Prohibitin 1 gene delivery promotes functional recovery in rats with spinal cord injury

Li, L.; Guo, Jia-Xiang; Wang, H.-D.; Yamin, Shi; Yuan, Yifang; Hou, Shuxun

doi:10.1016/j.neuroscience.2014.11.037

Cited by 28 publications

(20 citation statements)

References 45 publications

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“…This may provide a reasonable explanation for the locomotor function improvement in mice with SCT. The result gave a supplementary to the earlier reports about the effect of AKT on locomotor function [49][50][51]. More important, both NeuN, GAP-43, 5-HT and p-AKT/AKT showed similar changes.…”

Section: Bdnf Overexpression May Lead To Thermal Hyperalgesiasupporting

confidence: 81%

BDNF Overexpression Exhibited Bilateral Effect on Neural Behavior in SCT Mice Associated with AKT Signal Pathway

et al. 2016

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Spinal cord injury (SCI), a severe health problem in worldwide, was commonly associated with functional disability and reduced quality of life. As the expression of brain-derived neurotrophic factor (BDNF) was substantial event in injured spinal cord, we hypothesized whether BDNF-overexpression could be in favor of the recovery of both sensory function and hindlimb function after SCI. By using BDNF-overexpression transgene mice [CMV-BDNF 26 (CB26) mice] we assessed the role of BDNF on the recovery of neurological behavior in spinal cord transection (SCT) model. BMS score and tail-flick test was performed to evaluate locomotor function and sensory function, respectively. Immunohistochemistry was employed to detect the location and the expression of BDNF, NeuN, 5-HT, GAP-43, GFAP as well as CGRP, and the level of p-AKT and AKT were examined through western blot analysis. BDNF overexpressing resulted in significant locomotor functional recovery from 21 to 28 days after SCT, compared with wild type (WT)+SCT group. Meanwhile, the NeuN, 5-HT and GAP-43 positive cells were markedly increased in ventral horn in BDNF overexpression animals, compared with WT mice with SCT. Moreover, the crucial molecular signal, p-AKT/AKT has been largely up-regulated, which is consistent with the improvement of locomotor function. However, in this study, thermal hyperpathia encountered in sham (CB26) group and WT+SCT mice and further aggravated in CB26 mice after SCT. Also, following SCT, the significant augment of positive-GFAP astrocytes and CGRP fibers were found in WT+SCT mice, and further increase was seen in BDNF over-expression transgene mice. BDNF-overexpression may not only facilitate the recovery of locomotor function via AKT pathway, but also contributed simultaneously to thermal hyperalgesia after SCT.

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Section: Bdnf Overexpression May Lead To Thermal Hyperalgesiasupporting

confidence: 81%

BDNF Overexpression Exhibited Bilateral Effect on Neural Behavior in SCT Mice Associated with AKT Signal Pathway

et al. 2016

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“…Mitochondrial respiration and ATP formation were measured according to the method described previously (Patel et al, ; Li et al, ). Mitochondrial formation of H 2 O 2 and O 2 − was determined according to the method described by Elks et al, ().…”

Section: Methodsmentioning

confidence: 99%

D‐β‐hydroxybutyrate promotes functional recovery and relieves pain hypersensitivity in mice with spinal cord injury

Jiao

Zhu

et al. 2017

British J Pharmacology

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“…been reported that the PHB complex is located in the mitochondrial inner membrane and is essential for mitochondrial function and cell survival. The main mechanism of this protective role may be PHB-1-mediated inhibition of the intrinsic apoptotic pathway by maintaining the DCm, inhibiting cytochrome c release and caspase-3 activation, and enhancing the transcription and translation of antiapoptotic genes, such as Bcl2 and Bclxl (48)(49)(50). Therefore, our data provide new evidence to demonstrate that the exosomes derived from HBMECs contribute to the survival of SCLC cells through the elevated S100A16-mediated inhibition of mitochondrial inner membrane depolarization.…”

Section: Discussionmentioning

confidence: 58%

Brain microvascular endothelial cell exosome–mediated S100A16 up‐regulation confers small‐cell lung cancer cell survival in brain

Miao

Jiang

et al. 2018

FASEB j.

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Small cell lung cancer (SCLC) is the most aggressive histologic subtype of lung cancer, with a strong predilection for early brain metastases. Despite efforts and advances in new therapeutics for SCLC, the prognosis of patients with SCLC with brain metastases is consistently poor. Therefore, a better understanding of the mechanisms of SCLC brain metastasis is important in improving current treatments. In this study, elevated S100A16 levels were associated with SCLC brain metastases, which was a possible secondary event arising from the brain metastatic microenvironment. Using an in vitro cell coculture system, we found that the coculturing of SCLC cells with human brain microvascular endothelial cells (HBMECs) led to an increased expression of S100A16 in SCLC cells. Conversely, treatment of HBMECs with GW4869, an inhibitor of exosome release, significantly blocked this effect in the cocultured SCLC cells. Alternatively, the results from Western blot analyses and immunofluorescence indicated that the HBMEC exosomes purified by ultracentrifugation also induced the elevation and translocation from the cytoplasm to the nucleus of S100A16 in the recipient SCLC cells. The inhibition experiments demonstrated that elevated S100A16 contributed a benefit of HBMEC exosomes for the survival of the recipient SCLC cells under stress. Moreover, the elevation of S100A16 in SCLC cells prevented the loss of mitochondrial membrane potential (Δψm) and enhanced resistance to apoptosis under stressful conditions, which were determined by Annexin V/propidium iodide and JC-1 assay. Further results showed that the S100A16-mediated protective effect was caused by the presence of an important element in Δψm, prohibitin (PHB)-1, a protein in the mitochondrial inner membrane. Conversely, the delivery of PHB-1 siRNAs into S100A16 overexpressing SCLC cells weakened these protective effects. Our findings suggest that elevated S100A16 plays an active role in facilitating the survival of SCLC cells through modulating the mitochondrial function, identifying S100A16 as an important potential target in SCLC brain metastasis.-Xu, Z.-H., Miao, Z.-W., Jiang, Q.-Z., Gan, D.-X., Wei, X.-G., Xue, X.-Z., Li, J.-Q., Zheng, F., Qin, X.-X., Fang, W.-G., Chen, Y.-H., Li. B. Brain microvascular endothelial cell exosome-mediated S100A16 up-regulation confers small cell lung cancer cell survival in brain.

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Prohibitin 1 gene delivery promotes functional recovery in rats with spinal cord injury

Cited by 28 publications

References 45 publications

BDNF Overexpression Exhibited Bilateral Effect on Neural Behavior in SCT Mice Associated with AKT Signal Pathway

BDNF Overexpression Exhibited Bilateral Effect on Neural Behavior in SCT Mice Associated with AKT Signal Pathway

D‐β‐hydroxybutyrate promotes functional recovery and relieves pain hypersensitivity in mice with spinal cord injury

Brain microvascular endothelial cell exosome–mediated S100A16 up‐regulation confers small‐cell lung cancer cell survival in brain

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