All‐trans retinoic acid inhibits cobalt chloride‐induced apoptosis in PC12 cells: Role of the dimethylarginine dimethylaminohydrolase/asymmetric dimethylarginine pathway

Wang, Shan; Hu, Chang-Ping; Jiang, De-Jian; Peng, Jun; Zhou, Zhi; Yuan, Qiong; Nie, Sheng; Jiang, Jun-Lin; Li, Yuan‐Jian; Huang, Kang

doi:10.1002/jnr.21999

Cited by 24 publications

(15 citation statements)

References 37 publications

(43 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The recent study has indicated that the activity of DDAH and the expression of DDAH2 (mRNA and protein) was significantly decreased in cobalt chloride (CoCl 2 )-induced apoptosis. In contrast, DDAH2 overexpression inhibited the proapoptotic effects of CoCl2 [47]. CoCl 2 significantly increased the level of endogenous nitric oxide synthase inhibitor asymmetric dimethylarginine (ADMA), which markedly increased intracellular ROS production and promoted inflammatory responses, resulting in caspase-3-dependent apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Proteome changes of lungs artificially infected with H-PRRSV and N-PRRSV by two-dimensional fluorescence difference gel electrophoresis

Xiao

Wang

Jia

et al. 2010

Virol J

View full text Add to dashboard Cite

BackgroundPorcine reproductive and respiratory syndrome with PRRS virus (PRRSV) infection, which causes significant economic losses annually, is one of the most economically important diseases affecting swine industry worldwide. In 2006 and 2007, a large-scale outbreak of highly pathogenic porcine reproductive and respiratory syndrome (PRRS) happened in China and Vietnam. However little data is available on global host response to PRRSV infection at the protein level, and similar approaches looking at mRNA is problematic since mRNA levels do not necessarily predict protein levels. In order to improve the knowledge of host response and viral pathogenesis of highly virulent Chinese-type PRRSV (H-PRRSV) and Non-high-pathogenic North American-type PRRSV strains (N-PRRSV), we analyzed the protein expression changes of H-PRRSV and N-PRRSV infected lungs compared with those of uninfected negative control, and identified a series of proteins related to host response and viral pathogenesis.ResultsAccording to differential proteomes of porcine lungs infected with H-PRRSV, N-PRRSV and uninfected negative control at different time points using two-dimensional fluorescence difference gel electrophoresis (2D-DIGE) and mass spectrometry identification, 45 differentially expressed proteins (DEPs) were identified. These proteins were mostly related to cytoskeleton, stress response and oxidation reduction or metabolism. In the protein interaction network constructed based on DEPs from lungs infected with H-PRRSV, HSPA8, ARHGAP29 and NDUFS1 belonged to the most central proteins, whereas DDAH2, HSPB1 and FLNA corresponded to the most central proteins in those of N-PRRSV infected.ConclusionsOur study is the first attempt to provide the complex picture of pulmonary protein expression during H-PRRSV and N-PRRSV infection under the in vivo environment using 2D-DIGE technology and bioinformatics tools, provides large scale valuable information for better understanding host proteins-virus interactions of these two PRRSV strains.

show abstract

Section: Discussionmentioning

confidence: 99%

Proteome changes of lungs artificially infected with H-PRRSV and N-PRRSV by two-dimensional fluorescence difference gel electrophoresis

Xiao

Wang

Jia

et al. 2010

Virol J

View full text Add to dashboard Cite

show abstract

“…In the present study, we investigated the effects of Hcy on endogenous H 2 S production in neuronal cells and the underlying mechanism by studying PC12 cells, a clonal rat pheochromocytoma cell line that is widely used for studying the cellular biology of neurons (Duan et al 2009;Li et al 1998;Wang et al 2009). We demonstrated for the first time that Hcy significantly inhibits endogenous H 2 S synthesis in PC12 cells through suppressing the expression and activity of CBS, the major enzyme responsible for endogenous H 2 S generation in PC12 cells (Tang et al 2010a), and stimulating the activation of ERK1/ 2 and that the inhibitory effect of Hcy on endogenous H 2 S synthesis contributes to its neurotoxicity.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Endogenous Hydrogen Sulfide Generation is Associated with Homocysteine-Induced Neurotoxicity: Role of ERK1/2 Activation

et al. 2010

View full text Add to dashboard Cite

Both elevated homocysteine and decreased hydrogen sulfide (H(2)S) are observed in the brains of Alzheimer's disease (AD) patients. Reactive oxygen species (ROS) overproduction contributes to the neurotoxicity of homocysteine; however, H(2)S is an endogenous antioxidant gas. Therefore, the aim of this study was to investigate whether the imbalance of proportion to this endogenous protective antioxidant gas is involved in homocysteine-caused neurotoxicity. We show that homocysteine inhibits the generation of endogenous H(2)S and the expression and activity of cystathionine-β-synthetase (CBS), the main enzyme responsible for the generation of H(2)S in PC12 cells. S-Adenosylmethionine, an activator of CBS, not only prevents homocysteine-induced inhibition of endogenous H(2)S production but also attenuates homocysteine-triggered cytotoxicity and accumulation of ROS. We find that activation of ERK1/2 occurs in homocysteine-treated PC12 cells and blockade of ERK1/2 with U0126 abolished the homocysteine-induced cytotoxicity and inhibitory effect on endogenous H(2)S generation. These results indicate that homocysteine neurotoxicity involves reduction of H(2)S production, which is caused by inhibition of CBS and mediated by activation of ERK1/2. Our study suggests a promising future of H(2)S-based therapies for neurodegenerative diseases such as AD.

show abstract

“…The levels of another type of antioxidant, cytoplasmic biliverdin reductase A (BLVRA), showed a 91% increase at the 6 h treatment time-point. DDAH2, involved in the nitric oxide (NO) pathway as well as in apoptosis regulation (Wang et al, 2009), was increased by 40% at 48 h in IL-18 treated cells vs. untreated controls. IL-18 showed a concentration dependent DDAH2 increase at 72 h (Figure 3A).…”

Section: Resultsmentioning

confidence: 99%

Interleukin-18 alters protein expressions of neurodegenerative diseases-linked proteins in human SH-SY5Y neuron-like cells

Sutinen

Korolainen

Häyrinen

et al. 2014

Front. Cell. Neurosci.

View full text Add to dashboard Cite

Chronic inflammation and oxidative stress (OS) are present in Alzheimer's disease (AD) brains in addition to neuronal loss, Amyloid-β (Aβ) plaques and hyperphosphorylated tau-protein neurofibrillary tangles (NFTs). Previously we showed that levels of the pro-inflammatory cytokine, interleukin-18 (IL-18), are elevated in post-mortem AD brains. IL-18 can modulate the tau kinases, Cdk5 and GSK3β, as well as Aβ-production. IL-18 levels are also increased in AD risk diseases, including type-2 diabetes and obesity. Here, we explored other IL-18 regulated proteins in neuron-like SH-SY5Y cells. Differentiated SH-SY5Y cells, incubated with IL-18 for 24, 48, or 72 h, were analyzed by two-dimensional gel electrophoresis (2D-DIGE). Specific altered protein spots were chosen and identified with mass spectrometry (MS) and verified by western immunoblotting (WIB). IL-18 had time-dependent effects on the SH-SY5Y proteome, modulating numerous protein levels/modifications. We concentrated on those related to OS (DDAH2, peroxiredoxins 2, 3, and 6, DJ-1, BLVRA), Aβ-degradation (MMP14, TIMP2), Aβ-aggregation (Septin-2), and modifications of axon growth and guidance associated, collapsin response mediator protein 2 (CRMP2). IL-18 significantly increased antioxidative enzymes, indicative of OS, and altered levels of glycolytic α- and γ-enolase and multifunctional 14-3-3γ and -ε, commonly affected in neurodegenerative diseases. MMP14, TIMP2, α-enolase and 14-3-3ε, indirectly involved in Aβ metabolism, as well as Septin-2 showed changes that increase Aβ levels. Increased 14-3-3γ may contribute to GSK3β driven tau hyperphosphorylation and CRMP2 Thr514 and Ser522 phosphorylation with the Thr555-site, a target for Rho kinase, showing time-dependent changes. IL-18 also increased caspase-1 levels and vacuolization of the cells. Although our SH-SY5Y cells were not aged, as neurons in AD, our work suggests that heightened or prolonged IL-18 levels can drive protein changes of known relevance to AD pathogenesis.

show abstract

All‐trans retinoic acid inhibits cobalt chloride‐induced apoptosis in PC12 cells: Role of the dimethylarginine dimethylaminohydrolase/asymmetric dimethylarginine pathway

Cited by 24 publications

References 37 publications

Proteome changes of lungs artificially infected with H-PRRSV and N-PRRSV by two-dimensional fluorescence difference gel electrophoresis

Proteome changes of lungs artificially infected with H-PRRSV and N-PRRSV by two-dimensional fluorescence difference gel electrophoresis

Inhibition of Endogenous Hydrogen Sulfide Generation is Associated with Homocysteine-Induced Neurotoxicity: Role of ERK1/2 Activation

Interleukin-18 alters protein expressions of neurodegenerative diseases-linked proteins in human SH-SY5Y neuron-like cells

Contact Info

Product

Resources

About