Changes in neuronal protein 22 expression and cytoskeletal association in the alcohol‐dependent and withdrawn rat brain

Depaz, Iris; Heras, Rachel de las; Kroon, Paulus A.; Wilce, Peter A.

doi:10.1002/jnr.20563

Cited by 24 publications

(16 citation statements)

References 41 publications

(47 reference statements)

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“…, 2005). NP22 colocalizes with all three major components of neuronal microtubules, tau, α‐tubulin and MAP2 (Depaz et al. , 2005), and with F‐actin (Depaz et al.…”

Section: Discussionmentioning

confidence: 99%

“…NP22 colocalizes with all three major components of neuronal microtubules, tau, α‐tubulin and MAP2 (Depaz et al. , 2005), and with F‐actin (Depaz et al. , 2005), which is highly expressed in dendrites, synapses, dendritic spines and postsynaptic densities (Markham & Fifkova, 1986; Fifkova & Morales, 1992; Adam & Matus, 1996; Halpain, 2000) .…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Exercise affects energy metabolism and neural plasticity‐related proteins in the hippocampus as revealed by proteomic analysis

Ding¹,

Vaynman²,

Souda³

et al. 2006

Eur J of Neuroscience

153

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Studies were conducted to evaluate the effect of a brief voluntary exercise period on the expression pattern and post-translational modification of multiple protein classes in the rat hippocampus using proteomics. An analysis of 80 protein spots of relative high abundance on two-dimensional gels revealed that approximately 90% of the proteins identified were associated with energy metabolism and synaptic plasticity. Exercise up-regulated proteins involved in four aspects of energy metabolism, i.e. glycolysis, ATP synthesis, ATP transduction and glutamate turnover. Specifically, we found increases in fructose-bisphosphate aldolase C, phosphoglycerate kinase 1, mitochondrial ATP synthase, ubiquitous mitochondrial creatine kinase and glutamate dehydrogenase 1. Exercise also up-regulated specific synaptic-plasticity-related proteins, the cytoskeletal protein alpha-internexin and molecular chaperones (chaperonin-containing TCP-1, neuronal protein 22, heat shock 60-kDa protein 1 and heat shock protein 8). Western blot was used to confirm the direction and magnitude of change in ubiquitous mitochondrial creatine kinase, an enzyme essential for transducing mitochondrial-derived ATP to sites of high-energy demand such as the synapse. Protein phosphorylation visualized by Pro-Q Diamond fluorescent staining showed that neurofilament light polypeptide, glial fibrillary acidic protein, heat shock protein 8 and transcriptional activator protein pur-alpha were more intensely phosphorylated with exercise as compared with sedentary control levels. Our results, together with the fact that most of the proteins that we found to be up-regulated have been implicated in cognitive function, support a mechanism by which exercise uses processes of energy metabolism and synaptic plasticity to promote brain health.

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“…, 2005). NP22 colocalizes with all three major components of neuronal microtubules, tau, α‐tubulin and MAP2 (Depaz et al. , 2005), and with F‐actin (Depaz et al.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Exercise affects energy metabolism and neural plasticity‐related proteins in the hippocampus as revealed by proteomic analysis

Ding¹,

Vaynman²,

Souda³

et al. 2006

Eur J of Neuroscience

153

View full text Add to dashboard Cite

show abstract

“…An in vitro study using rat brain has demonstrated that phosphorylation of microtubule-associated proteins, which modulate the functional properties of microtubules, is altered by ethanol exposure [93]. A study using hepatoma-derived cells has shown altered integrity of proteins associated with microtubules following ethanol exposure [94].Altered expression of neuronal protein 22, which interacts with microfilament and microtubule matrices, may also be involved in the pathogenesis of alcoholic neuropathy [95]. Thus, defects in axonal transport and cytoskeletal properties of axons may be one of the important pathways involved in alcohol induced peripheral neuropathy.…”

Section: Effects On Axonal Transport and Cytoskeletal Propertiesmentioning

confidence: 99%

Alcoholic neuropathy: possible mechanisms and future treatment possibilities

Chopra

Tiwari

2012

Brit J Clinical Pharma

191

103

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Chronic alcohol consumption produces painful peripheral neuropathy for which there is no reliable successful therapy, mainly due to lack of understanding of its pathobiology. Alcoholic neuropathy involves coasting caused by damage to nerves that results from long term excessive drinking of alcohol and is characterized by spontaneous burning pain, hyperalgesia and allodynia. The mechanism behind alcoholic neuropathy is not well understood, but several explanations have been proposed. These include activation of spinal cord microglia after chronic alcohol consumption, oxidative stress leading to free radical damage to nerves, activation of mGlu5 receptors in the spinal cord and activation of the sympathoadrenal and hypothalamo-pituitary-adrenal (HPA) axis. Nutritional deficiency (especially thiamine deficiency) and/or the direct toxic effect of alcohol or both have also been implicated in alcohol-induced neuropathic pain. Treatment is directed towards halting further damage to the peripheral nerves and restoring their normal functioning. This can be achieved by alcohol abstinence and a nutritionally balanced diet supplemented by all B vitamins. However, in the setting of ongoing alcohol use, vitamin supplementation alone has not been convincingly shown to be sufficient for improvement in most patients. The present review is focused around the multiple pathways involved in the development of peripheral neuropathy associated with chronic alcohol intake and the different therapeutic agents which may find a place in the therapeutic armamentarium for both prevention and management of alcoholic neuropathy.

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“…These genes are basically co-dominant in classes 5 and 3, representing pulmonary carcinoids (COID) and small cell lung cancer (SCLC), respectively. TAGLN3 associates with and regulates F-actin, α-tubulin, tau and MAP2 [50]. CRMP1 is a phosphoprotein and controls microtubules [51].…”

Section: Resultsmentioning

confidence: 99%

Identification of Single- and Multiple-Class Specific Signature Genes from Gene Expression Profiles by Group Marker Index

Tsai¹,

Aguan

Pal

et al. 2011

PLoS ONE

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Informative genes from microarray data can be used to construct prediction model and investigate biological mechanisms. Differentially expressed genes, the main targets of most gene selection methods, can be classified as single- and multiple-class specific signature genes. Here, we present a novel gene selection algorithm based on a Group Marker Index (GMI), which is intuitive, of low-computational complexity, and efficient in identification of both types of genes. Most gene selection methods identify only single-class specific signature genes and cannot identify multiple-class specific signature genes easily. Our algorithm can detect de novo certain conditions of multiple-class specificity of a gene and makes use of a novel non-parametric indicator to assess the discrimination ability between classes. Our method is effective even when the sample size is small as well as when the class sizes are significantly different. To compare the effectiveness and robustness we formulate an intuitive template-based method and use four well-known datasets. We demonstrate that our algorithm outperforms the template-based method in difficult cases with unbalanced distribution. Moreover, the multiple-class specific genes are good biomarkers and play important roles in biological pathways. Our literature survey supports that the proposed method identifies unique multiple-class specific marker genes (not reported earlier to be related to cancer) in the Central Nervous System data. It also discovers unique biomarkers indicating the intrinsic difference between subtypes of lung cancer. We also associate the pathway information with the multiple-class specific signature genes and cross-reference to published studies. We find that the identified genes participate in the pathways directly involved in cancer development in leukemia data. Our method gives a promising way to find genes that can involve in pathways of multiple diseases and hence opens up the possibility of using an existing drug on other diseases as well as designing a single drug for multiple diseases.

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Changes in neuronal protein 22 expression and cytoskeletal association in the alcohol‐dependent and withdrawn rat brain

Cited by 24 publications

References 41 publications

Exercise affects energy metabolism and neural plasticity‐related proteins in the hippocampus as revealed by proteomic analysis

Exercise affects energy metabolism and neural plasticity‐related proteins in the hippocampus as revealed by proteomic analysis

Alcoholic neuropathy: possible mechanisms and future treatment possibilities

Identification of Single- and Multiple-Class Specific Signature Genes from Gene Expression Profiles by Group Marker Index

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