Xing-Jun Liu

Chinese Academy of Sciences, Peping, Beijing, China

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Publications (3)25.41 Total impact

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    ABSTRACT: Fibroblast growth factor (FGF) 7, a member of FGF family, is initially found to be secreted from mesenchymal cells to repair epithelial tissues. However, its functions in the nervous system are largely unknown. The present study showed that FGF7 was a neuromodulator localized in the large dense-core vesicles (LDCVs) in nociceptive neurons. FGF7 was mainly expressed in small-diameter neurons of the dorsal root ganglion (DRG) and could be transported to the dorsal spinal cord. Interestingly, FGF7 was mostly stored in LDCVs that did not contain neuropeptide substance P. Electrophysiological recordings in the spinal cord slice showed that buffer-applied FGF7 increased the amplitude of excitatory post-synaptic current evoked by stimulating the sensory afferent fibers. Behavior tests showed that intrathecally applied FGF7 potentiated the formalin-induced acute nociceptive response. Moreover, both acute and inflammatory nociceptive responses were significantly reduced in Fgf7-deficient mice. These results suggest that FGF7 exerts an excitatory modulation of nociceptive afferent transmission. © The Author (2015). Published by Oxford University Press on behalf of Journal of Molecular Cell Biology, IBCB, SIBS, CAS. All rights reserved.
    Journal of Molecular Cell Biology 03/2015; DOI:10.1093/jmcb/mjv019 · 8.43 Impact Factor
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    ABSTRACT: Emerging evidence suggests that the suppressive modulators released from nociceptive afferent neurons contribute to pain regulation. However, the suppressive modulators expressed in small-diameter neurons of the dorsal root ganglion remain to be further identified. The present study shows that the activin C expressed in small dorsal root ganglion neurons is required for suppressing inflammation-induced nociceptive responses. The expression of activin C in small dorsal root ganglion neurons of rats was markedly downregulated during the early days of peripheral inflammation induced by intraplantar injection of the complete Freund's adjuvant. Intrathecal treatment with the small interfering RNA targeting activin βC or the antibodies against activin C could enhance the formalin-induced nociceptive responses, and impair the recovery from the complete Freund's adjuvant-induced thermal hyperalgesia. Intrathecally applied activin C could reduce nociceptive responses induced by formalin or complete Freund's adjuvant. Moreover, activin C was found to inhibit the inflammation-induced phosphorylation of extracellular signal-regulated kinase in the dorsal root ganglia and the dorsal spinal cord. Thus, activin C functions as an endogenous suppressor of inflammatory nociceptive transmission and may have a therapeutic potential for treatment of inflammatory pain.
    Brain 02/2012; 135(Pt 2):391-403. DOI:10.1093/brain/awr350 · 10.23 Impact Factor
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    ABSTRACT: 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 (DRG) of rats and upregulated after intraplantar injection of complete Freund's adjuvant (CFA). Immunohistochemistry showed that BNP was expressed in calcitonin gene-related peptide (CGRP)-containing small neurons and IB4 (isolectin B4)-positive neurons, whereas NPR-A was present in CGRP-containing neurons. Application of BNP reduced the firing frequency of small DRG neurons in the presence of glutamate through opening large-conductance Ca2+-activated K+ channels (BKCa channels). Furthermore, intrathecal injection of BNP yielded inhibitory effects on formalin-induced flinching behavior and CFA-induced thermal hyperalgesia in rats. Blockade of BNP signaling by BNP antibodies or cGMP-dependent protein kinase (PKG) inhibitor KT5823 [(9S,10R,12R)-2,3,9,10,11,12-hexahydro-10-methoxy-2,9-dimethyl-1-oxo-9,12-epoxy-1H-diindolo[1,2,3-fg:3',2',1'-kl]pyrrolo[3,4-i][1,6]benzodiazocine-10-carboxylic acid methyl ester] impaired the recovery from CFA-induced thermal hyperalgesia. Thus, BNP negatively regulates nociceptive transmission through presynaptic receptor NPR-A, and activation of the BNP/NPR-A/PKG/BKCa channel pathway in nociceptive afferent neurons could be a potential strategy for inflammatory pain therapy.
    The Journal of Neuroscience : The Official Journal of the Society for Neuroscience 08/2010; 30(32):10927-38. DOI:10.1523/JNEUROSCI.0657-10.2010 · 6.75 Impact Factor