Fluoxetine up-regulates expression of cellular FLICE-inhibitory protein and inhibits LPS-induced apoptosis in hippocampus-derived neural stem cell

Chiou, Shih Hwa; Chen, Shih‐Jen; Peng, Chi Hsien; Chang, Yu Li; Ku, Hung Hai; Hsu, Wen Ming; Ho, Larry L.T.; Lee, Chen Hsen

doi:10.1016/j.bbrc.2006.02.180

Cited by 88 publications

(51 citation statements)

References 36 publications

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“…31,32 Here, our results reveal that, at least in fibroblasts, cAMP induces the expression of both MKP-1 and c-FLIP L (Figure 5a to dephosphorylate each one of these kinases varies depending on the cell system and its environmental conditions. 36,37 Conditional expression of MKP-1 was found to abolish UV-induced JNK activity, and inhibit UV-induced apoptosis.…”

Section: Discussionmentioning

confidence: 86%

Cyclic AMP inhibits JNK activation by CREB-mediated induction of c-FLIPL and MKP-1, thereby antagonizing UV-induced apoptosis

Zhang

Wang²,

Zhu³

et al. 2008

Cell Death Differ

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The cyclic AMP (cAMP) signaling pathway has been reported to either promote or suppress apoptosis, in a cell contextdependent manner. Our previous study has shown that cAMP, by protein kinase A (PKA)-cAMP response element-binding protein (CREB)-dynein light chain (DLC) pathway, negatively regulates mitogen-activated protein kinase p38 activation, thereby contributing to tumor necrosis factor (TNF)-a-induced apoptosis in certain types of cells. However, it remains largely unknown how cAMP suppresses apoptosis. Here we report that cAMP antagonized UV-induced apoptosis in Rat-1 and NIH 3T3 cells. Despite that cAMP significantly suppressed UV-induced p38 activation, inhibition of p38 activity showed no significant effect on UV-induced cell death in both cell lines. Further studies revealed that cAMP antagonized UV-induced apoptosis by inhibition of cJun N-terminal protein kinase (JNK) activation. The induction of the long form of cellular FLICE-inhibitory protein (c-FLIP L ) and mitogen-activated protein kinase phosphatase-1 (MKP-1), but not DLC and p21WAF1 by CREB was required for cAMP-mediated inhibition of JNK activation. The suppression by cAMP of UV-induced apoptosis was reversed by c-FLIP L small-interfering RNA (siRNA) or MKP-1 siRNA, which released the inhibition of JNK activation by cAMP. Thus, our results provide a molecular mechanism by which cAMP suppresses JNK activation and antagonizes apoptosis.

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Section: Discussionmentioning

confidence: 86%

Cyclic AMP inhibits JNK activation by CREB-mediated induction of c-FLIPL and MKP-1, thereby antagonizing UV-induced apoptosis

Zhang

Wang²,

Zhu³

et al. 2008

Cell Death Differ

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show abstract

“…This indicates that although induced apoptosis is usually associated with changes in the amount of apoptotic gene transcripts, induced without changes in the transcript level of these genes probably due to posttranscriptional induction/regulation of the pathway. Previous studies examined the effects of FLX on apoptosis with different types of cell, such as adult neurons, hepatocytes, lymphoma cells, and neuroblastoma cells (Chen et al, 2007;Chiou et al, 2006;Koch et al, 2003;Lee et al, 2001;Levkovitz et al, 2005;Nahon et al, 2005;Serafeim et al, 2003). However, these studies used nonhuman CNS cells and animal models.…”

Section: Discussionmentioning

confidence: 99%

“…Previous reports have shown conflicting evidence regarding the effect of FLX on apoptosis. Some studies showed an increase in apoptotic activity due to FLX in different cell lines using various methods (Koch et al, 2003;Levkovitz et al, 2005;Serafeim et al, 2003), while others found an increase in antiapoptotic activity (Chen et al, 2007;Chiou et al, 2006;Lee et al, 2001;Nahon et al, 2005). These conflicting findings may have resulted from differences in cell lines, FLX concentrations, or the duration of treatment.…”

Section: Discussionmentioning

confidence: 99%

Increased cellular turnover in response to fluoxetine in neuronal precursors derived from human embryonic stem cells

et al. 2010

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“…It has been shown that chronic antidepressant treatment (e.g., with fluoxetine) has been shown to up-regulate neurogenesis (Malberg, 2004). Fluoxetine has previously been reported to prevent MDMA ("ecstasy")-induced degeneration of serotonergic nerve endings (Sanchez et al, 2001) and to increase the proliferation of neuronal stem cells derived from the hippocampus (Chiou et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Fluoxetine and Sertraline Attenuate Postischemic Brain Injury in Mice

Shin

Kang

Lee

et al. 2009

Korean J Physiol Pharmacol

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ABBREVIATIONS: SSRIs, serotonin reuptake inhibitors; HO-1, heme oxygenase-1; HIF-1α, hypoxia-inducible factor-1α; BBB, blood-brain barrier; rCBF, regional cerebral blood flow; MABP, mean arterial blood pressure; LL, lower limit; HSP-32, heat-shock protein. Medicine, Korea This study aimed to investigate whether selective serotonin reuptake inhibitors (SSRIs) attenuate brain injury and facilitate recovery following photothrombotic cortical ischemia in mice. Male ICR mice were anesthetized and systemically administered Rose Bengal. Permanent focal ischemia was induced in the medial frontal and somatosensory cortices by irradiating the skull with cold light laser. The animals were treated with fluoxetine or sertraline once a day for 14 d starting 1 h after ischemic insult. Treatment with fluoxetine and sertraline significantly reduced the infarct size. The Evans blue extravasation indices of the fluoxetine-and sertraline-treated groups were significantly lower than that of the vehicle group. Treatment with fluoxetine and sertraline shifted the lower limit of the mean arterial blood pressure for cerebral blood flow autoregulation toward normal, and significantly increased the expression of heme oxygenase-1 (HO-1) and hypoxia-inducible factor-1α (HIF-1α) proteins in the ischemic region. These results suggest that SSRIs, such as fluoxetine and sertraline, facilitate recovery following photothrombotic cortical ischemia via enhancement of HO-1 and HIF-1α proteins expression, thereby providing a benefit in therapy of cerebral ischemia.

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Fluoxetine up-regulates expression of cellular FLICE-inhibitory protein and inhibits LPS-induced apoptosis in hippocampus-derived neural stem cell

Cited by 88 publications

References 36 publications

Cyclic AMP inhibits JNK activation by CREB-mediated induction of c-FLIPL and MKP-1, thereby antagonizing UV-induced apoptosis

Cyclic AMP inhibits JNK activation by CREB-mediated induction of c-FLIPL and MKP-1, thereby antagonizing UV-induced apoptosis

Increased cellular turnover in response to fluoxetine in neuronal precursors derived from human embryonic stem cells

Fluoxetine and Sertraline Attenuate Postischemic Brain Injury in Mice

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