Oligodendroglial cyclic AMP response element‐binding protein: A member of the CREB family of transcription factors

Sato‐Bigbee, Carmen; Chan, Edward L.; Yu, Robert K.

doi:10.1002/jnr.490380604

Cited by 36 publications

(37 citation statements)

References 28 publications

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“…Furthermore, intracerebroventricular administration of IGF-I has shown antidepressant-like behavioral effects with increased serotonin transmissions in rodent models (Hoshaw et al, 2008). CREB is also highly expressed in oligodendrocytes (SatoBigbee and Yu, 1993;Sato-Bigbee et al, 1994). Studies have shown that IGF-I can induce multipotent adult neural progenitor cells to become oligodendrocytes (Hsieh et al, 2004).…”

Section: Antidepressant Treatment May Increase Functioning Of Oligodementioning

confidence: 99%

Hyperforin promotes mitochondrial function and development of oligodendrocytes

Wang

Zhang

et al. 2011

Journal of Neurochemistry

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Major depressive disorder is a common severe psychiatric disorder with unknown etiology. Recent studies show that the loss and malfunction of oligodendrocytes are closely related to the neuropathological changes in depression, which can be reversed by antidepressant treatment. St. John's wort is an effective and safe herbal treatment for depression in several clinical trials. However, the underlying mechanism of its therapeutic effects is unclear. In this study, we evaluated the effects of hyperforin, a iii ACKNOWLEDGEMENTS

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Section: Antidepressant Treatment May Increase Functioning Of Oligodementioning

confidence: 99%

Hyperforin promotes mitochondrial function and development of oligodendrocytes

Wang

Zhang

et al. 2011

Journal of Neurochemistry

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“…We have previously shown the presence of the transcription factor cAMP response element binding protein (CREB) in oligodendrocytes (Sato-Bigbee and Yu, 1993;Sato-Bigbee et al, 1994). CREB belongs to a family of transcription factors which includes various isoforms of CREB modulator protein (CREM) and activation transcription factors (ATF) (Hai et a]., 1989;Habener, 1990;Lalli and Sassone-Corsi, 1994).…”

Section: Introductionmentioning

confidence: 96%

“…The efficiency of CREB as a transcriptional activator of cAMP responsive genes is modulated by its phosphorylation at serine 133 by CAMP-dependent protein kinase A (PKA) (Yamamoto et al, 1989). Our previous results indicated that the CREB protein present in oligodendrocytes contains the transactivating region designated as the alpha region (Sato-Bigbee et al, 1994). This alpha region, which is absent in the negative regulator CREB-2, interacts with the PKA phosphorylation motif to stimulate transcription .…”

Section: Introductionmentioning

confidence: 97%

“…This alpha region, which is absent in the negative regulator CREB-2, interacts with the PKA phosphorylation motif to stimulate transcription . We have shown previously that in oligodendroglial cells isolated from rat brain at different postnatal ages, CREB expression was maximal at 14 days suggesting a role in a developmental period that immediately precedes the peak of myelination (Sato-Bigbee and Yu, 1993;Sato-Bigbee et al, 1994). Studies on the role of transcription factors in primary cultures of eukaryotic cells represent a challenging problem.…”

Section: Introductionmentioning

confidence: 98%

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Treatment of oligodendrocytes with antisense deoxyoligonucleotide directed against CREB mRNA: Effect on the cyclic AMP-dependent induction of myelin basic protein expression

Sato‐Bigbee

DeVries

1996

J. Neurosci. Res.

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We have shown previously that in oligodendrocytes, the transcription factor cyclic AMP response element binding protein (CREB) is maximally expressed immediately prior to the most rapid period of myelination in rat brain. We have begun to investigate the role of this protein during myelination by downregulating CREB synthesis in cultured oligodendrocytes using an antisense deoxyoligonucleotide directed against CREB mRNA. Neonatal oligodendrocytes were grown for 4 days in a chemically defined medium (CDM) after which intracellular delivery of CREB antisense oligonucleotide was facilitated by using a liposome preparation. Control cultures were treated in a similar manner but in the presence of CREB sense oligomer. Immediately after transfection, cells were cultured for 3 days in CDM in the presence or absence of the cyclic AMP (cAMP) analogue N6,O21‐dibutyryl cAMP (db‐cAMP). In these cultures, myelin basic protein (MBP) expression was investigated by immunocytochemistry and Western blot analysis. Treatment of control cultures with db‐cAMP resulted in a significant increase in the number of MBP positive cells which was abolished when the cells were treated with CREB antisense oligonucleotide. MBP positive cells in control cultures treated with db‐cAMP have extended and highly branched MBP positive processes. In contrast, MBP positive cells in either control cultures grown in the absence of db‐cAMP or cultures grown in the presence of db‐cAMP but treated with CREB antisense oligonucleotide showed shorter and less complex processes and the MBP immunoreactivity appeared to be concentrated in the cell body. These observations suggest that CREB is at least one of the mediators in the induction of oligodendrocyte differentiation by cAMP. © 1996 Wiley‐Liss, Inc.

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“…cAMP plays an important role in inducing oligodendrocyte differentiation and myelin synthesis (10,11). Furthermore, the transcription factor, cAMP response element-binding protein (CREB) is a key mediator of stimulus-induced cAMPmediated nuclear responses that underlie survival of neurons.…”

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confidence: 99%

Rolipram, a Phosphodiesterase Type IV Inhibitor, Exacerbates Periventricular White Matter Lesions in Rat Pups

et al. 2008

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Periventricular white matter injury is the leading cause of cerebral palsy in premature infants for which no effective treatments are available. Our previous studies have demonstrated that pharmacological activation of the cAMP response element-binding protein (CREB) signaling pathway, before hypoxic-ischemia protected against neuronal injury in neonatal rats. We examined whether rolipram, a phosphodiesterase type IV inhibitor, treatment after hypoxic-ischemia is protective against white matter injury in neonatal rats. Rats were exposed to hypoxia-ischemia (HI) on P7 and then treated with daily injections of various doses of rolipram (P7-P11). Immunohistochemical staining for myelin basic protein, ED1, glial fibrillary acidic protein, CREB and O1 were examined on P11. We found that the periventricular white matter and deep cortical lesions were exacerbated by rolipram administration after HI injury. The lesions in the rolipram-treated group also showed increased astrogliosis and increased CREB phosphorylation in the activated microglia and astrocytes. Furthermore, the rolipram-posttreated HI group had markedly depleted preoligodendrocytes in the ipsilateral hemisphere, which may be related to decreased preoligodendrocytes proliferation after rolipram treatment per se. These data suggest that rolipram treatment after hypoxic-ischemia is not protective; in contrast, rolipram may exacerbate hypoxic-ischemic white matter injury in neonatal rat brains. N early 90% of low-birth weight infants now survive with the advances in neonatal intensive care. Of the survivors, however, 10 -15% have cerebral palsy, and 25-50% have manifest cognitive and behavioral deficits (1). Periventricular white matter injury, or leukomalacia (PVL), is the major form of brain injury in preterm babies. The neuropatholgical findings are characterized by distinct cystic white matter lesions and, commonly, a more diffuse loss of white matter volume and secondary ventriculomegaly (2). Notably, despite the significant long-term morbidity, there is currently no specific treatment for these disorders.Although, the exact cause of PVL in human infants is currently unknown, hypoxia-ischemia (HI) is believed to be a significant cause (3). Cell-type specific factors are also likely to underlie the mechanisms of PVL. Data from a recent study demonstrated that PVL in humans was related to oxidative damage that particularly targeted cells of the oligodendrocyte lineage; whereas neuronal and glial cells were markedly more resistant (4). The timing of appearance of preoligodendrocytes (preOLs) coincides with the high-risk period for PVL (5). Considerable data demonstrate that preOLs are highly susceptible to oxidative stress and hypoxic-ischemia injury (6 -9). Compared with mature oligodendrocytes, preOLs express lower levels of antioxidant enzymes (6). These data suggest that acceleration of preOLs maturation might be a feasible strategy to reduce the severity of PVL.cAMP plays an important role in inducing oligodendrocyte differentiation and myeli...

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Oligodendroglial cyclic AMP response element‐binding protein: A member of the CREB family of transcription factors

Cited by 36 publications

References 28 publications

Hyperforin promotes mitochondrial function and development of oligodendrocytes

Hyperforin promotes mitochondrial function and development of oligodendrocytes

Treatment of oligodendrocytes with antisense deoxyoligonucleotide directed against CREB mRNA: Effect on the cyclic AMP-dependent induction of myelin basic protein expression

Rolipram, a Phosphodiesterase Type IV Inhibitor, Exacerbates Periventricular White Matter Lesions in Rat Pups

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