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Title

Thyroid hormone antagonizes tumor necrosis factor-α signaling in pituitary cells through the induction of dual specificity phosphatase 1

AuthorsLasa, Marina CSIC ORCID; Gil-Araujo, Beatriz CSIC; Palafox, Marta; Aranda, Ana CSIC ORCID
KeywordsNf-kappa-b
Activated protein-kinase
Rat gh3 cells
Gene-expression
P38 mapk
Tnf-alpha
Tyrosine phosphorylation
Molecular-mechanisms
Receptor-gamma
Messenger-rna
Issue Date1-Feb-2010
PublisherEndocrine Society
CitationMolecular Endocrinology 24(2): 412-422 (2010)
AbstractPituitary function has been shown to be regulated by an increasing number of factors, including cytokines and hormones, such as TNF alpha and T-3. Both the proinflammatory cytokine TNF alpha and T-3 have been suggested to be involved in the maintenance of tissue homeostasis in the anterior pituitary gland. In this report we show that T-3 negatively interferes with MAPK p38 and nuclear factor-kappa B (NF-kappa B) activation by TNF alpha in GH4C1 cells. Our data demonstrate that MAPK p38 is specifically activated upon exposure to TNF alpha and that T-3 abolishes this activation in a time-dependent manner by a mechanism that involves the induction of the MAPK phosphatase, DUSP1. Our data show that the pool of up-regulated DUSP1 by T-3 is mainly localized to the cytosol, and that TNF alpha does not affect this localization. On the other hand, we show that T-3 impairs the activation of the NF-kappa B pathway induced by TNF alpha, producing a significant decrease in NF-kappa B-dependent transcription, phosphorylation of I kappa B alpha, translocation of p65/NF-kappa B to the nucleus, and p65/NF-kappa B transactivation potential. Interestingly, the overexpression of DUSP1 inhibits the NF-kappa B activation achieved by either TNF alpha or ectopic expression of the upstream inducer of MAPK p38. Conversely, DUSP1 depletion abrogates the inhibitory effect of T-3 on the induction of NF-kappa B-dependent transcription by TNF alpha. Overall, our results indicate that T-3 antagonizes TNF alpha signaling in rat pituitary tumor cells through the induction of DUSP1.
Publisher version (URL)http://dx.doi.org/10.1210/me.2009-0298
URIhttp://hdl.handle.net/10261/37089
DOI10.1210/me.2009-0298
ISSN0888-8809
Appears in Collections:(IIBM) Artículos

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