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您的检索式：作者名="Judith A.Strong"
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| 1 | Differential Inhibition of Nav1.7 and Neuropathic Pain by Hybridoma-Produced and Recombinant Monoclonal Antibodies that Target Nav1.7显示文摘The voltage-gated Na^+ channel subtype Nav1.7 is important for pain and itch in rodents and humans. We previously showed that a Nav1.7-targeting monoclonal antibody(SVmab) reduces Na+ currents and pain and itch responses in mice. Here, we investigated whether recombinant SVmab(rSVmab) binds to and blocks Nav1.7 similar to SVmab. ELISA tests revealed that SVmab was capable of binding to Nav1.7-expressing HEK293 cells,mouse DRG neurons, human nerve tissue, and the voltagesensor domain Ⅱ of Nav1.7. In contrast, rSVmab showed no or weak binding to Nav1.7 in these tests. Patch-clamp recordings showed that SVmab, but not rSVmab, markedly inhibited Na+ currents in Nav1.7-expressing HEK293 cells. Notably, electrical field stimulation increased the blocking activity of SVmab and rSVmab in Nav1.7-expressing HEK293 cells. SVmab was more effective than rSVmab in inhibiting paclitaxel-induced mechanical allodynia. SVmab also bound to human DRG neurons and inhibited their Na^+ currents. Finally, potential reasons for the differential efficacy of SVmab and rSVmab and future directions are discussed. | Sangsu Bang Jiho Yoo Xingrui Gong Di Liu Qingjian Han Xin Luo Wonseok Chang Gang Chen Sang-Taek Im Yong Ho Kim Judith A.Strong Ma-Zhong Zhang Jun-Ming Zhang Seok-Yong Lee Ru-Rong Ji | 2018 | Neuroscience Bulletin2018，34，1： | 2 |
| 2 | The Antinociceptive Effect of Sympathetic Block is Mediated by Transforming Growth Factor β in a Mouse Model of Radiculopathy显示文摘Although sympathetic blockade is clinically used to treat pain,the underlying mechanisms remain unclear.We developed a localized microsympathectomy(mSYMPX),by cutting the grey rami entering the spinal nerves near the rodent lumbar dorsal root ganglia(DRG).In a chemotherapy-induced peripheral neuropathy model,mSYMPX attenuated pain behaviors via DRG macrophages and the anti-inflammatory actions of transforming growth factor-β(TGF-β)and its receptor TGF-βR1.Here,we examined the role of TGF-βin sympathetic-mediated radiculopathy produced by local inflammation of the DRG(LID).Mice showed mechanical hypersensitivity and transcriptional and protein upregulation of TGF-β1 and TGF-βR1 three days after LID.Microsympathectomy prevented mechanical hypersensitivity and further upregulated Tgfb1 and Tgfbr1.Intrathecal delivery of TGF-β1 rapidly relieved the LID-induced mechanical hypersensitivity,and TGF-βR1 antagonists rapidly unmasked the mechanical hypersensitivity after LID+mSYMPX.In situ hybridization showed that Tgfb1 was largely expressed in DRG macrophages,and Tgfbr1 in neurons.We suggest that TGF-βsignaling is a general underlying mechanism of local sympathetic blockade. | Debora Denardin Luckemeyer Wenrui Xie Arthur Silveira Prudente Katherine A.Qualls Raquel Tonello Judith A.Strong Temugin Berta Jun-Ming Zhang | 2023 | Neuroscience Bulletin2023，39，9： | 0 |
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