Mapping of NPR-B immunoreactivity in the brainstem of Macaca fascicularis

Abdelalim, Essam M.; Tooyama, Ikuo

doi:10.1007/s00429-011-0313-1

Cited by 13 publications

(12 citation statements)

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“…While all NPRs have been identified in brainstem trigeminal nuclei [32–34], little is known about the possible role of the natriuretic peptide system at TG level where nociceptive signals are transduced [35–37]. A recent clinical report has shown that BNP levels are raised in the jugular vein blood during a migraine attack [38].…”

Section: Introductionmentioning

confidence: 99%

B-Type Natriuretic Peptide-Induced Delayed Modulation of TRPV1 and P2X3 Receptors of Mouse Trigeminal Sensory Neurons

et al. 2013

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Important pain transducers of noxious stimuli are small- and medium-diameter sensory neurons that express transient receptor vanilloid-1 (TRPV1) channels and/or adenosine triphosphate (ATP)-gated P2X3 receptors whose activity is upregulated by endogenous neuropeptides in acute and chronic pain models. Little is known about the role of endogenous modulators in restraining the expression and function of TRPV1 and P2X3 receptors. In dorsal root ganglia, evidence supports the involvement of the natriuretic peptide system in the modulation of nociceptive transmission especially via the B-type natriuretic peptide (BNP) that activates the natriuretic peptide receptor-A (NPR-A) to downregulate sensory neuron excitability. Since the role of BNP in trigeminal ganglia (TG) is unclear, we investigated the expression of BNP in mouse TG in situ or in primary cultures and its effect on P2X3 and TRPV1 receptors of patch-clamped cultured neurons. Against scant expression of BNP, almost all neurons expressed NPR-A at membrane level. While BNP rapidly increased cGMP production and Akt kinase phosphorylation, there was no early change in passive neuronal properties or responses to capsaicin, α,β-meATP or GABA. Nonetheless, 24 h application of BNP depressed TRPV1 mediated currents (an effect blocked by the NPR-A antagonist anantin) without changing responses to α,β-meATP or GABA. Anantin alone decreased basal cGMP production and enhanced control α,β-meATP-evoked responses, implying constitutive regulation of P2X3 receptors by ambient BNP. These data suggest a slow modulatory action by BNP on TRPV1 and P2X3 receptors outlining the role of this peptide as a negative regulator of trigeminal sensory neuron excitability to nociceptive stimuli.

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Section: Introductionmentioning

confidence: 99%

B-Type Natriuretic Peptide-Induced Delayed Modulation of TRPV1 and P2X3 Receptors of Mouse Trigeminal Sensory Neurons

et al. 2013

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“…Proteins were detected by using antibodies against NPR-C (Abcam) [15], p53 (Santa Cruz Biotechnology), Oct4 (sc-5279; Santa Cruz Biotechnology), Nanog (Bethyl Laboratories), NPR-A (Santa Cruz Biotechnology), NPR-B (Santa Cruz Biotechnology) [16], BNP (Chemicon), and b-actin (sc-47778; Santa Cruz Biotechnology). The secondary antibodies were peroxidase-conjugated IgG ( Jackson ImmunoResearch Lab, Inc.).…”

Section: Western Blottingmentioning

confidence: 99%

“…Therefore, to explore the relationship between NPR-C and p53, we treated ES cells with mitomycin C (MMC), an activator of the DNA damage p53/apoptosis pathway [22]. ES cells cultured in serum-free medium were treated for 6 h with MMC (5 mg/mL) alone or with MMC and cANF (4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23) (an NPR-C-specific agonist) together, and then we examined the expression of p53. As expected, MMC-treated cells showed a significant increase in the level of p53 protein.…”

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confidence: 99%

“…To confirm that cANF (4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23) protects ES cells from DNA damage through NPR-C, control siRNA-treated and NPR-C siRNA-treated cells were treated for 6 h with cANF (4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23) and MMC together, and then, the expressions of p53 and Nanog were measured. Although the pretreatment of ES cells with cANF (4)(5)(6)(7)(8)(9)(10)(11)(12)(13)…”

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confidence: 99%

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NPR-C Protects Embryonic Stem Cells from Apoptosis by Regulating p53 Levels

Abdelalim

Tooyama

2012

Stem Cells and Development

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The identification of intrinsic factors required for propagation of self-renewing embryonic stem (ES) cells is important to improve the efficiency of expansion of ES cells for therapeutic purposes. Here, we report a novel role for natriuretic peptide receptor-C (NPR-C) in the survival of murine ES cells. We found that NPR-C was highly expressed in ES cells and was downregulated during ES cell differentiation. Knockdown of NPR-C in ES cells by using a small-interfering RNA resulted in apoptotic cell death, and the induction of p53 protein expression. Conversely, chemical inhibition of p53 by α-pifithrin significantly reduced apoptosis in NPR-C-deficient cells. cANF((4-23)), a selective NPR-C agonist, protected ES cells against oxidative stress-induced apoptosis, and blocked activation of p53 and Nanog suppression in the presence of DNA-damaging agents. Thus, NPR-C is required to control DNA damage-induced p53 levels to maintain ES cell self-renewal.

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“…Several studies showed that BNP plays an essential role in cardiovascular homeostasis (Woodard and Rosado, 2007; Potter et al, 2009). However, other reports demonstrated that BNP and its receptors are expressed in several cell types that are not related to cardiovascular control, indicating BNP involvement in several functions (Cameron et al, 1996; Suda et al, 1998; Abdelalim et al, 2007, 2008a,b, 2013; Cao and Yang, 2008; Abdelalim and Tooyama, 2009, 2011a,b). …”

Section: Introductionmentioning

confidence: 99%

Localization of Brain Natriuretic Peptide Immunoreactivity in Rat Spinal Cord

Abdelalim¹,

Bellier²,

Tooyama³

2016

Front. Neuroanat.

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Brain natriuretic peptide (BNP) exerts its functions through NP receptors. Recently, BNP has been shown to be involved in a wide range of functions. Previous studies reported BNP expression in the sensory afferent fibers in the dorsal horn (DH) of the spinal cord. However, BNP expression and function in the neurons of the central nervous system are still controversial. Therefore, in this study, we investigated BNP expression in the rat spinal cord in detail using reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry. RT-PCR analysis showed that BNP mRNA was present in the spinal cord and dorsal root ganglion (DRG). BNP immunoreactivity was observed in different structures of the spinal cord, including the neuronal cell bodies and neuronal processes. BNP immunoreactivity was observed in the DH of the spinal cord and in the neurons of the intermediate column (IC) and ventral horn (VH). Double-immunolabeling showed a high level of BNP expression in the afferent fibers (laminae I–II) labeled with calcitonin gene-related peptide (CGRP), suggesting BNP involvement in sensory function. In addition, BNP was co-localized with CGRP and choline acetyltransferase (ChAT) in the motor neurons of the VH. Together, these results indicate that BNP is expressed in sensory and motor systems of the spinal cord, suggesting its involvement in several biological actions on sensory and motor neurons via its binding to NP receptor-A (NPR-A) and/or NP receptor-B (NPR-B) at the spinal cord level.

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Mapping of NPR-B immunoreactivity in the brainstem of Macaca fascicularis

Cited by 13 publications

References 50 publications

B-Type Natriuretic Peptide-Induced Delayed Modulation of TRPV1 and P2X3 Receptors of Mouse Trigeminal Sensory Neurons

B-Type Natriuretic Peptide-Induced Delayed Modulation of TRPV1 and P2X3 Receptors of Mouse Trigeminal Sensory Neurons

NPR-C Protects Embryonic Stem Cells from Apoptosis by Regulating p53 Levels

Localization of Brain Natriuretic Peptide Immunoreactivity in Rat Spinal Cord

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