Resistin protects against 6‐hydroxydopamine‐induced cell death in dopaminergic‐like MES23.5 cells

Lu, Dah Yuu; Chen, Jia Hong; Tan, Tzu Wei; Huang, Chih Yang; Yeh, Wei Lan; Hsu, Hsiang‐Chen

doi:10.1002/jcp.24163

Cited by 31 publications

(15 citation statements)

References 69 publications

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“…In addition to adiponectin, other adipokines also exert neuroprotective effect in PD. Resistin has been reported to protect against 6-hydroxydopamine (6-OHDA)-induced cell death with the underlying mechanisms of inhibiting oxidative stress and apoptosis [45]. Leptin was able to preserve cell survival in neuronal SH-SY5Y cells against MPP+ toxicity by maintaining ATP levels and MMP accompanied by increased uncoupling protein-2 (UCP2) expression [46].…”

Section: Discussionmentioning

confidence: 98%

Adiponectin offers protection against L166P mutant DJ-1-induced neuronal cytotoxicity mediated by APPL1-dependent AMPK activation

Geng

Liu

2013

International Journal of Neuroscience

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Parkinson's disease (PD) is the second most common neurodegenerative disease in the world. L166P mutant DJ-1 has been linked with a genetic form of the disease. Preventing neurotoxicity of DJ-1 familial mutations has become a new therapeutic target for PD. Adiponectin, the most abundantly secreted adipokine, has displayed its protective roles in pathologies of various types of diseases. In this study, we investigate whether adiponectin is protective against neurotoxicity induced by familial L166P mutant DJ-1 in PD. Our results demonstrate that adiponectin treatment could attenuate increased levels of reactive oxygen species and nitric oxide induced by the DJ-1L166P mutation. In addition, adiponectin could rescue impaired mitochondrial membrane potential induced by DJ-1L166P. Importantly, we verified that both adiponectin receptors, type 1 (AdipoR1) and type 2 (AdipoR2), are expressed in human neuroblastoma M17 cells. Our results also demonstrate that the protective effects of adiponectin against DJ-1L166P-induced neuronal cytotoxicity under 1-methyl-4-phenylpyridinium ion (MPP+) treatment require binding of adiponectin to its cell surface receptors. Finally, we found that the protective effects of adiponectin against DJ-1L166P depend on AMP-activated protein kinase (AMPK) activation mediated by the endosomal adaptor protein, APPL1 (adaptor protein with phosphotyrosine binding, pleckstrin homology domains and leucine zipper motif). These data suggest that adiponectin may have potential for implementation in novel therapies against PD.

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Section: Discussionmentioning

confidence: 98%

Adiponectin offers protection against L166P mutant DJ-1-induced neuronal cytotoxicity mediated by APPL1-dependent AMPK activation

Geng

Liu

2013

International Journal of Neuroscience

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“…The procedures of MTT and SRB assays determining cell viability were conducted according to previous reports [33–35]. After treatment with various concentrations of osthole for 24 h, cell culture media were aspirated.…”

Section: Methodsmentioning

confidence: 99%

p53 Is a Key Regulator for Osthole-Triggered Cancer Pathogenesis

Huang

Tsai

Chen

et al. 2014

BioMed Research International

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Osthole has been reported to have antitumor activities via the induction of apoptosis and inhibition of cancer cell growth and metastasis. However, the detailed molecular mechanisms underlying the anticancer effects of osthole in human colon cancer remain unclear. In the present study, we have assessed osthole-induced cell death in two different human colon cancer cell lines, HCT116 and SW480. Our results also showed that osthole activated proapoptotic signaling pathways in human colon cancer cells. By using cell culture insert system, osthole reduced cell motility in both human colon cancer cell lines. This study also provides evidence supporting the potential of osthole in p53 activation. Expression of p53, an apoptotic protein, was remarkably upregulated in cells treated with osthole. Importantly, the levels of phosphorylation of p53 on Ser15 (p-p53) and acetylation of p53 on Lys379 (acetyl-p53) were increased under osthole treatment. Our results also demonstrated that p53 was activated followed by generation of reactive oxygen species (ROS) and activation of c-Jun N-terminal kinase (JNK). Our study provides novel insights of p53-mediated responses under osthole treatment. Taken together, we concluded that osthole induces cancer cell death and inhibits migratory activity in a controlled manner and is a promising candidate for antitumor drug development.

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“…Live cells was measured by using the 3-(4,5-cimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay according to our previous study [34], [35]. Culture medium was aspirated after indicated treatment, and cells were washed with PBS twice.…”

Section: Methodsmentioning

confidence: 99%

Combination Treatment of Tamoxifen with Risperidone in Breast Cancer

Yeh

Lin

et al. 2014

PLoS ONE

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Tamoxifen has long been used and still is the most commonly used endocrine therapy for treatment of both early and advanced estrogen receptor-positive breast cancer in pre- and post-menopause women. Tamoxifen exerts its cytotoxic effect primarily through cytostasis which is associated with the accumulation of cells in the G0/G1 phase of the cell cycle. Apoptotic activity can also be exerted by tamoxifen which involves cleavage of caspase 9, caspase 7, caspase 3, and poly-ADP-ribose polymerase (PARP). Down-regulation of anti-apoptotic proteins Bcl-2 and Bcl-xL and up-regulation of pro-apoptotic proteins Bax and Bak have also been observed. In addition, stress response protein of GRP 94 and GRP 78 have also been induced by tamoxifen in our study. However, side effects occur during tamoxifen treatment in breast cancer patients. Researching into combination regimen of tamoxifen and drug(s) that relieves tamoxifen-induced hot flushes is important, because drug interactions may decrease tamoxifen efficacy. Risperidone has been shown to be effective in reducing or eliminating hot flushes on women with hormonal variations. In this present study, we demonstrated that combination of tamoxifen with risperidone did not interfered tamoxifen-induced cytotoxic effects in both in vitro and in vivo models, while fluoxetine abrogated the effects of tamoxifen. This is the first paper suggesting the possibility of combination treatment of tamoxifen with risperidone in breast cancer patients, providing a conceivable resolution of tamoxifen-induced side effects without interfering the efficacy of tamoxifen against breast cancer.

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Resistin protects against 6‐hydroxydopamine‐induced cell death in dopaminergic‐like MES23.5 cells

Cited by 31 publications

References 69 publications

Adiponectin offers protection against L166P mutant DJ-1-induced neuronal cytotoxicity mediated by APPL1-dependent AMPK activation

Adiponectin offers protection against L166P mutant DJ-1-induced neuronal cytotoxicity mediated by APPL1-dependent AMPK activation

p53 Is a Key Regulator for Osthole-Triggered Cancer Pathogenesis

Combination Treatment of Tamoxifen with Risperidone in Breast Cancer

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