Modulation of Bcl-2 expression

Singer, Cherie A.; Rogers, Keith L.; Dorsa, Daniel M.

doi:10.1097/00001756-199808030-00025

Cited by 159 publications

(15 citation statements)

References 12 publications

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“…E2 exerts neuroprotective action in various model systems where it reduces neuronal damage caused by serum deprivation (43,44), ␤-amyloid treatment (45,46), and exposure to glutamate (46,47). In the present study we found that E2 protects HiB5 cells against toxicity induced by AMPA and A␤ peptide.…”

Section: Discussionsupporting

confidence: 61%

Estrogen-dependent Transcription of the NEL-like 2 (NELL2) Gene and Its Role in Protection from Cell Death

Choi

Kim

et al. 2010

Journal of Biological Chemistry

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NELL2 (neural tissue-specific epidermal growth factor-like repeat domain-containing protein) is a secreted glycoprotein that is predominantly expressed in neural tissues. We reported previously that NELL2 mRNA abundance in brain is increased by estrogen (E2) treatment and that NELL2 is involved in the E2-dependent organization of a sexually dimorphic nucleus in the preoptic area. In this study we cloned the mouse NELL2 promoter and found it to contain two half-E2 response elements. Electrophoretic mobility shift assays and promoter assays showed that E2 and its receptors (ER␣ and ER␤) stimulated NELL2 transcription by binding to the two half-E2 response elements. Hippocampal neuroprogenitor HiB5 cells expressing recombinant NELL2 showed increased cell survival under cell death-inducing conditions. Blockade of endogenous synthesis of NELL2 in HiB5 cells abolished the cell survival effect of E2 and resulted in a decrease in phosphorylation of extracellular signal-regulated kinase 1 and 2 (ERK1/2). These data suggest that the NELL2 gene is trans-activated by E2 and contributes to mediating the survival promoting effects of E2 via intracellular signaling pathway of ERK.A gene encoding neural epidermal growth factor (EGF) 4 -like protein (NEL) was first identified in the chick embryo (1). A subsequent study reported two mammalian homologs of the chick NEL gene, NEL-like 1 (NELL1) and NEL-like 2 (NELL2), isolated from a human fetal brain cDNA library (2). NELL2 has a greater sequence similarity to chicken NEL than NELL1 and is strongly expressed in mammalian brain in an apparent neuronspecific manner (3-5). NELL2 is a secreted, N-glycosylated protein (3). A large fraction of NELL2 is secreted into culture medium from transfected COS7 and HiB5 cells (3, 6) and from in ovo-transfected chicken spinal cord cells (7). The released NELL2 promotes proliferation and differentiation of neural cells (7) and increases survival of in vitro cultured primary cortical and hippocampal neurons (8).NELL2 is also involved in promoting the neuronal survival required for the formation of a sexually dimorphic nucleus of the preoptic area (SDN-POA) in male rats (6). The volume of the SDN-POA in male rats is much larger than females (for review, see Ref. 9). This has been known to result from the actions of estrogen (E2) on cells of the male SDN-POA (9). E2 exerts multiple effects on developmental processes taking place in the mammalian central nervous system, such as neurogenesis, survival, and differentiation of different neuronal populations (for review, see Ref. 10). A prominent function of E2 in the nervous system is to protect neurons from cell death (for review, see Ref. 11). E2 produced locally by aromatization of circulating testosterone promotes survival of the SDN-POA in neonatal male rats, whereas this effect is not observed in females because fetoneonatal E2 binding protein blocks E2 action in the female brain (12-14). Because blockade of NELL2 synthesis in the neonatal male rat brain resulted in a decreased size of SDN-POA (6),...

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Section: Discussionsupporting

confidence: 61%

Estrogen-dependent Transcription of the NEL-like 2 (NELL2) Gene and Its Role in Protection from Cell Death

Choi

Kim

et al. 2010

Journal of Biological Chemistry

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“…Estradiol prevents cell death by the regulation of genes related to apoptosis [16]. Our results showed that the level of Bcl-2 was decreased in ischemic damage region, whereas the level of Bax was significantly increased.…”

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confidence: 46%

Estrogen Modulates Bcl-2 Family Proteins in Ischemic Brain Injury

Won

Kim

Koh

2006

The Journal of Veterinary Medical Science

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ABSTRACT. Estradiol acts as a neuroprotective factor against brain injury. This study investigated whether estradiol modulates the Bcl-2 family proteins in ischemic brain injury. Adult female rats were ovariectomized and treated with estradiol prior to middle cerebral artery occlusion (MCAO). Brains were collected 24 hr after MCAO, and infarct volumes were analyzed. Estradiol significantly reduces the infarct volume and decreases the positive cells of TUNEL staining in cerebral cortex. In ischemic cerebral cortex, the level of Bcl-2 was decreased, and the level of Bax was significantly increased. Estradiol prevents the injury-induced decrease of Bcl-2 and increase of Bax. In conclusion, our findings suggest that estradiol plays a potent protective role in brain injury through the regulation of Bcl-2 family proteins.

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“…T regulates the expression of antiapoptotic genes such as bcl-2 in the spinal nucleus of the bulbocavernosus in male rats (42). 17␤-Estradiol (E 2 ), a metabolite of T, promotes the expression of several antiapoptotic genes (43)(44)(45)(46)(47)(48). In zebra finches, neuronal injury is accompanied by an increase in expression of aromatase, an enzyme that converts T to E 2 (49), and inhibition of aromatase increases apoptosis near the injury (50).…”

Section: Discussionmentioning

confidence: 99%

Rapid seasonal-like regression of the adult avian song control system

Thompson

Bentley²,

Brenowitz

2007

Proc. Natl. Acad. Sci. U.S.A.

101

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We analyzed how rapidly avian song control nuclei regress after testosterone (T) withdrawal. Regression of neuronal attributes resulting from T withdrawal has been observed in several animal models. The time course over which regression occurs is not known, however. To address this issue, we castrated adult male white-crowned sparrows and rapidly shifted them to short-day photoperiods after being held under breeding conditions (longday photoperiod and systemic T exposure) for 3 weeks. We found that the volume of one song nucleus, HVC, regressed 22% within 12 h after T withdrawal. Changes in HVC neuron density after T withdrawal were dynamic; density increased at 12 h and then decreased by 4 days. HVC neuron number was reduced by 26% by 4 days. The volumes of Area X and the robust nucleus of the arcopallium (RA) were significantly regressed by 7 and 20 days, respectively. RA somatic area and neuronal spacing were significantly reduced by 2 days. The rapidity of HVC regression is unprecedented among vertebrate models of hormone-sensitive neural circuits. These results reveal that the rapid regression of the song control system provides a model for the important role sex steroid hormones play in mediating adult neural plasticity and in neuroprotection.birdsong ͉ neurodegeneration ͉ neuroprotection ͉ plasticity ͉ testosterone

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Modulation of Bcl-2 expression

Cited by 159 publications

References 12 publications

Estrogen-dependent Transcription of the NEL-like 2 (NELL2) Gene and Its Role in Protection from Cell Death

Estrogen-dependent Transcription of the NEL-like 2 (NELL2) Gene and Its Role in Protection from Cell Death

Estrogen Modulates Bcl-2 Family Proteins in Ischemic Brain Injury

Rapid seasonal-like regression of the adult avian song control system

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