Contribution of single-minded 2 to hyperglycaemia-induced neurotoxicity

Wang, Xiaolan; Song, Yi; Chen, Lu; Zhuang, Guobing; Zhang, Jing; Li, Man; Meng, Xianhong

doi:10.1016/j.neuro.2013.01.003

Cited by 12 publications

(14 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…STZ-treated rats exhibited significant increase in blood glucose level and decrease in body weight as we described previously [52]. Excessive IL-1β and IL-18 are a common cause of Alzheimer's disease and other neurodegeneration diseases [15,18].…”

Section: Cleaved Il-1β Increases In Diabetic Rat Cerebral Corticessupporting

confidence: 73%

“…Diabetic rat model was induced as described previously [52]. Briefly, diabetes was induced by a 60 mg/kg intraperitoneal injection of streptozocin (STZ, 60 mg/kg, Sigma, St. Louis, MO, USA), an agent that is toxic to the pancreatic beta cells, dissolved in sterile sodium citrate buffer solution (0.1 mol/L citric acid and 0.2 mol/L sodium phosphate, pH 4.5).…”

Section: Induction Of Diabetes In Ratsmentioning

confidence: 99%

“…Western blot analyses were performed as previously described [52]. Briefly, primary antibodies to anti-NLRP1 (1:500, Cell Signalling Technology), anti-ASC (1:200, Santa Cruz Biotechnology, CA, USA), anti-caspase-1 (1:100, Santa Cruz Biotechnology), IL-1β (1:500, Millipore, MA, USA) overnight at 4°C followed by incubation with horseradish peroxidaselabeled IgG (1:5000) were used in this study.…”

Section: Western Blot Analysismentioning

confidence: 99%

“…Cell death was assessed by the uptake of the fluorescent exclusion dye propidium iodide (PI) as we described previously [52]. After neurons were plated in 12-well plates for at least 5 days, they were pretreated with 10 μM Z-YVAD-FMK for 1 h before adding glucose for 24 h. Cells were then washed with phosphate buffered saline and then stained with 10 μg/ mL PI (Sigma) and 1 μg/mL Hoechst 33342 (Sigma) at 37°C.…”

Section: Pi Stainingmentioning

confidence: 99%

“…Data are presented as mean±SEM. *P <0.05 vs. Ctrl manufacturer's protocol and done as we described previously [52]. Briefly, neurons were planted into 96-well clusters with a density of 5×10 4 cells/well.…”

Section: Evaluation Of Cell Viabilitymentioning

confidence: 99%

See 4 more Smart Citations

Nod-Like Receptor Protein 1 Inflammasome Mediates Neuron Injury under High Glucose

et al. 2013

Self Cite

View full text Add to dashboard Cite

Diabetic encephalopathy is one of the most common complications of diabetes. Inflammatory events during diabetes may be an important mechanism of diabetic encephalopathy. Inflammasome is a multiprotein complex consisting of Nod-like receptor proteins (NLRPs), apoptosis-associated speck-like protein (ASC), and caspase 1 or 5, which functions to switch on the inflammatory process and the release of inflammatory factors. The present study hypothesized that the formation and activation of NLRP1 inflammasome turns on neuroinflammation and neuron injury during hyperglycemia. The results demonstrated that the levels of interleukin-1 beta (IL-1β) were increased in the cortex of streptozocin (STZ)-induced diabetic rats. The levels of mature IL-1β and IL-18 were also elevated in culture medium of neurons treated with high glucose (50 mM). The expression of three essential components of the NLRP1 inflammasome complex, namely, NLRP1, ASC, and caspase 1, was also upregulated in vivo and in vitro under high glucose. Silencing the ASC gene prevented the caspase-1 activation, and inhibiting caspase 1 activity blocked hyperglycemia-induced release of inflammatory factors and neuron injury. Moreover, we found that pannexin 1 mediated the actvitation of NLRP1 inflammasome under high glucose. These results suggest that hyperglycemia induces neuroinflammation through activation of NLRP1 inflammasome, which represents a novel mechanism of diabetes-associated neuron injury.

show abstract

Section: Cleaved Il-1β Increases In Diabetic Rat Cerebral Corticessupporting

confidence: 73%

Section: Induction Of Diabetes In Ratsmentioning

confidence: 99%

Section: Western Blot Analysismentioning

confidence: 99%

Section: Pi Stainingmentioning

confidence: 99%

Section: Evaluation Of Cell Viabilitymentioning

confidence: 99%

See 3 more Smart Citations

Nod-Like Receptor Protein 1 Inflammasome Mediates Neuron Injury under High Glucose

et al. 2013

Self Cite

View full text Add to dashboard Cite

show abstract

Ethanol Activation of PKA Mediates Single-Minded 2 Expression in Neuronal Cells

et al. 2014

View full text Add to dashboard Cite

Prenatal ethanol exposure can cause extensive apoptotic neurodegeneration throughout the developing central nervous system (CNS), which results in cognitive deficits and memory decline. However, the underlying mechanisms need further study. Single-minded 2 (Sim2), a transcriptional repressor, is reportedly involved in diseases that impair learning and memory, such as Down syndrome (DS) and Alzheimer's disease. It is still unknown whether Sim2 is involved in regulating ethanol-mediated neuronal injury that might ultimately lead to neuronal dysfunction and subsequent learning and memory deficits. To study the effects of ethanol on Sim2 expression and neuronal injury, we used animal models and cell culture experiments. Our results indicated that in SH-SY5Y cells, ethanol exposure increased Sim2 expression and levels of cleaved caspase 3, which is a marker for cells undergoing apoptosis. Silencing Sim2 expression attenuated caspase 3 activation and cellular apoptosis. We also found that protein kinase A (PKA) activation induced Sim2 expression, as did ethanol. Inhibiting the PKA signaling pathway with H-89 decreased Sim2 expression and cleavage of caspase 3 that was induced by ethanol in vivo and in vitro. We further found that PKA regulated Sim2 expression at the transcriptional level. These results demonstrate that ethanol leads to increased Sim2 expression via the PKA pathway, ultimately resulting in apoptotic cell death.

show abstract

Asiaticoside attenuates diabetes-induced cognition deficits by regulating PI3K/Akt/NF-κB pathway

Yin

Chen

et al. 2015

Behavioural Brain Research

View full text Add to dashboard Cite

Contribution of single-minded 2 to hyperglycaemia-induced neurotoxicity

Cited by 12 publications

References 32 publications

Nod-Like Receptor Protein 1 Inflammasome Mediates Neuron Injury under High Glucose

Nod-Like Receptor Protein 1 Inflammasome Mediates Neuron Injury under High Glucose

Ethanol Activation of PKA Mediates Single-Minded 2 Expression in Neuronal Cells

Asiaticoside attenuates diabetes-induced cognition deficits by regulating PI3K/Akt/NF-κB pathway

Contact Info

Product

Resources

About