Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/53526
Title: Melatonin prevents apoptosis and enhances HSP27 mRNA expression induced by heat shock in HL-60 cells: possible involvement of the MT2 receptor
Authors: Cabrera, J
Quintana, J 
Reiter, RJ
Loro, J 
Cabrera, F
Estevez, F 
UNESCO Clasification: 32 Ciencias médicas
Keywords: Hyperthermia-Induced Apoptosis
G-Protein
Ischemia-Reperfusion
Signal-Transduction
Oxidative Damage, et al
Issue Date: 2003
Publisher: 0742-3098
Journal: Journal of Pineal Research 
Abstract: Previous studies have reported that melatonin protects cells and tissues against stressful stimuli. In the present study using HL-60 cells, we show that cells acquire increased resistance to apoptosis normally induced by heat shock when they are incubated with melatonin. This effect of melatonin is saturable at nanomolar concentrations and appears to be mediated by the MT2 subtype melatonin receptor. The high affinity melatonin receptor agonist, 2-iodomelatonin, reproduced the melatonin effect while it was fully blocked by the selective MT2 antagonist 4-phenyl-2-propionamidotetraline. The melatonin response to heat shock-induced apoptosis was pertussis toxin sensitive and, interestingly, the non-selective MT1/MT2 melatonin receptor ligand luzindole was found to display agonistic activity. Furthermore, we provide evidence that melatonin enhanced HSP27 mRNA expression as a result of heat shock - HSP27, is known to play an important role in the defense of cells against apoptosis induced by stressful agents. Together, these results demonstrate that melatonin, likely via receptor mechanisms, interferes with the apoptotic pathway activated by heat shock.
URI: http://hdl.handle.net/10553/48406
ISSN: 0742-3098
DOI: 10.1034/j.1600-079X.2003.00071.x
Source: Journal of Pineal Research[ISSN 0742-3098],v. 35, p. 231-238 (Noviembre 2003)
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