
dc.languageeng-
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescie-
dc.relation.ispartofLife Sciences-
dc.subjectLactation-
dc.subjectProlactin receptor binding-
dc.subjectProlactin receptor gene expression-
dc.subject.meshLactation - physiology-
dc.subject.meshReceptors, Prolactin - biosynthesis - metabolism-
dc.subject.meshSpleen - metabolism - ultrastructure-
dc.subject.meshSubstrate Specificity-
dc.subject.meshThymus Gland - metabolism - ultrastructure-
dc.titleLactation increases prolactin receptor expression in spleen and thymus of rats-
dc.typeArticle-
dc.identifier.emailLoh, TT: ttloh@hkucc.hku.hk-
dc.identifier.emailSheng, HP: hpsheng@hkucc.hku.hk-
dc.identifier.doi10.1016/S0024-3205(98)00246-X-
dc.identifier.pmid9674945-
dc.identifier.scopuseid_2-s2.0-0032486425-
dc.identifier.hkuros36795-
dc.identifier.volume63-
dc.identifier.issue2-
dc.identifier.spage111-
dc.identifier.epage119-
dc.identifier.isiWOS:000074133200005-
dc.publisher.placeUnited States-
dc.identifier.issnl0024-3205-

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