ANP-mediated cGMP signaling and phosphodiesterase inhibition in the rat cervical spinal cord

Vente, Jan de; Ittersum, Marjanne Markerink‐van; Vles, Johan S.H.

doi:10.1016/j.jchemneu.2006.02.005

Cited by 11 publications

(5 citation statements)

References 55 publications

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“…We find that the BNP-induced inhibitory effects on neuronal excitability and nociceptive behavior were attenuated by PKG inhibitor KT5823, suggesting a requirement of cGMP/PKG signaling for the BNP action. Coordinately, cGMP is detected in afferent fibers in the superficial dorsal horn of spinal cord (Vles et al, 2000;de Vente et al, 2006). Intracellular concentration of cGMP is determined by the ratio of synthesis and breakdown.…”

Section: Inhibition Of Inflammatory Pain By Activating Bnp/npr-a/pkg/mentioning

confidence: 99%

“…Intracellular concentration of cGMP is determined by the ratio of synthesis and breakdown. The NPR-A-mediated cGMP generation can be enhanced in the presence of different phosphodiesterase inhibitors (de Vente et al, 2006). Accordingly, inhibition of cGMP degradation by intrathecal administration of the phosphodiesterase 5 inhibitor sildenafil reduces inflammatory pain induced by formalin (Torres-Lopez et al, 2002;Araiza-Saldana et al, 2005).…”

Section: Inhibition Of Inflammatory Pain By Activating Bnp/npr-a/pkg/mentioning

confidence: 99%

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Inhibition of Inflammatory Pain by Activating B-Type Natriuretic Peptide Signal Pathway in Nociceptive Sensory Neurons

Zhang¹,

Liu²,

Gong³

et al. 2010

J. Neurosci.

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B-type natriuretic peptide (BNP) has been known to be secreted from cardiac myocytes and activate its receptor, natriuretic peptide receptor-A (NPR-A), to reduce ventricular fibrosis. However, the function of BNP/NPR-A pathway in the somatic sensory system has been unknown. In the present study, we report a novel function of BNP in pain modulation. Using microarray and immunoblot analyses, we found that BNP and NPR-A were expressed in the dorsal root ganglion (

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Section: Inhibition Of Inflammatory Pain By Activating Bnp/npr-a/pkg/mentioning

confidence: 99%

Section: Inhibition Of Inflammatory Pain By Activating Bnp/npr-a/pkg/mentioning

confidence: 99%

Inhibition of Inflammatory Pain by Activating B-Type Natriuretic Peptide Signal Pathway in Nociceptive Sensory Neurons

Zhang¹,

Liu²,

Gong³

et al. 2010

J. Neurosci.

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“…Interestingly, phosphodiesterase-4D is a key interacting enzyme responsible for downstream inhibition of cyclic adenosine mono-phosphate (cAMP)-mediated activity within neural tissues. 16 Other mutations in critical DNA damage response genes (PRKDC (50%; 2/4) were also detected but occurred at lower confidence MAFs (MAF=48.25 and 2.65, respectively) (Figure 2; Supplemental Table I). …”

Section: Resultsmentioning

confidence: 99%

Neuroendocrine Merkel Cell Carcinoma Is Associated with Mutations in Key DNA Repair, Epigenetic and Apoptosis Pathways: A Case-Based Study Using Targeted Massively Parallel Sequencing

et al. 2014

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Introduction: Merkel cell carcinoma (MCC) is a rare neuroendocrine carcinoma with a poorly understood molecular etiology. We implemented a comprehensive deep sequencing approach to identify mutations in the tumor DNA from a cohort of patients treated at our institution over the past 15 years. Our results indicate mutations that may constitute therapeutic targets in MCC. Methods: Five patients were treated for MCC within the study interval. Patients with adequate tissue (n = 4), positive neuroendocrine differentiation (chromogranin, synaptophysin, and cytokeratin 20), and histopathological confirmation of MCC were included in the study. DNA was extracted from archival tumor tissue samples and analyzed by massively parallel sequencing using a targeted, multiplex PCR approach followed by semiconductor sequencing. Results: We demonstrate high-penetrance nonsense mutations in PDE4DIP (n = 4) as well as various missense mutations in the DNA damage response (PRKDC, AURKB, ERCC5, ATR, and ATRX) and epigenetic modulating enzymes (MLL3). Conclusion: We describe several mutations in potential disease-relevant genes and pathways. These targets should be evaluated in a larger cohort to determine their role in the molecular pathogenesis of MCC.

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“…Activation of NPRA resulted in addition of cGMP/PKG signaling [ 18 ]. The NPRA-mediated cGMP could be elevated by different phosphodiesterase inhibitors [ 27 ]. Coordinately, inhibition of cGMP degradation reduces inflammatory pain induced by formalin after intrathecal injection of the phosphodiesterase five inhibitor sildenafil [ 28 , 29 ].…”

Section: Discussionmentioning

confidence: 99%

Brain natriuretic peptide suppresses pain induced by BmK I, a sodium channel-specific modulator, in rats

Tan

et al. 2016

J Headache Pain

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BackgroundA previous study found that brain natriuretic peptide (BNP) inhibited inflammatory pain via activating its receptor natriuretic peptide receptor A (NPRA) in nociceptive sensory neurons. A recent study found that functional NPRA is expressed in almost all the trigeminal ganglion (TG) neurons at membrane level suggesting a potentially important role for BNP in migraine pathophysiology.MethodsAn inflammatory pain model was produced by subcutaneous injection of BmK I, a sodium channel-specific modulator from venom of Chinese scorpion Buthus martensi Karsch. Quantitative PCR, Western Blot, and immunohistochemistry were used to detect mRNA and protein expression of BNP and NPRA in dorsal root ganglion (DRG) and dorsal horn of spinal cord. Whole-cell patch clamping experiments were conducted to record large-conductance Ca2+-activated K+ (BKCa) currents of membrane excitability of DRG neurons. Spontaneous and evoked pain behaviors were examined.ResultsThe mRNA and protein expression of BNP and NPRA was up-regulated in DRG and dorsal horn of spinal cord after BmK I injection. The BNP and NPRA was preferentially expressed in small-sized DRG neurons among which BNP was expressed in both CGRP-positive and IB4-positive neurons while NPRA was preferentially expressed in CGRP-positive neurons. BNP increased the open probability of BKCa channels and suppressed the membrane excitability of small-sized DRG neurons. Intrathecal injection of BNP significantly inhibited BmK-induced pain behaviors including both spontaneous and evoked pain behaviors.ConclusionsThese results suggested that BNP might play an important role as an endogenous pain reliever in BmK I-induced inflammatory pain condition. It is also suggested that BNP might play a similar role in other pathophysiological pain conditions including migraine.

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ANP-mediated cGMP signaling and phosphodiesterase inhibition in the rat cervical spinal cord

Cited by 11 publications

References 55 publications

Inhibition of Inflammatory Pain by Activating B-Type Natriuretic Peptide Signal Pathway in Nociceptive Sensory Neurons

Inhibition of Inflammatory Pain by Activating B-Type Natriuretic Peptide Signal Pathway in Nociceptive Sensory Neurons

Neuroendocrine Merkel Cell Carcinoma Is Associated with Mutations in Key DNA Repair, Epigenetic and Apoptosis Pathways: A Case-Based Study Using Targeted Massively Parallel Sequencing

Brain natriuretic peptide suppresses pain induced by BmK I, a sodium channel-specific modulator, in rats

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