Pineal function: Impact of microarray analysis

Klein, David C.; Bailey, Michael; Carter, David A.; Kim, Jong–So; Shi, Qiong; Ho, Anthony K.; Chik, Constance L.; Gaildrat, Pascaline; Morin, Fabrice; Ganguly, Shantanu; Rath, Martin F.; Møller, Morten Hylander; Sugden, David; Rangel, Zoila G.; Munson, Peter J.; Weller, Joan L.; Coon, Steven L.

doi:10.1016/j.mce.2009.07.010

Cited by 41 publications

(36 citation statements)

References 110 publications

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“…The mammalian pineal gland is a neuroendocrine organ, which converts photoperiodic information into the nocturnal hormonal signal of melatonin [12]. In most mammals, the pineal gland is located directly on the dorsal part of the brain stem at the mesencephalic-diencephalic border, whereas in rodents it is subdivided into a superficial part located on top of the brain just caudal to the hemispheres and a deep part consisting of a collection of pinealocytes located between the habenular and posterior commissures.…”

Section: Development and Circadian Function Of The Mammalian Pineamentioning

confidence: 99%

Homeobox Genes in the Rodent Pineal Gland: Roles in Development and Phenotype Maintenance

et al. 2012

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The pineal gland is a neuroendocrine gland responsible for nocturnal synthesis of melatonin. During early development of the rodent pineal gland from the roof of the diencephalon, homeobox genes of the orthodenticle homeobox (Otx)- and paired box (Pax)-families are expressed and are essential for normal pineal development consistent with the well-established role that homeobox genes play in developmental processes. However, the pineal gland appears to be unusual because strong homeobox gene expression persists in the pineal gland of the adult brain. Accordingly, in addition to developmental functions, homeobox genes appear to be key regulators in postnatal phenotype maintenance in this tissue. In this paper, we review ontogenetic and phylogenetic aspects of pineal development and recent progress in understanding the involvement of homebox genes in rodent pineal development and adult function. A working model is proposed for understanding the sequential action of homeobox genes in controlling development and mature circadian function of the mammalian pinealocyte based on knowledge from detailed developmental and daily gene expression analyses in rats, the pineal phenotypes of homebox gene-deficient mice and studies on development of the retinal photoreceptor; the pinealocyte and retinal photoreceptor share features not seen in other tissues and are likely to have evolved from the same ancestral photodetector cell.

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Section: Development and Circadian Function Of The Mammalian Pineamentioning

confidence: 99%

Homeobox Genes in the Rodent Pineal Gland: Roles in Development and Phenotype Maintenance

et al. 2012

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“…Serotonin is then acetylated to form N-acetylserotonin by the enzyme arylakylamine N-acetyltransferase while N-acetylserotonin is converted into melatonin by the enzyme hydroxyindole-O-methyl transferase [37, 38]. Once formed melatonin is not stored within the pineal gland it diffuses into the capillary blood and the cerebrospinal fluid (CSF) [39, 40].…”

Section: Melatonin In Admentioning

confidence: 99%

Melatonin and Its Agonist Ramelteon in Alzheimer′s Disease: Possible Therapeutic Value

Srinivasan

Kaur

Pandi-Perumal³

et al. 2010

International Journal of Alzheimer's Disease

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Alzheimer's disease (AD) is an age-associated neurodegenerative disease characterized by the progressive loss of cognitive function, loss of memory and insomnia, and abnormal behavioral signs and symptoms. Among the various theories that have been put forth to explain the pathophysiology of AD, the oxidative stress induced by amyloid β-protein (Aβ) deposition has received great attention. Studies undertaken on postmortem brain samples of AD patients have consistently shown extensive lipid, protein, and DNA oxidation. Presence of abnormal tau protein, mitochondrial dysfunction, and protein hyperphosphorylation all have been demonstrated in neural tissues of AD patients. Moreover, AD patients exhibit severe sleep/wake disturbances and insomnia and these are associated with more rapid cognitive decline and memory impairment. On this basis, the successful management of AD patients requires an ideal drug that besides antagonizing Aβ-induced neurotoxicity could also correct the disturbed sleep-wake rhythm and improve sleep quality. Melatonin is an effective chronobiotic agent and has significant neuroprotective properties preventing Aβ-induced neurotoxic effects in a number of animal experimental models. Since melatonin levels in AD patients are greatly reduced, melatonin replacement has the potential value to be used as a therapeutic agent for treating AD, particularly at the early phases of the disease and especially in those in whom the relevant melatonin receptors are intact. As sleep deprivation has been shown to produce oxidative damage, impaired mitochondrial function, neurodegenerative inflammation, and altered proteosomal processing with abnormal activation of enzymes, treatment of sleep disturbances may be a priority for arresting the progression of AD. In this context the newly introduced melatonin agonist ramelteon can be of much therapeutic value because of its highly selective action on melatonin MT1/MT2 receptors in promoting sleep.

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“…The binding of CREB to the CRE-L and CRE.2 binding sites results in the activation of the IA-2 promoter and an increase in IA-2 mRNA and IA-2 protein. The widespread distribution of CREB and CREB-binding sites throughout the genome [21] may explain the high levels of IA-2 seen in some tissues [22, 23] and tumors [24, 25] where DCV have not been detected. Viewing the IA-2 promoter region from an even broader perspective, when the 5′-upstream region from −1300 to +115 was examined by the TRES program, a number of other potential transcription binding sites and CREB activators were identified [26–30].…”

Section: Discussionmentioning

confidence: 99%

The minimal promoter region of the dense-core vesicle protein IA-2: transcriptional regulation by CREB

Cai

Hirai

et al. 2014

Acta Diabetol

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IA-2 is a transmembrane protein found in the dense core vesicles (DCV) of neuroendocrine cells and one of the major autoantigens in type 1 diabetes. DCV are involved in the secretion of hormones (e.g., insulin) and neurotransmitters. Stimulation of pancreatic β cells with glucose upregulates the expression of IA-2 and an increase of IA-2 results in an increase of the number of DCV. Little is known, however, about the promoter region of IA-2 or the transcriptional factors that regulate the expression of this gene. In the present study, we constructed eight deletion fragments from the upstream region of the IA-2 transcription start site and linked them to a luciferase reporter. By this approach we have identified a short bp region (−216 to +115) that has strong promoter activity. We also identified a transcription factor, CREB (cAMP Responsive Element Binding Protein), which binds to two CREB-related binding sites located in this region. The binding of CREB to these sites enhanced IA-2 transcription by more than 5 fold. We confirmed these findings by site-directed mutagenesis, chromatin immunoprecipitation (ChIP) assays and RNAi inhibition. Based on these findings we conclude that the PKA pathway is a critical, but not the exclusive signaling pathway involved in IA-2 gene expression.

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Pineal function: Impact of microarray analysis

Cited by 41 publications

References 110 publications

Homeobox Genes in the Rodent Pineal Gland: Roles in Development and Phenotype Maintenance

Homeobox Genes in the Rodent Pineal Gland: Roles in Development and Phenotype Maintenance

Melatonin and Its Agonist Ramelteon in Alzheimer′s Disease: Possible Therapeutic Value

The minimal promoter region of the dense-core vesicle protein IA-2: transcriptional regulation by CREB

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