| Autor: |
Cláudia Emanuele Carvalho-Sousa, Sanseray eda Silveira Cruz-Machado, Eduardo Koji Tamura, Pedro A C. M. Fernandes, Luciana ePinato, Sandra M Muxel, Erika eCecon, Regina P. Markus |
| Jazyk: |
angličtina |
| Rok vydání: |
2011 |
| Předmět: |
|
| Zdroj: |
Frontiers in Endocrinology, Vol 2 (2011) |
| Druh dokumentu: |
article |
| ISSN: |
1664-2392 |
| DOI: |
10.3389/fendo.2011.00010 |
| Popis: |
The pineal gland, which is the gland that translates darkness into an endocrine signal by releasing melatonin at night, is now considered a key player in the mounting of an innate immune response. Tumor necrosis factor (TNF), the first pro-inflammatory cytokine to be released by an inflammatory response, suppresses the translation of the key enzyme of melatonin synthesis (arylalkylamine-N-acetyltransferase-alkyl-N-acetyltransferase, Aa-nat). Here we show that TNF receptors of the subtype 1 (TNF-R1) are expressed by astrocytes, microglia and pinealocytes. We also show that the activation of TNF triggers the nuclear factor kappa B (NFKB) pathway in pinealocytes by reducing the cytoplasmic level of the inhibitory nuclear factor kappa B protein of the subtype A (NFKBIA). The TNF-induced nuclear translocation of the p50/p50 NFKB transcription factor lacks a transactivation domain, and this phenomenon explains how TNF blocks the transcription of Aa-nat. In addition, the p65/RelA nuclear translocation was read-out following the expression of inducible nitric oxide synthase (iNOS) and the synthesis of nitric oxide NO. The increase in the transcription of genes activated by NFKB opens a new perspective for understanding the implication of the pineal gland in pathophysiological conditions. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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