Naofen, a novel WD40-repeat protein, mediates spontaneous and tumor necrosis factor-induced apoptosis

Feng, Guo-Gang; Li, Chang; Huang, Lei; Tsunekawa, Koji; Sato, Yuko; Fujiwara, Yoshihiro; Komatsu, T.; Honda, Takashi; Fan, Junhua; Goto, Hidemi; Koide, Tatsurou; Hasegawa, Takaaki; Ishikawa, Naohisa

doi:10.1016/j.bbrc.2010.02.133

Cited by 11 publications

(22 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…WD repeat-containing protein 35 (WDR35) is a novel member of the WDR protein family [3]. Previously, we reported that enhanced WDR35 expression may mediate apoptosis in several animal models [4]–[6].…”

Section: Introductionmentioning

confidence: 99%

Enhanced Expression of WD Repeat-Containing Protein 35 via CaMKK/AMPK Activation in Bupivacaine-Treated Neuro2a Cells

et al. 2014

Self Cite

View full text Add to dashboard Cite

We previously reported that bupivacaine induces reactive oxygen species (ROS) generation, p38 mitogen-activated protein kinase (MAPK) activation and nuclear factor-kappa B activation, resulting in an increase in expression of WD repeat-containing protein 35 (WDR35) in mouse neuroblastoma Neuro2a cells. However, the identity of signaling upstream of p38 MAPK pathways to WDR35 expression remains unclear. It has been shown that AMP-activated protein kinase (AMPK) can activate p38 MAPK through diverse mechanisms. In addition, several kinases acting upstream of AMPK have been identified including Ca2+/calmodulin-dependent protein kinase kinase (CaMKK). Recent studies reported that AMPK may be involved in bupivacaine-induced cytotoxicity in Schwann cells and in human neuroblastoma SH-SY5Y cells. The present study was undertaken to test whether CaMKK and AMPK are involved in bupivacaine-induced WDR35 expression in Neuro2a cells. Our results showed that bupivacaine induced activation of AMPK and p38 MAPK in Neuro2a cells. The AMPK inhibitors, compound C and iodotubercidin, attenuated the bupivacaine-induced activation of AMPK and p38 MAPK, resulting in an inhibition of the bupivacaine-induced increase in WDR35 expression. Treatment with the CaMKK inhibitor STO-609 also attenuated the bupivacaine-induced activation of AMPK and p38 MAPK, resulting in an inhibition of the bupivacaine-induced increase in WDR35 expression. These results suggest that bupivacaine activates AMPK and p38 MAPK via CaMKK in Neuro2a cells, and that the CaMKK/AMPK/p38 MAPK pathway is involved in regulating WDR35 expression.

show abstract

Section: Introductionmentioning

confidence: 99%

Enhanced Expression of WD Repeat-Containing Protein 35 via CaMKK/AMPK Activation in Bupivacaine-Treated Neuro2a Cells

et al. 2014

Self Cite

View full text Add to dashboard Cite

show abstract

“…We previously reported that WDR35 activates caspase-3 and promotes tumor necrosis factor (TNF)-α−induced apoptosis in HEK293 cells [3]. We also reported that enhanced expression of WDR35 may mediate the activation of caspase-3 through a mitochondrial signaling pathway in LPS-induced hepatocyte apoptosis [5].…”

Section: Discussionmentioning

confidence: 96%

“…The primers and TaqMan MGB probe for mouse c-Jun (Mm00495062_s1) and WDR35 (Mm00552650_m1) were purchased from Applied Biosystems. The amount of c-Jun or WDR35 PCR product was calculated relative to the internal control beta-actin (ACTB, Mm00607939_s1; Applied Biosystems), glyceraldehyde-3-phosphate dehydrogenase (GAPDH, Mm99999915_g1), or 18S ribosomal RNA (18S rRNA, Mm03928990_g1), and was compared between experimental and control groups by the ΔΔC T method, as reported previously [3], [14]. The difference of internal control did not affect the results in qPCR experiments.…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Enhanced Expression of WD Repeat-Containing Protein 35 via Nuclear Factor-Kappa B Activation in Bupivacaine-Treated Neuro2a Cells

et al. 2014

Self Cite

View full text Add to dashboard Cite

The family of WD repeat proteins comprises a large number of proteins and is involved in a wide variety of cellular processes such as signal transduction, cell growth, proliferation, and apoptosis. Bupivacaine is a sodium channel blocker administered for local infiltration, nerve block, epidural, and intrathecal anesthesia. Recently, we reported that bupivacaine induces reactive oxygen species (ROS) generation and p38 mitogen-activated protein kinase (MAPK) activation, resulting in an increase in the expression of WD repeat-containing protein 35 (WDR35) in mouse neuroblastoma Neuro2a cells. It has been shown that ROS activate MAPK through phosphorylation, followed by activation of nuclear factor-kappa B (NF-κB) and activator protein 1 (AP-1). The present study was undertaken to test whether NF-κB and c-Jun/AP-1 are involved in bupivacaine-induced WDR35 expression in Neuro2a cells. Bupivacaine activated both NF-κB and c-Jun in Neuro2a cells. APDC, an NF-κB inhibitor, attenuated the increase in NF-κB activity and WDR35 protein expression in bupivacaine-treated Neuro2a cells. GW9662, a selective peroxisome proliferator-activated receptor-γ antagonist, enhanced the increase in NF-κB activity and WDR35 protein expression in bupivacaine-treated Neuro2a cells. In contrast, c-Jun siRNA did not inhibit the bupivacaine-induced increase in WDR35 mRNA expression. These results indicate that bupivacaine induces the activation of transcription factors NF-κB and c-Jun/AP-1 in Neuro2a cells, while activation of NF-κB is involved in bupivacaine-induced increases in WDR35 expression.

show abstract

“…In a mouse mutation screen for developmental phenotypes, Mill et al [18] identified a mutation in the WDR35 gene as a cause of midgestation lethality associated with abnormalities characteristic of defects in the Hedgehog signaling pathway. Recently, we cloned rat WDR35, also referred to as naofen [19]. Very recently, we have found that bupivacaine, a local anesthetic, increases intracellular ROS levels and activates p38 MAPK in mouse neuroblastoma Neuro2a cells, resulting in apoptosis via an increase in the expression of WDR35 (under revision).…”

Section: Introductionmentioning

confidence: 99%

Enhanced expression of WD repeat-containing protein 35 (WDR35) stimulated by domoic acid in rat hippocampus: involvement of reactive oxygen species generation and p38 mitogen-activated protein kinase activation

et al. 2013

Self Cite

View full text Add to dashboard Cite

BackgroundDomoic acid (DA) is an excitatory amino acid analogue of kainic acid (KA) that acts via activation of glutamate receptors to elicit a rapid and potent excitotoxic response, resulting in neuronal cell death. Recently, DA was shown to elicit reactive oxygen species (ROS) production and induce apoptosis accompanied by activation of p38 mitogen-activated protein kinase (MAPK) in vitro. We have reported that WDR35, a WD-repeat protein, may mediate apoptosis in several animal models. In the present study, we administered DA to rats intraperitoneally, then used liquid chromatography/ion trap tandem mass spectrometry (LC-MS/MS) to identify and quantify DA in the brains of the rats and performed histological examinations of the hippocampus. We further investigated the potential involvement of glutamate receptors, ROS, p38 MAPK, and WDR35 in DA-induced toxicity in vivo.ResultsOur results showed that intraperitoneally administered DA was present in the brain and induced neurodegenerative changes including apoptosis in the CA1 region of the hippocampus. DA also increased the expression of WDR35 mRNA and protein in a dose- and time-dependent manner in the hippocampus. In experiments using glutamate receptor antagonists, the AMPA/KA receptor antagonist NBQX significantly attenuated the DA-induced increase in WDR35 protein expression, but the NMDA receptor antagonist MK-801 did not. In addition, the radical scavenger edaravone significantly attenuated the DA-induced increase in WDR35 protein expression. Furthermore, NBQX and edaravone significantly attenuated the DA-induced increase in p38 MAPK phosphorylation.ConclusionIn summary, our results indicated that DA activated AMPA/KA receptors and induced ROS production and p38 MAPK phosphorylation, resulting in an increase in the expression of WDR35 in vivo.

show abstract

Naofen, a novel WD40-repeat protein, mediates spontaneous and tumor necrosis factor-induced apoptosis

Cited by 11 publications

References 15 publications

Enhanced Expression of WD Repeat-Containing Protein 35 via CaMKK/AMPK Activation in Bupivacaine-Treated Neuro2a Cells

Enhanced Expression of WD Repeat-Containing Protein 35 via CaMKK/AMPK Activation in Bupivacaine-Treated Neuro2a Cells

Enhanced Expression of WD Repeat-Containing Protein 35 via Nuclear Factor-Kappa B Activation in Bupivacaine-Treated Neuro2a Cells

Enhanced expression of WD repeat-containing protein 35 (WDR35) stimulated by domoic acid in rat hippocampus: involvement of reactive oxygen species generation and p38 mitogen-activated protein kinase activation

Contact Info

Product

Resources

About