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26 September 2014, Volume 9 Issue 18 Previous Issue    Next Issue

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Decorin treatment of spinal cord injury Maryam Esmaeili, Martin Berry, Ann Logan, Zubair Ahmed 2014, 9 (18):  1653-1656.  doi: 10.4103/1673-5374.141797 Abstract ( 294 )   PDF (179KB) ( 910 )   Save The scarring response after a penetrant central nervous system injury results from the interaction between invading leptominingeal/pericyte-derived fibroblasts and endogenous reactive astrocytes about the wound margin. Extracellular matrix and scar-derived axon growth inhibitory molecules fill the lesion site providing both a physical and chemical barrier to regenerating axons. Decorin, a small leucine-rich chondroitin-dermatan sulphate proteoglycan expressed by neurons and astrocytes in the central nervous system, is both anti-fibrotic and anti-inflammatory and attenuates the formation and partial dissolution of established and chronic scars. Here, we discuss the potential of using Decorin to antagonise scarring in the central nervous system. Related Articles | Metrics

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Histological assessment in peripheral nerve tissue engineering Víctor Carriel, Ingrid Garzón, Miguel Alaminos, Maria Cornelissen 2014, 9 (18):  1657-1660.  doi: 10.4103/1673-5374.141798 Abstract ( 308 )   PDF (1064KB) ( 816 )   Save The histological analysis of peripheral nerve regeneration is one of the most used methods to demonstrate the success of the regeneration through nerve conduits. Nowadays, it is possible to evaluate different parameters of nerve regeneration by using histological, histochemical, immunohistochemical and ultrastructural techniques. The histochemical methods are very sensible and are useful tools to evaluate the extracellular matrix remodeling and the myelin sheath, but they are poorly specific. In contrast, the immunohistochemical methods are highly specific and are frequently used for the identification of the regenerated axons, Schwann cells and proteins associated to nerve regeneration or neural linage. The ultrastructural techniques offer the possibility to perform a high resolution morphological and quantitative analysis of the nerve regeneration. However, the use of a single histological method may not be enough to assess the degree of regeneration, and the combination of different histological techniques could be necessary. References | Related Articles | Metrics

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Genetic factors for nerve susceptibility to injuries – lessons from PMP22 deficiency Jun Li 2014, 9 (18):  1661-1664.  doi: 10.4103/1673-5374.141800 Abstract ( 250 )   PDF (225KB) ( 912 )   Save Genetic factors may be learnt from families with gene mutations that render nerve-injury susceptibility even to ordinary physical activities. A typical example is hereditary neuropathy with liability to pressure palsies (HNPP). HNPP is caused by a heterozygous deletion of PMP22 gene. PMP22 deficiency disrupts myelin junctions (such as tight junction and adherens junctions), leading to abnormally increased myelin permeability that explains the nerve susceptibility to injury. This finding should motivate investigators to identify additional genetic factors contributing to nerve vulnerability of injury. References | Related Articles | Metrics

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Bone marrow mesenchymal stem cells repair spinal cord ischemia/reperfusion injury by promoting axonal growth and anti-autophagy Fei Yin, Chunyang Meng, Rifeng Lu, Lei Li, Ying Zhang, Hao Chen, Yonggang Qin, Li Guo 2014, 9 (18):  1665-1671.  doi: 10.4103/1673-5374.141801 Abstract ( 297 )   PDF (2592KB) ( 1181 )   Save Bone marrow mesenchymal stem cells can differentiate into neurons and astrocytes after transplantation in the spinal cord of rats with ischemia/reperfusion injury. Although bone marrow mesenchymal stem cells are known to protect against spinal cord ischemia/reperfusion injury through anti-apoptotic effects, the precise mechanisms remain unclear. In the present study, bone marrow mesenchymal stem cells were cultured and proliferated, then transplanted into rats with ischemia/reperfusion injury via retro-orbital injection. Immunohistochemistry and immunofluorescence with subsequent quantification revealed that the expression of the axonal regeneration marker, growth associated protein-43, and the neuronal marker, microtubule-associated protein 2, significantly increased in rats with bone marrow mesenchymal stem cell transplantation compared with those in rats with spinal cord ischemia/reperfusion injury. Furthermore, the expression of the autophagy marker, microtubule-associated protein light chain 3B, and Beclin 1, was significantly reduced in rats with the bone marrow mesenchymal stem cell transplantation compared with those in rats with spinal cord ischemia/reperfusion injury. Western blot analysis showed that the expression of growth associated protein-43 and neurofilament-H increased but light chain 3B and Beclin 1 decreased in rats with the bone marrow mesenchymal stem cell transplantation. Our results therefore suggest that bone marrow mesenchymal stem cell transplantation promotes neurite growth and regeneration and prevents autophagy. These responses may likely be mechanisms underlying the protective effect of bone marrow mesenchymal stem cells against spinal cord ischemia/reperfusion injury. References | Related Articles | Metrics

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Oxidative phosphorylated neurofilament protein M protects spinal cord against ischemia/reperfusion injury Haitao Wang, Su Pan, Xiaoyu Yang, Benqing Zhu, Dalin Wang 2014, 9 (18):  1672-1677.  doi: 10.4103/1673-5374.141803 Abstract ( 471 )   PDF (1316KB) ( 992 )   Save Previous studies have shown that neurofilament protein M expression is upregulated in the early stage of spinal cord ischemia/reperfusion injury, indicating that this protein may play a role in the injury process. In the present study, we compared protein expression in spinal cord tissue of rabbits after 25 minutes of ischemia followed by 0, 12, 24, or 48 hours of reperfusion with that of sham operated rabbits, using proteomic two-dimensional gel electrophoresis and mass spectrometry. In addition, the nerve repair-related neurofilament protein M with the unregulated expression was detected with immunohistochemistry and western blot analysis. Two-dimensional gel electrophoresis and mass spectrometry showed that, compared with the sham group, upregulation of protein expression was most significant in the spinal cords of rabbits that had undergone ischemia and 24 hours of reperfusion. Immunohistochemical analysis revealed that neurofilament protein M was located in the membrane and cytoplasm of neuronal soma and axons at each time point after injury. Western blot analysis showed that neurofilament protein M expression increased with reperfusion time until it peaked at 24 hours and returned to baseline level after 48 hours. Furthermore, neurofilament protein M is phosphorylated under oxidative stress, and expression changes were parallel for the phosphorylated and non-phosphorylated forms. Neurofilament protein M plays an important role in spinal cord ischemia/reperfusion injury, and its functions are achieved through oxidative phosphorylation. References | Related Articles | Metrics

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Ginsenoside Rd inhibits apoptosis following spinal cord ischemia/reperfusion injury Baogang Wang, Qingsan Zhu, Xiaxia Man, Li Guo, Liming Hao 2014, 9 (18):  1678-1687.  doi: 10.4103/1673-5374.141802 Abstract ( 259 )   PDF (3253KB) ( 652 )   Save Ginsenoside Rd has a clear neuroprotective effect against ischemic stroke. We aimed to verify the neuroprotective effect of ginsenoside Rd in spinal cord ischemia/reperfusion injury and explore its anti-apoptotic mechanisms. We established a spinal cord ischemia/reperfusion injury model in rats through the occlusion of the abdominal aorta below the level of the renal artery for 1 hour. Successfully established models were injected intraperitoneally with 6.25, 12.5, 25 or 50 mg/kg per day ginsenoside Rd. Spinal cord morphology was observed at 1, 3, 5 and 7 days after spinal cord ischemia/reperfusion injury. Intraperitoneal injection of ginsenoside Rd in ischemia/reperfusion injury rats not only improved hindlimb motor function and the morphology of motor neurons in the anterior horn of the spinal cord, but it also reduced neuronal apoptosis. The optimal dose of ginsenoside Rd was 25 mg/kg per day and the optimal time point was 5 days after ischemia/reperfusion. Immunohistochemistry and western blot analysis showed ginsenoside Rd dose-dependently inhibited expression of pro-apoptotic Caspase 3 and down-regulated the expression of the apoptotic proteins ASK1 and JNK in the spinal cord of rats with spinal cord ischemia/reperfusion injury. These findings indicate that ginsenoside Rd exerts neuroprotective effects against spinal cord ischemia/reperfusion injury and the underlying mechanisms are achieved through the inhibition of ASK1-JNK pathway and the down-regulation of Caspase 3 expression. References | Related Articles | Metrics

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Factors affecting directional migration of bone marrow mesenchymal stem cells to the injured spinal cord Peng Xia, Su Pan, Jieping Cheng, Maoguang Yang, Zhiping Qi, Tingting Hou, Xiaoyu Yang 2014, 9 (18):  1688-1695.  doi: 10.4103/1673-5374.141804 Abstract ( 183 )   PDF (1798KB) ( 968 )   Save Microtubule-associated protein 1B plays an important role in axon guidance and neuronal migration. In the present study, we sought to discover the mechanisms underlying microtubule-associated protein 1B mediation of axon guidance and neuronal migration. We exposed bone marrow mesenchymal stem cells to okadaic acid or N-acetyl-D-erythro-sphingosine (an inhibitor and stimulator, respectively, of protein phosphatase 2A) for 24 hours. The expression of the phosphorylated form of type I microtubule-associated protein 1B in the cells was greater after exposure to okadaic acid and lower after N-acetyl-D-erythro-sphingosine. We then injected the bone marrow mesenchymal stem cells through the ear vein into rabbit models of spinal cord contusion. The migration of bone marrow mesenchymal stem cells towards the injured spinal cord was poorer in cells exposed to okadaic acid- and N-acetyl-D-erythro-sphingosine than in non-treated bone marrow mesenchymal stem cells. Finally, we blocked phosphatidylinositol 3-kinase (PI3K) and extracellular signal-regulated kinase 1/2 (ERK1/2) pathways in rabbit bone marrow mesenchymal stem cells using the inhibitors LY294002 and U0126, respectively. LY294002 resulted in an elevated expression of phosphorylated type I microtubule-associated protein 1B, whereas U0126 caused a reduction in expression. The present data indicate that PI3K and ERK1/2 in bone marrow mesenchymal stem cells modulate the phosphorylation of microtubule-associated protein 1B via a cross-signaling network, and affect the migratory efficiency of bone marrow mesenchymal stem cells towards injured spinal cord. References | Related Articles | Metrics

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Schwann cells originating from skin-derived precursors promote peripheral nerve regeneration in rats Ping Zhang, Xiaocheng Lu, Jianghai Chen, Zhenbing Chen 2014, 9 (18):  1696-1702.  doi: 10.4103/1673-5374.141805 Abstract ( 220 )   PDF (1301KB) ( 1483 )   Save Artificial guidance channels containing Schwann cells can promote the regeneration of injured peripheral nerve over long distances. However, primary Schwann cells are not suitable for autotransplantation. Under specific conditions, skin-derived progenitors can be induced to differentiate into Schwann cells. Therefore, adult rat dorsal skin (dermis)-derived progenitors were isolated and induced to differentiate with DMEM/F12 containing B27, neuregulin 1, and forskolin. Immunofluorescence staining and reverse transcription polymerase chain reaction (RT-PCR) confirmed that the resultant cells were indeed Schwann cells. Artificial guidance channels containing skin-derived progenitors, Schwann cells originating from skin-derived progenitors, or primary Schwann cells were used to bridge 5 mm sciatic nerve defects. Schwann cells originating from skin-derived progenitors significantly promoted sciatic nerve axonal regeneration. The significant recovery of injured rat sciatic nerve function after the transplantation of Schwann cells originating from skin-derived progenitors was confirmed by electromyogram. The therapeutic effect of Schwann cells originating from skin-derived progenitors was better than that of skin-derived progenitors. These findings indicate that Schwann cells originating from skin-derived precursors can promote peripheral nerve regeneration in rats. References | Related Articles | Metrics

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Craniocerebral injury promotes the repair of peripheral nerve injury Wei Wang, Jun Gao, Lei Na, Hongtao Jiang, Jingfeng Xue, Zhenjun Yang, Pei Wang 2014, 9 (18):  1703-1708.  doi: 10.4103/1673-5374.141807 Abstract ( 203 )   PDF (2743KB) ( 557 )   Save The increase in neurotrophic factors after craniocerebral injury has been shown to promote fracture healing. Moreover, neurotrophic factors play a key role in the regeneration and repair of peripheral nerve. However, whether craniocerebral injury alters the repair of peripheral nerve injuries remains poorly understood. Rat injury models were established by transecting the left sciatic nerve and using a free-fall device to induce craniocerebral injury. Compared with sciatic nerve injury alone after 6–12 weeks, rats with combined sciatic and craniocerebral injuries showed decreased sciatic functional index, increased recovery of gastrocnemius muscle wet weight, recovery of sciatic nerve ganglia and corresponding spinal cord segment neuron morphologies, and increased numbers of horseradish peroxidase-labeled cells. These results indicate that craniocerebral injury promotes the repair of peripheral nerve injury. Related Articles | Metrics

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Edaravone promotes functional recovery after mechanical peripheral nerve injury Teng Zhang, Zhengwei Li, Jianli Dong, Feng Nan, Tao Li, Qing Yu 2014, 9 (18):  1709-1715.  doi: 10.4103/1673-5374.141808 Abstract ( 295 )   PDF (1042KB) ( 1005 )   Save Edaravone has been shown to reduce ischemia/reperfusion-induced peripheral nerve injury. However, the therapeutic effect of edaravone on peripheral nerve injury caused by mechanical factors is unknown. In the present study, we established a peripheral nerve injury model by crushing the sciatic nerve using hemostatic forceps, and then administered edaravone 3 mg/kg intraperitoneally. The sciatic functional index and superoxide dismutase activity of the sciatic nerve were increased, and the malondialdehyde level was decreased in animals in the edaravone group compared with those in the model group. Bcl-2 expression was increased, but Bax expression was decreased in anterior horn cells of the L4–6 spinal cord segments. These results indicated that edaravone has a neuroprotective effect following peripheral nerve injury caused by mechanical factors through alleviating free radical damage to cells and inhibiting lipid peroxidation, as well as regulating apoptosis-related protein expression. Related Articles | Metrics

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Sciatic nerve injury repair: a visualized analysis of research fronts and development trends Guangyao Liu, Rui Jiang, Yan Jin 2014, 9 (18):  1716-1722.  doi: 10.4103/1673-5374.141810 Abstract ( 326 )   PDF (524KB) ( 1098 )   Save A total of 3,446 publications regarding sciatic nerve injury repair and protection indexed by Web of Science during 2000–2004 were used for a detailed analysis of temporal-spatial distribution characteristics. Reference co-citation networks of the 100 top-cited publications as per the number of total citations were created using the Web of Science database and the information visualization tool, CiteSpaceIII. The key words that showed high frequency in these publications were included for analyzing the research fronts and development trends for sciatic nerve injury repair and protection. Through word frequency trend analysis, studies on bone marrow mesenchymal stem cells, adipose-derived stem cells, and skeletal muscle-derived multipotent stem cells combined with tissue-engineered scaffold material will become the forefronts in the field of sciatic nerve injury repair and protection in the near future. Related Articles | Metrics

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Restoration and protection of brachial plexus injury:  hot topics in the last decade Kaizhi Zhang, Zheng Lv, Jun Liu, He Zhu, Rui Li 2014, 9 (18):  1723-1728.  Abstract ( 251 )   PDF (388KB) ( 792 )   Save Brachial plexus injury is frequently induced by injuries, accidents or birth trauma. Upper limb function may be partially or totally lost after injury, or left permanently disabled. With the development of various medical technologies, different types of interventions are used, but their effectiveness is wide ranging. Many repair methods have phasic characteristics, i.e., repairs are done in different phases. This study explored research progress and hot topic methods for protection after brachial plexus injury, by analyzing 1,797 articles concerning the repair of brachial plexus injuries, published between 2004 and 2013 and indexed by the Science Citation Index database. Results revealed that there are many methods used to repair brachial plexus injury, and their effects are varied. Intervention methods include nerve transfer surgery, electrical stimulation, cell transplantation, neurotrophic factor therapy and drug treatment. Therapeutic methods in this field change according to the hot topic of research. Related Articles | Metrics