360 Expression of Opioid Genes in Neuropathic and Inflammatory Pain

Parkitna, Jan Rodriguez; Obara, Ilona; Korostyński, Michał; Kaminska, Dorota; Makuch, Wioletta; Przewłocka, Barbara; Przewłocki, Ryszard

doi:10.1016/j.ejpain.2007.03.375

Cited by 12 publications

(17 citation statements)

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“…Using OX-42 and GFAP as microglial and astrocytic activation markers, respectively, they revealed an early microglial and delayed astrocytic activation in the spinal cord following SPCN . This temporal pattern was confirmed by surface markers indicative of microglial (ITGAM, TLR4, CD14, TIMP-1, ICAM-1, and chemokine receptor-like 1) and astrocytic (GFAP) activation at the transcriptional levels (Parkitna et al, 2006;Tanga et al, 2004). Furthermore, a sequential activation of the mitogenactivated protein (MAP) kinase ERK (extracellular signal-regulated kinase) in neurons, then microglia, and finally astrocytes in SNL model was reported recently (Zhuang et al, 2005).…”

Section: Spinal Glial Activation In Neuropathic Pain Modelssupporting

confidence: 57%

“…The involvement of glia in neuropathic pain gives us great hint that glia might be a key modulator during inflammatory pain. Despite some conflicting reports (Clark et al, 2007;Lin et al, 2007;Lindia et al, 2005;Parkitna et al, 2006), most evidence showed that spinal microglia and astrocytes were activated by subcutaneous injections of complete Freund's adjuvant (Lindia et al, 2005;Raghavendra et al, 2004b), phospholipase A2 (Raghavendra et al, 2000), snake venom , formalin (Guo et al, 2005;Lan et al, 2007;Sweitzer et al, 1999;Watkins et al, 1997) and zymosan (Sweitzer et al, 1999). Studies from Deleo's group showed sustained microglia activation at the transcriptional level as evident by the upregulation of the mRNA encoding for the microglial markers: Mac-1, TLR4, and CD14 at the lumbar spinal cord during the acute, subacute and chronic phases of CFA-induced peripheral inflammation.…”

Section: Spinal Glial Activation In Inflammatory Pain Modelsmentioning

confidence: 98%

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Spinal glial activation contributes to pathological pain states

Cao

Zhang

2008

Neuroscience & Biobehavioral Reviews

221

170

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Section: Spinal Glial Activation In Neuropathic Pain Modelssupporting

confidence: 57%

Section: Spinal Glial Activation In Inflammatory Pain Modelsmentioning

confidence: 98%

Spinal glial activation contributes to pathological pain states

Cao

Zhang

2008

Neuroscience & Biobehavioral Reviews

221

170

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“…There are substantial differences between neuropathic-pain and inflammatory-pain states (e.g., etiology, pathology, and treatment strategy) (4,(26)(27)(28). Because mechanical allodynia is the most common and disabling stimulus-evoked symptom of neuralgia and is often difficult to treat, we determined whether BAM 8-22 can also reduce neuropathic mechanical allodynia in mice.…”

Section: Intrathecal Administration Of Bam 8-22 Inhibits Persistent Imentioning

confidence: 99%

Mas-related G-protein–coupled receptors inhibit pathological pain in mice

Guan

Tang

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

116

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An important objective of pain research is to identify novel drug targets for the treatment of pathological persistent pain states, such as inflammatory and neuropathic pain. Mas-related G-protein-coupled receptors (Mrgprs) represent a large family of orphan receptors specifically expressed in small-diameter nociceptive primary sensory neurons. To determine the roles of Mrgprs in persistent pathological pain states, we exploited a mouse line in which a chromosomal locus spanning 12 Mrgpr genes was deleted (KO). Initial studies indicated that these KO mice show prolonged mechanical-and thermal-pain hypersensitivity after hind-paw inflammation compared with wildtype littermates. Here, we show that this mutation also enhances the windup response of dorsal-horn wide dynamic-range neurons, an electrophysiological model for the triggering of central pain sensitization. Deletion of the Mrgpr cluster also blocked the analgesic effect of intrathecally applied bovine adrenal medulla peptide [8][9][10][11][12][13][14][15][16][17][18][19][20][21][22], an MrgprC11 agonist, on both inflammatory heat hyperalgesia and neuropathic mechanical allodynia. Spinal application of bovine adrenal medulla peptide 8-22 also significantly attenuated windup in wild-type mice, an effect eliminated in KO mice. These data suggest that members of the Mrgpr family, in particular MrgprC11, may constitute an endogenous inhibitory mechanism for regulating persistent pain in mice. Agonists for these receptors may, therefore, represent a class of antihyperalgesics for treating persistent pain with minimal side effects because of the highly specific expression of their targets.inflammation | neuropeptides | sensory neurons | Mrgpr

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“…The ANOVA is applied to identify genes which show a significant difference among experimental conditions. ANOVA does not identify which experimental conditions show the difference; therefore, we also apply the Tukey test as a post-hoc test to identify which experimental conditions show significant difference, see for example Pavlidis (2003), Parkitna et al (2006), Goeman and Bühlmann (2007), and Zollanvari et al (2009). As comparison criterion between methods we consider the true positive rate (TPR) and false discovery rate (FDR).…”

Section: Introductionmentioning

confidence: 99%

“…In order to estimate parameters of interest from posterior distribution the authors propose an importance sampling method. But, in situations with a control and more than one treatment, remains common to apply analysis of variance (ANOVA) followed by a Tukey test to identify which treatment caused the difference; see for example Pavlidis (2003), Parkitna et al (2006), and Goeman and Bühlmann (2007).…”

Section: Introductionmentioning

confidence: 99%

Identifying differentially expressed genes using the Polya urn scheme

Saraiva

Suzuki

Milan

2017

CSAM

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A common interest in gene expression data analysis is to identify genes that present significant changes in expression levels among biological experimental conditions. In this paper, we develop a Bayesian approach to make a gene-by-gene comparison in the case with a control and more than one treatment experimental condition. The proposed approach is within a Bayesian framework with a Dirichlet process prior. The comparison procedure is based on a model selection procedure developed using the discreteness of the Dirichlet process and its representation via Polya urn scheme. The posterior probabilities for models considered are calculated using a Gibbs sampling algorithm. A numerical simulation study is conducted to understand and compare the performance of the proposed method in relation to usual methods based on analysis of variance (ANOVA) followed by a Tukey test. The comparison among methods is made in terms of a true positive rate and false discovery rate. We find that proposed method outperforms the other methods based on ANOVA followed by a Tukey test. We also apply the methodologies to a publicly available data set on Plasmodium falciparum protein.

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360 Expression of Opioid Genes in Neuropathic and Inflammatory Pain

Cited by 12 publications

References 0 publications

Spinal glial activation contributes to pathological pain states

Spinal glial activation contributes to pathological pain states

Mas-related G-protein–coupled receptors inhibit pathological pain in mice

Identifying differentially expressed genes using the Polya urn scheme

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