C-jun phosphorylation contributes to down regulation of neuronal nitric oxide synthase protein and motoneurons death in injured spinal cords following root-avulsion of the brachial plexus

Wang, L.-L.; Zhao, Xiang; Yan, Liwei; Wang, Y.-Q.; Cheng, Xiuyuan; Fu, Rao; Zhou, Lihua

doi:10.1016/j.neuroscience.2011.04.070

Cited by 26 publications

(38 citation statements)

References 57 publications

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“…Our study also showed that c-jun phosphorylation acts as the upstream molecule that inhibits the nNOS expression in injured spinal cords within the first 2 weeks after root-avulsion injury. Additionally, a functional relationship between c-jun and nNOS in motoneurons is possible (17).…”

Section: Discussionmentioning

confidence: 99%

Suppression of c-jun influences nNOS expression in differentiated PC12 cells

Cheng

Liu

Wang

et al. 2012

Molecular Medicine Reports

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Section: Discussionmentioning

confidence: 99%

Suppression of c-jun influences nNOS expression in differentiated PC12 cells

Cheng

Liu

Wang

et al. 2012

Molecular Medicine Reports

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“…Avulsion of the right C7 and C8 ventral roots was performed as described in our previous publication [7,68] and further modified in the present study. Briefly, the rat was anesthetized with intraperitoneal injections of 10% chloral hydrate (350 mg/kg).…”

Section: Methodsmentioning

confidence: 99%

Lithium enhances survival and regrowth of spinal motoneurons after ventral root avulsion

Tang

Ling

et al. 2014

BMC Neurosci

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BackgroundDuring the clinical treatment of the brachial plexus root avulsion (BPRA), reimplantation surgery can not completely repair the motor function of the hand because the axonal growth velocity of the spinal motoneurons (MNs) is too slow to re-innervate the intrinsic hand muscles before muscle atrophy. Here, we investigated whether lithium can enhance the regenerative capacity of the spinal MNs in a rat model of BPRA.ResultsThe avulsion and immediate reimplantation of the C7 and C8 ventral roots were performed and followed with daily intraperitoneal administration of a therapeutic concentrationof LiCl. After a 20 week long-term rehabilitation, the motor function recovery of the injured forepaw was studied by a grasping test. The survival and regeneration of MNs were checked by choline acetyltransferase (ChAT) immunofluorescence and by Fluoro-Gold (FG) retrograde labeling through the median and ulnar nerves of the ventral horn MNs. The number and diameter of the nerve fibers in the median nerve were assessed by toluidine blue staining. Our results showed that lithium plus reimplantation therapy resulted in a significantly higher grasping strength of the digits of the injured forepaw. Lithium plus reimplantation allowed 45.1% ± 8.11% of ChAT-positive MNs to survive the injury and increased the number and diameter of nerve fibers in the median nerve. The number of FG-labeled regenerative MNs was significantly elevated in all of the reimplantation animals. Our present data proved that lithium can enhance the regenerative capacity of spinal MNs.ConclusionsThese results suggest that immediate administration of lithium could be used to assist reimplantation surgery in repairing BPRA injuries in clinical treatment.

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“…It is possible that either the induction of pro-apoptotic and/or the reduction of prosurvival pathways may influence the transcriptional control of nNOS expression and/or its translation and activity. As recently shown the activation of the JNK pathway may lead to the reduction of nNOS protein expression [27], therefore the observed decrease in nNOS protein expression after a cytokine mixture treatment may result, at least partially, from the cytokine-induced JNK activation, a well established phenomenon in pancreatic beta cells [28][29][30]. Other possible regulatory mechanisms could also include changes in the alternative splicing of nNOS mRNA as well as inactivation of nNOS activity, for instance by disturbances in the intracellular calcium pool and Hsp90 availability.…”

Section: Discussionmentioning

confidence: 96%

“…JANEX-1 [20], antiinflammatory cytokines [21], prostacyclin [22] or some plant extracts [23] prevents cytokine-induced iNOS expression and cytokine toxicity in insulin-secreting cells [1,24,25]. The expression of nNOS is controlled by alternative splicing and the transcription factor CREB [26] and its activity can be regulated by Hsp90, calmodulin and other factors [1,26,27]. 5.…”

Section: Discussionmentioning

confidence: 99%