Prolactin inhibits auto- and cross-induction of thyroid hormone and estrogen receptor and vitellogenin genes in adult Xenopus (Amphibia) hepatocytes

Detalhes bibliográficos
Autor(a) principal: Rabelo,Elida M.L.
Data de Publicação: 1997
Outros Autores: Tata,Jamshed R.
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Brazilian Journal of Genetics
Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-84551997000400010
Resumo: It is well known that virtually every tissue of the amphibian larvae is highly sensitive to the mutually antagonistic actions of thyroid hormone (TH) and prolactin (PRL), but it is not known if adult amphibian tissues respond similarly to these two hormones. We have previously shown that very low doses of triiodothyronine (T3) rapidly and strongly potentiate the activation of silent vitellogenin (Vit) genes by estrogen (E2) and the autoinduction of estrogen receptor (ER) transcripts in primary cultures of adult Xenopus hepatocytes. This response to T3 is accompanied by the upregulation of thyroid hormone receptor <FONT FACE="Symbol">b</FONT> (TR<FONT FACE="Symbol">b</FONT>) mRNA. Using Northern blot and RNase protection assays, we now show that ovine PRL added for 12 h along with 2 x 10-9 M T3 will completely prevent potentiation of E2 induction of Vit mRNA in primary cultures of adult Xenopus hepatocytes. PRL also abolished the auto-upregulation of TR<FONT FACE="Symbol">b</FONT> mRNA and the cross-activation of autoinduction of ER mRNA. Thus, we show for the first time that the anti-TH action of PRL that is manifested in Xenopus tadpole tissues during metamorphosis is retained in adult liver, and suggest that the mutually antagonistic actions of the two hormones may be brought about by similar molecular mechanisms in larval and adult amphibian tissues
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spelling Prolactin inhibits auto- and cross-induction of thyroid hormone and estrogen receptor and vitellogenin genes in adult Xenopus (Amphibia) hepatocytesIt is well known that virtually every tissue of the amphibian larvae is highly sensitive to the mutually antagonistic actions of thyroid hormone (TH) and prolactin (PRL), but it is not known if adult amphibian tissues respond similarly to these two hormones. We have previously shown that very low doses of triiodothyronine (T3) rapidly and strongly potentiate the activation of silent vitellogenin (Vit) genes by estrogen (E2) and the autoinduction of estrogen receptor (ER) transcripts in primary cultures of adult Xenopus hepatocytes. This response to T3 is accompanied by the upregulation of thyroid hormone receptor <FONT FACE="Symbol">b</FONT> (TR<FONT FACE="Symbol">b</FONT>) mRNA. Using Northern blot and RNase protection assays, we now show that ovine PRL added for 12 h along with 2 x 10-9 M T3 will completely prevent potentiation of E2 induction of Vit mRNA in primary cultures of adult Xenopus hepatocytes. PRL also abolished the auto-upregulation of TR<FONT FACE="Symbol">b</FONT> mRNA and the cross-activation of autoinduction of ER mRNA. Thus, we show for the first time that the anti-TH action of PRL that is manifested in Xenopus tadpole tissues during metamorphosis is retained in adult liver, and suggest that the mutually antagonistic actions of the two hormones may be brought about by similar molecular mechanisms in larval and adult amphibian tissuesSociedade Brasileira de Genética1997-12-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-84551997000400010Brazilian Journal of Genetics v.20 n.4 1997reponame:Brazilian Journal of Geneticsinstname:Sociedade Brasileira de Genética (SBG)instacron:SBG10.1590/S0100-84551997000400010info:eu-repo/semantics/openAccessRabelo,Elida M.L.Tata,Jamshed R.eng1998-10-06T00:00:00Zoai:scielo:S0100-84551997000400010Revistahttps://www.gmb.org.br/brazilian-journal-of-geneticsONGhttps://old.scielo.br/oai/scielo-oai.phpsede@sgb.org.br || sede@sgb.org.br0100-84550100-8455opendoar:1998-10-06T00:00Brazilian Journal of Genetics - Sociedade Brasileira de Genética (SBG)false
dc.title.none.fl_str_mv Prolactin inhibits auto- and cross-induction of thyroid hormone and estrogen receptor and vitellogenin genes in adult Xenopus (Amphibia) hepatocytes
title Prolactin inhibits auto- and cross-induction of thyroid hormone and estrogen receptor and vitellogenin genes in adult Xenopus (Amphibia) hepatocytes
spellingShingle Prolactin inhibits auto- and cross-induction of thyroid hormone and estrogen receptor and vitellogenin genes in adult Xenopus (Amphibia) hepatocytes
Rabelo,Elida M.L.
title_short Prolactin inhibits auto- and cross-induction of thyroid hormone and estrogen receptor and vitellogenin genes in adult Xenopus (Amphibia) hepatocytes
title_full Prolactin inhibits auto- and cross-induction of thyroid hormone and estrogen receptor and vitellogenin genes in adult Xenopus (Amphibia) hepatocytes
title_fullStr Prolactin inhibits auto- and cross-induction of thyroid hormone and estrogen receptor and vitellogenin genes in adult Xenopus (Amphibia) hepatocytes
title_full_unstemmed Prolactin inhibits auto- and cross-induction of thyroid hormone and estrogen receptor and vitellogenin genes in adult Xenopus (Amphibia) hepatocytes
title_sort Prolactin inhibits auto- and cross-induction of thyroid hormone and estrogen receptor and vitellogenin genes in adult Xenopus (Amphibia) hepatocytes
author Rabelo,Elida M.L.
author_facet Rabelo,Elida M.L.
Tata,Jamshed R.
author_role author
author2 Tata,Jamshed R.
author2_role author
dc.contributor.author.fl_str_mv Rabelo,Elida M.L.
Tata,Jamshed R.
description It is well known that virtually every tissue of the amphibian larvae is highly sensitive to the mutually antagonistic actions of thyroid hormone (TH) and prolactin (PRL), but it is not known if adult amphibian tissues respond similarly to these two hormones. We have previously shown that very low doses of triiodothyronine (T3) rapidly and strongly potentiate the activation of silent vitellogenin (Vit) genes by estrogen (E2) and the autoinduction of estrogen receptor (ER) transcripts in primary cultures of adult Xenopus hepatocytes. This response to T3 is accompanied by the upregulation of thyroid hormone receptor <FONT FACE="Symbol">b</FONT> (TR<FONT FACE="Symbol">b</FONT>) mRNA. Using Northern blot and RNase protection assays, we now show that ovine PRL added for 12 h along with 2 x 10-9 M T3 will completely prevent potentiation of E2 induction of Vit mRNA in primary cultures of adult Xenopus hepatocytes. PRL also abolished the auto-upregulation of TR<FONT FACE="Symbol">b</FONT> mRNA and the cross-activation of autoinduction of ER mRNA. Thus, we show for the first time that the anti-TH action of PRL that is manifested in Xenopus tadpole tissues during metamorphosis is retained in adult liver, and suggest that the mutually antagonistic actions of the two hormones may be brought about by similar molecular mechanisms in larval and adult amphibian tissues
publishDate 1997
dc.date.none.fl_str_mv 1997-12-01
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-84551997000400010
url http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-84551997000400010
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv 10.1590/S0100-84551997000400010
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv text/html
dc.publisher.none.fl_str_mv Sociedade Brasileira de Genética
publisher.none.fl_str_mv Sociedade Brasileira de Genética
dc.source.none.fl_str_mv Brazilian Journal of Genetics v.20 n.4 1997
reponame:Brazilian Journal of Genetics
instname:Sociedade Brasileira de Genética (SBG)
instacron:SBG
instname_str Sociedade Brasileira de Genética (SBG)
instacron_str SBG
institution SBG
reponame_str Brazilian Journal of Genetics
collection Brazilian Journal of Genetics
repository.name.fl_str_mv Brazilian Journal of Genetics - Sociedade Brasileira de Genética (SBG)
repository.mail.fl_str_mv sede@sgb.org.br || sede@sgb.org.br
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