Diurnal variation in p42/44 mitogen-activated protein kinase in the rat pineal gland

Ho, Angela; Macková, Martina; Price, Luke M.; Chik, Constance L.

doi:10.1016/s0303-7207(03)00260-0

Cited by 19 publications

(19 citation statements)

References 34 publications

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“…In rodents, p38 MAPK is activated in response to light in the SCN during the subjective night, matching the phase gating of ERK in the hamster SCN (Pizzio, Hainich, Ferreyra, Coso, & Golombek, 2003). In cultured rat pineal gland, p38 MAPK activation is similar to ERK in that both are rhythmic in an LD cycle, peaking during the subjective night (Chik, Mackova, Price, & Ho, 2004; Ho, Mackova, Price, & Chik, 2003). However, blockage of p38 signaling had no effect on the activation of CREB in cortical neurons, demonstrating that p38 probably does not signal through the CREB-mediated clock resetting pathway (Arthur et al, 2004).…”

Section: The Function Of Mapks In Circadian Input Pathwaysmentioning

confidence: 98%

“…The pineal gland, a neuroendocrine component of the clock that contributes to overall rhythmicity of the organism, produces the hormone melatonin that is secreted at night into the circulatory system to relay temporal information to peripheral oscillators (Dibner et al, 2010; Ho et al, 2003). In the rat pineal gland, the ERK pathway is activated by the sympathetic nervous system and is rhythmically activated in an LD cycle with a peak during the subjective night (Ho et al, 2003).…”

Section: The Role Of Mapk Pathways In Circadian Outputmentioning

confidence: 99%

Section: The Role Of Mapk Pathways In Circadian Outputmentioning

confidence: 99%

“…In the rat pineal gland, the ERK pathway is activated by the sympathetic nervous system and is rhythmically activated in an LD cycle with a peak during the subjective night (Ho et al, 2003). In this tissue, ERK regulates the synthesis of a rate-limiting precursor in melatonin synthesis that generates the rhythm in melatonin production (Ho et al, 2003). A direct photic stimulation of a pineal gland in explant culture results in suppression of p-ERK and a simultaneous decrease in melatonin precursor, suggesting that p-ERK connects neural stimulation to the production of melatonin (Ho et al, 2003).…”

Section: The Role Of Mapk Pathways In Circadian Outputmentioning

confidence: 99%

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Diverse Roles for MAPK Signaling in Circadian Clocks

Goldsmith

Bell-Pedersen

2013

Advances in Genetics

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The mitogen-activated protein kinase (MAPK) family of genes aids cells in sensing both extracellular and intracellular stimuli, and emerging data indicate that MAPKs have fundamental, yet diverse, roles in the circadian biological clock. In the mammalian sup-rachiasmatic nucleus (SCN), MAPK pathways can function as inputs allowing the endogenous clock to entrain to 24 h environmental cycles. MAPKs can also interact physically and/or genetically with components of the molecular circadian oscillator, implying that MAPKs can affect the cycling of the clock. Finally, circadian rhythms in MAPK pathway activation exist in many different tissue types and in model organisms, providing a mechanism to coordinately control the expression tissue-specific target genes at the proper time of day. As such, it should probably not come as a surprise that MAPK signaling pathways and circadian clocks affect similar biological processes and defects in either pathway lead to many of the same types of human diseases, highlighting the need to better define the mechanisms that link these two fundamental pathways together.

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Section: The Function Of Mapks In Circadian Input Pathwaysmentioning

confidence: 98%

Section: The Role Of Mapk Pathways In Circadian Outputmentioning

confidence: 99%

Section: The Role Of Mapk Pathways In Circadian Outputmentioning

confidence: 99%

Section: The Role Of Mapk Pathways In Circadian Outputmentioning

confidence: 99%

See 2 more Smart Citations

Diverse Roles for MAPK Signaling in Circadian Clocks

Goldsmith

Bell-Pedersen

2013

Advances in Genetics

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“…First, p38 MAPK phosphorylation levels oscillate in the rat and chick pineal gland where these kinases have been shown to control the period and phase of circadian rhythms (Hayashi et al, 2003;Hasegawa and Cahill, 2004). Second, daily and circadian rhythms of ERK activations occur respectively in the rat pineal gland (Ho et al, 2003), and in both Syrian hamster and mouse SCN (Obrietan et al, 1998;Pizzio et al, 2003). In the mouse SCN, ERK is known to participate to the entrainment of rhythms by light cycles (Butcher et al, 2002;Dziema et al, 2003).…”

mentioning

confidence: 99%

c-Jun N-terminal kinase inhibitor SP600125 modulates the period of mammalian circadian rhythms

et al. 2007

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Circadian rhythms are endogenous cycles with periods close to, but not exactly equal to, 24 h. In mammals, circadian rhythms are generated in the suprachiasmatic nucleus (SCN) of the hypothalamus as well as several peripheral cell types, such as fibroblasts. Protein kinases are key regulators of the circadian molecular machinery. We investigated the role of the c-Jun N-terminal kinases (JNK), which belong to the mitogen-activated protein kinases family, in the regulation of circadian rhythms. In rat-1 fibroblasts, the p46 kDa, but not the p54 kDa, isoforms of JNK expressed circadian rhythms in phosphorylation. The JNK-inhibitor SP600125 dose-dependently extended the period of Period1-luciferase rhythms in rat-1 fibroblasts from 24.23±0.17-31.48±0.07 h. This treatment also dose-dependently delayed the onset of the bioluminescence rhythms. The effects of SP600125 on explant cultures from Period1-luciferase transgenic mice and Period2 Luciferase knockin mice appeared tissue-specific. SP600125 lengthened the period in SCN, pineal gland, and lung explants in Period1-luciferase and Period2 Luciferase mice. However, in the kidneys circadian rhythms were abolished in Period1-luciferase, while circadian rhythms were not affected by SP600125 treatment in Period2 Luciferase mice. Valproic acid, already known to affect period length, enhanced JNK phosphorylation and, as predicted, shortened the period of the Period1-bioluminescence rhythms in rat-1 fibroblasts. In conclusion, our results showed that SP600125 treatment, as well as valproic acid, alters JNK phosphorylation levels, and modulates the period length in various tissues. We conclude that JNK phosphorylation levels may help to set the period length of mammalian circadian rhythms. Keywords SCN; peripheral oscillators; Period genes; valproic acid; real time bioluminescence monitoringDeveloped through evolution to adjust to environmental conditions, self-sustained circadian oscillators generate daily fluctuations in behavior and physiology with a period of approximately 24 h. The study of the mammalian circadian clock at molecular levels has progressed dramatically over the past decade (Fukuhara and Tosini, 2003;Schibler et al., 2003;Gachon et al., 2004). In mammals, the central circadian clock is localized to the suprachiasmatic nucleus (SCN) of the hypothalamus, which synchronizes circadian events within the body. Peripheral circadian clocks have been found in many types of cells and tissues, e.g. fibroblasts, pineal gland, heart, liver, kidney, lung, and so on. Sustained circadian rhythm can be generated not only in a SCN neuron, but also in a fibroblast and other tissues and organs. Numerous studies of the molecular clock mechanism have suggested that these circadian pacemakers consist of transcriptional/translational autoregulatory feedback loops of several clock gene products (Hastings and Herzog, 2004;Ko and Takahashi, 2006). The stability of clock proteins, regulated through phosphorylation and dephosphorylation via protein kinases and phosphatases, is ...

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Rhythmic Diurnal Synthesis and Signaling of Retinoic Acid in the Rat Pineal Gland and Its Action to Rapidly Downregulate ERK Phosphorylation

et al. 2018

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Vitamin A is important for the circadian timing system; deficiency disrupts daily rhythms in activity and clock gene expression, and reduces the nocturnal peak in melatonin in the pineal gland. However, it is currently unknown how these effects are mediated. Vitamin A primarily acts via the active metabolite, retinoic acid (RA), a transcriptional regulator with emerging non-genomic activities. We investigated whether RA is subject to diurnal variation in synthesis and signaling in the rat pineal gland. Its involvement in two key molecular rhythms in this gland was also examined: kinase activation and induction of Aanat, which encodes the rhythm-generating melatonin synthetic enzyme. We found diurnal changes in expression of several genes required for RA signaling, including a RA receptor and synthetic enzymes. The RA-responsive gene Cyp26a1 was found to change between day and night, suggesting diurnal changes in RA activity. This corresponded to changes in RA synthesis, suggesting rhythmic production of RA. Long-term RA treatment in vitro upregulated Aanat transcription, while short-term treatment had no effect. RA was also found to rapidly downregulate extracellular signal-regulated kinase (ERK) 1/2 phosphorylation, suggesting a rapid non-genomic action which may be involved in driving the molecular rhythm in ERK1/2 activation in this gland. These results demonstrate that there are diurnal changes in RA synthesis and activity in the rat pineal gland which are partially under circadian control. These may be key to the effects of vitamin A on circadian rhythms, therefore providing insight into the molecular link between this nutrient and the circadian system.

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Diurnal variation in p42/44 mitogen-activated protein kinase in the rat pineal gland

Cited by 19 publications

References 34 publications

Diverse Roles for MAPK Signaling in Circadian Clocks

Diverse Roles for MAPK Signaling in Circadian Clocks

c-Jun N-terminal kinase inhibitor SP600125 modulates the period of mammalian circadian rhythms

Rhythmic Diurnal Synthesis and Signaling of Retinoic Acid in the Rat Pineal Gland and Its Action to Rapidly Downregulate ERK Phosphorylation

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