Methamphetamine toxicity-induced calcineurin activation, nuclear translocation of nuclear factor of activated T-cells and elevation of cyclooxygenase 2 levels are averted by calpastatin overexpression in neuroblastoma SH-SY5Y cells

Chetsawang, Jirapa; Nudmamud-Thanoi, Sutisa; Phonchai, Ruchee; Abubakar, Zuroida; Govitrapong, Piyarat; Chetsawang, Banthit

doi:10.1016/j.neuro.2018.06.011

Cited by 8 publications

(2 citation statements)

References 33 publications

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“…The enzyme family, cyclooxygenease (COX), can be obtained starting from the cytokines, including the interleukin materials, and TNF-α. From the cytokines, the NF-κB and NFAT pathways produce COX [6,7,8,9]. The combination of AA and COX will generate PGE2, at a rate that will be limited either by the source material of AA or the enzyme COX.…”

Section: Molecular Pathways Resultant In Fevermentioning

confidence: 99%

Dynamics and Internal Control of Body Temperature in Response to Infectious Agents and Other Causal Factors

Schaper¹

2019

Preprint

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Thermoregulation is crucial to homeostasis but the mechanisms by which body temperature is controlled are still largely mysterious, especially in response to infectious agents and other exogenous stressors. This research develops a model of body temperature dynamics with a new hypothesis of integrated pathways associated with the cardiovascular and nervous system. For the first time, chemical and neural signals are coordinated to mathematically characterize body temperature dynamics. Quantitative insight and model predictive capability for the dynamics and internal control of body temperature is developed in which a feedback-only controller is newly introduced. Further, the proposed multivariable feedback controller, is comprised of a superposition of proportional responses to signals and its rate of change in association with cardiovascular and neural pathways and is thus evaluated in a framework of linear equations to form a closed-loop model of body temperature control effects in response to causal factors, including those associated with the immune response. The model is validated by examination of the transient and spectral characteristics of a three-day case history involving temperature trajectories after routine exercise protocols inducing chills then fever in response to an initial standard vaccine injection of pneumococcal and influenza species. In addition, the model is applied to address and mathematically explain intriguing questions of thermoregulation, such as the mathematical description of fevers induced by infections, why chills often precede fever, and that fevers are due to a trade-off of robustness in favor of performance. The model is a comprehensive integration coordinating the cardiovascular and neural physiological systems to analyze, predict, and thereby produce regulation strategies to minimize body temperature deviations, especially in the presence of infections which are shown to fundamentally alter the inherent dynamic modes of the closed-loop temperature response.

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Section: Molecular Pathways Resultant In Fevermentioning

confidence: 99%

Dynamics and Internal Control of Body Temperature in Response to Infectious Agents and Other Causal Factors

Schaper¹

2019

Preprint

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“…COX-2 can catalyze the conversion of arachidonic acid into thromboxane A2, prostaglandin E2 and prostaglandin H2, which is associated with neuroinflammation, and contributes to the progression of neurodegenerative diseases [12]. A recent study had shown that COX-2 expression depends on the activation of calcineurin, which is associated with increased Ca 2þ concentration in the cytoplasm of neurons [13]. Selective inhibition of the binding of neuronal nitric oxide synthase to COX-2 can suppress NMDA-induced excitatory neurotoxicity and exert neuroprotective properties [14,15].…”

Section: Upregulation Of Ppar-c Inhibits Nmda-induced Neurotoxicity Tmentioning

confidence: 99%

Upregulation of PPAR-gamma activity inhibits cyclooxygenase 2 expression in cortical neurons with N-methyl-d-aspartic acid induced excitatory neurotoxicity

Weng

Chen

et al. 2019

Biotechnology & Biotechnological Equipment

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This study aimed to investigate the effect of upregulated peroxisome proliferator-activated receptor-gamma (PPAR-c) activity on cyclooxygenase 2 (COX-2) expression and N-methyl-Daspartic acid (NMDA)-induced excitatory neurotoxicity in primary cultured cortical neurons. Rat cortical neurons were cultured for 8 days in vitro, and divided into control, NMDA, MK-801 (selective NMDA antagonist), rosiglitazone (ROSI, PPAR-c agonist), GW9662 (PPAR-c antagonist), NS398 (selective COX-2 antagonist) and NS398 þ ROSI groups. Two hours after treatment in each group, cell viability, intracellular Ca 2þ concentrations, PPAR-c and COX-2 protein expression were detected by CCK-8 assay, flow cytometry and western blot assay, respectively. The results showed that compared with the control group, 100 lmol/L of NMDA significantly decreased the neuronal cell viability, increased Ca 2þ concentrations, which also increased the COX-2 protein expression and decreased PPAR-c expression in neurons. Compared with the NMDA group, the cell viability was increased, Ca 2þ concentrations and COX-2 protein expression were significantly decreased, PPAR-c expression was significantly increased in the MK-801, ROSI, NS398 and ROSI þ NS398 groups (both P < 0.01). This finding suggested that upregulation of PPAR-c activity can inhibit COX-2 expression, decrease Ca 2þ concentrations in primary cultured cortical neurons, and protect neurons against NMDA-induced excitatory neurotoxicity.

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Effect of Hypoxia on the Muscle Fiber Switching Signal Pathways CnA/NFATc1 and Myostatin in Mouse Myocytes

Wang²,

Bai

et al. 2019

Acta Histochemica

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Methamphetamine toxicity-induced calcineurin activation, nuclear translocation of nuclear factor of activated T-cells and elevation of cyclooxygenase 2 levels are averted by calpastatin overexpression in neuroblastoma SH-SY5Y cells

Cited by 8 publications

References 33 publications

Dynamics and Internal Control of Body Temperature in Response to Infectious Agents and Other Causal Factors

Dynamics and Internal Control of Body Temperature in Response to Infectious Agents and Other Causal Factors

Upregulation of PPAR-gamma activity inhibits cyclooxygenase 2 expression in cortical neurons with N-methyl-d-aspartic acid induced excitatory neurotoxicity

Effect of Hypoxia on the Muscle Fiber Switching Signal Pathways CnA/NFATc1 and Myostatin in Mouse Myocytes

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