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MicroRNAs: a novel promising therapeutic target for cerebral ischemia/reperfusion injury?

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Neural Regeneration Research 2015年第11期10卷 1799-1808页

作者： Xiao-li Min ting-yong wang Yi Cao Jia Liu Jin-tao Li ting-hua wang Institute of Neuroscience Kunming Medical University Faculty of Clinical Medicine Yunnan University of Traditional Chinese Medicine the First Affiliated Hospital of Yunnan University of Traditional Chinese Medicine School of Economics of Sichuan University Department of Neurosurgery the Second Affiliated Hospital of Kunming Medical University

To determine the molecular mechanism of cerebral ischemia/reperfusion injury, we examined the micro RNA（mi RNA） expression profile in rat cortex after focal cerebral ischemia/reperfusion injury using mi RNA microarrays and bioinformatic tools to systematically analyze Gene Ontology（GO） function classifications, as well as the signaling pathways of genes targeted by these differentially expressed mi RNAs. Our results show significantly changed mi RNA expression profiles in the reperfusion period after focal cerebral ischemia, with a total of 15 mi RNAs up-regulated and 44 mi RNAs down-regulated. Target genes of these differentially expressed mi RNAs were mainly involved in metabolic and cellular processes, which were identified as hub nodes of a mi RNA-GO-network. The most correlated pathways included D-glutamine and D-glutamate metabolism, the renin-angiotensin system, peroxisomes, the PPAR signaling pathway, SNARE interactions in vesicular transport, and the calcium signaling pathway. Our study suggests that mi RNAs play an important role in the pathological process of cerebral ischemia/reperfusion injury. Understanding mi RNA expression and function may shed light on the molecular mechanism of cerebral ischemia/reperfusion injury.

关键词： nerve regeneration microRNA therapeutic target cerebral ischemia/reperfusion injury miRNA expression profiles bioinformatics analysis Gene Ontology analysis molecular mechanism KEGG pathway neural regeneration

Brain-Derived Glia Maturation Factor b Participates in Lung Injury Induced by Acute Cerebral Ischemia by Increasing ROS in Endothelial Cells

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Neuroscience Bulletin 2018年第6期34卷 1077-1090页

作者： Fei-Fei Xu Zi-Bin Zhang Yang-Yang wang ting-hua wang Institute of Neurological Disease Department of Anesthesiology West China Hospital Sichuan University

Brain damage can cause lung injury. To explore the mechanism underlying the lung injury induced by acute cerebral ischemia(ACI), we established a middle cerebral artery occlusion(MCAO) model in male Sprague-Dawley rats. We focused on glia maturation factor b(GMFB) based on quantitative analysis of the global rat serum *** chain reaction, western blotting, and immunofluorescence revealed that GMFB was overexpressed in astrocytes in the brains of rats subjected to MCAO. We cultured rat primary astrocytes and confirmed that GMFB was also up-regulated in primary astrocytes after oxygen-glucose deprivation(OGD). We subjected the primary astrocytes to Gmfb RNA interference before OGD and collected the conditioned medium(CM) after *** then used the CM to culture pulmonary microvascular endothelial cells(PMVECs) acquired in advance and assessed their status. The viability of the PMVECs improved significantly when Gmfb was blocked. Moreover,ELISA assays revealed an elevation in GMFB concentration in the medium after OGD. Cell cultures containing recombinant GMFB showed increased levels of reactive oxygen species and a deterioration in the state of the *** conclusion, GMFB is up-regulated in astrocytes after ACI, and brain-derived GMFB damages PMVECs by increasing reactive oxygen species. GMFB might thus be an initiator of the lung injury induced by ACI.

关键词： Glial maturation factor b Acute cerebral ischemia Lung injury RNA interference Pulmonary microvascular endothelial cells Reactive oxygen species

Nitric Oxide Mediates Cytokinin Functions in Cell Proliferation and Meristem Maintenance in Arabidopsis

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Molecular Plant 2013年第4期6卷 1214-1225页

作者： Qi Shen Yu-ting wang hua Tian Fang-Qing Guo The National Key Laboratory of Plant Molecular Genetics and National Center for Plant Gene Research (Shanghai) Institute of Plant Physiology andEcology Shanghai Institutes for Biological Sciences Chinese Academy of Sciences 300 Fenglin Road Shanghai 200032 China

Cytokinin and nitric oxide （NO） have been characterized as signaling molecules to trigger cell division in tissue culture. Here, we show that the hypocotyl and root explants of Arabidopsis NO-deficient mutant nosl/noal exhibit severe defects in callus induction and shoot regeneration in response to cytokinin. Accordingly, depletion of NO caused by a NO scavenger leads to a severe inhibitory effect on callus induction. Moreover, cytokinin-induced NO production is impaired in nosl/noal in which cytokinin-triggered activation of cell cycle gene CYCD3;1 is inhibited, indicating that NO may act downstream of cytokinin in the control of cell proliferation through CYCD3;1. This hypothesis is further con- firmed by the genetic evidence that constitutive expression of CYCD3;1 complements the defects of nosl/noal mutant in meristematic activity in shoot, root, and floral tissues as well as in cytokinin-induced callus initiation and shoot regen- eration. Furthermore, we show that NO deficiency caused by loss of NOSl/NOA1 impairs cellular development such as the duration of the mitotic phase and timing of the transition to endocycles in nosl/noal mutant leaves, which can be reverted by constitutive expression of CYCD3;1. Taken together, these results demonstrate that NO mediates transcrip- tional activation of CYCD3,1 in regulating the mitotic cycles in response to cytokinins.

关键词： nitric oxide cytokinins cell proliferation CYCD3 1 shoot regeneration endocycles.

Breviscapine reduces neuronal injury caused by traumatic brain injury insult:partly associated with suppression of interleukin-6 expression

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Neural Regeneration Research 2017年第1期12卷 90-95页

作者： Ling Jiang Yue Hu Xiang He Qiang Lv ting-hua wang Qing-jie Xia Institute of Neurological Disease Department of Anesthesiology and Translation Neuroscience CenterWest China HospitalSichuan UniversityChengduSichuan ProvinceChina

Breviscapine,extracted from the herb Erigeron breviscapus,is widely used for the treatment of cardiovascular diseases,cerebral infarct,and stroke,but its mechanism of action remains *** study established a rat model of traumatic brain injury induced by controlled cortical impact,and injected 75 μg breviscapine via the right lateral *** found that breviscapine significantly improved neurobehavioral dysfunction at 6 and 9 days after ***,interleukin-6 expression was markedly down-regulated following breviscapine *** results suggest that breviscapine is effective in promoting neurological behavior after traumatic brain injury and the underlying molecular mechanism may be associated with the suppression of interleukin-6.

关键词： nerve regeneration breviscapine traumatic brain injury neuroprotective effect interleukin-6 neural regeneration

Synaptosomal-associated protein 25 may be an intervention target for improving sensory and locomotor functions after spinal cord contusion

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Neural Regeneration Research 2017年第6期12卷 969-976页

作者： Zhan-qiong Zhong Yang Xiang Xi Hu You-cui wang Xi Zeng Xiao-meng wang Qing-jie Xia ting-hua wang Xiao Zhang Experiment Technology Center of Preclinical Medicine of Chengdu Medical College School of Basic Medicine Chengdu University of Traditional Chinese Medicine Institute of Neurological Diseases Center for Translational Neuroscience Western China Hospital Sichuan University

Synaptosomal-associated protein 25 k Da（SNAP-25） is localized on the synapse and participates in exocytosis and neurotransmitter release. Decreased expression of SNAP-25 is associated with Alzheimer＇s disease and attention deficit/hyperactivity disorder. However, the expression of SNAP-25 in spinal cord contusion injury is still unclear. We hypothesized that SNAP-25 is associated with sensory and locomotor functions after spinal cord injury. We established rat models of spinal cord contusion injury to detect gene changes with a gene array. A decreased level of SNAP-25 was detected by quantitative real time-polymerase chain reaction and western blot assay at 1, 3, 7, 14 and 28 days post injury. SNAP-25 was localized in the cytoplasm of neurons of the anterior and posterior horns, which are involved in locomotor and sensory functions. Our data suggest that reduced levels of SNAP-25 are associated with sensory and locomotor functions in rats with spinal cord contusion injury.

关键词： sensory hyperactivity deficit cytoplasm localized unclear Chengdu autism neuronal minutes

Neuroprotective effects of BDNF and GDNF in intravitreally transplanted mesenchymal stem cells after optic nerve crush in mice

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International Journal of Ophthalmology(English edition) 2017年第1期10卷 35-42页

作者： Zong-Li Hu Ni Li Xin Wei Li Tang ting-hua wang Xiao-Ming Chen Department of Ophthalmology West China HospitalSichuan UniversityChengdu 610041Sichuan ProvinceChina Institute of Neurological Disease West China HospitalSichuan UniversityChengdu 610041Sichuan ProvinceChina

AIM： To assess the neuro-protective effect of bone marrow mesenchymal stem cells （BMSCs） on retinal ganglion cells （RGCs） following optic nerve crush in mice. METHODS： C56BL/6J mice were treated with intravitreal injection of PBS, BMSCs, BDNF-interference BMSCs （BIM）, and GDNF-interference BMSCs （GIM） following optic nerve crush, respectively. The number of surviving RGCs was determined by whole-mount retinas and frozen sections, while certain mRNA or protein was detected by q-PCR or ELISA, ***： The density （cell number/mm^2） of RGCs was 410.77±56.70 in the retina 21d after optic nerve crush without any treatment, compared to 1351.39±195.97 in the normal control （P〈0.05）. RGCs in BMSCs treated eyes was 625.07±89.64/mm^2, significantly higher than that of no or PBS treatment （P〈0.05）. While RGCs was even less in the retina with intravitreal injection of BIM （354.07±39.77） and GIM （326.67±33.37） than that without treatment （P〈0.05）. BMSCs injection improved the internal BDNF expression in ***： Optic nerve crush caused rust loss of RGCs and intravitreally transplanted BMSCs at some extent protected RGCs from death. The effect of BMSCs and level of BDNF in retinas are both related to BDNF and GDNF expression in BMSCs.

关键词： optic nerve crash retinal ganglion cells stemcells brain-derived neurotrophie factor glial cell line-derived neurotrophic factor

Application prospects of urine-derived stem cells in neurological and musculoskeletal diseases

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World Journal of Orthopedics 2024年第10期15卷 918-931页

作者： Hui-Si Yang Yue-Xiang Zheng Xue Bai Xiu-Ying He ting-hua wang Department of Neurology and National Traditional Chinese Medicine Clinical Research Base The Affiliated Traditional Chinese Medicine Hospital of Southwest Medical UniversityLuzhou 646000Sichuan ProvinceChina Department of Anesthesiology Institute of Neurological DiseaseWest China HospitalSichuan UniversityChengdu 610041Sichuan ProvinceChina Department of Anesthesiology Institute of Neurological DiseaseTranslational Neuroscience CenterWest China HospitalSichuan UniversityChengdu 610041Sichuan ProvinceChina

Urine-derived stem cells(USCs)are derived from urine and harbor the potential of proliferation and multidirectional ***,USCs could be reprogrammed into pluripotent stem cells[namely urine-derived induced pluripotent stem cells(UiPSCs)]through transcription factors,such as octamer binding transcription factor 4,sex determining region Y-box 2,kruppel-like factor 4,myelocytomatosis oncogene,and Nanog homeobox and protein lin-28,in which the first four are known as Yamanaka *** evidence supports that USCs and UiPSCs possess high potential of neurogenic,myogenic,and osteogenic differentiation,indicating that they may play a crucial role in the treatment of neurological and musculoskeletal ***,we summarized the origin and physiological characteristics of USCs and UiPSCs and their therapeutic application in neurological and musculoskeletal disorders in this review,which not only contributes to deepen our understanding of hallmarks of USCs and UiPSCs but also provides the theoretical basis for the treatment of neurological and musculoskeletal disorders with USCs and UiPSCs.

关键词： Urine-derived stem cells Urine-derived induced pluripotent stem cells Neurological diseases Musculoskeletal diseases Treatment prospect

Structural insights into substrate recognition and translocation of human peroxisomal ABC transporter ALDP

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Signal Transduction and Targeted Therapy 2023年第3期8卷 1269-1281页

作者： Chao Xiong Li-Na Jia Wei-Xi Xiong Xin-Tong Wu Liu-Lin Xiong ting-hua wang Dong Zhou Zhen Hong Zheng Liu Lin Tang Department of Neurology State Key Lab of Biotherapy and Cancer CenterWest China HospitalSichuan University and Collaborative Innovation Center for Biotherapy610041 ChengduSichuanChina Institute of Brain Science and Brain-inspired Technology of West China Hospital Sichuan UniversityChengduChina Institute of Neurological Disease State Key Lab of BiotherapyWest China HospitalSichuan University610041 ChengduSichuanChina School of Life and Health Kobilka Institute of Innovative Drug Discoverythe Chinese University of Hong Kong(Shenzhen)ShenzhenChina

Dysfunctions of ATP-binding cassette,subfamily D,member 1(ABCD1)cause X-linked adrenoleukodystrophy,a rare neurodegenerative disease that affects all human *** in the peroxisome membrane,ABCD1 plays a role in the translocation of very long-chain fatty acids for theirβ-***,the six cryo-electron microscopy structures of ABCD1 in four distinct conformational states were *** the transporter dimer,two transmembrane domains form the substrate translocation pathway,and two nucleotide-binding domains form the ATP-binding site that binds and hydrolyzes *** ABCD1 structures provide a starting point for elucidating the substrate recognition and translocation mechanism of *** of the four inward-facing structures of ABCD1 has a vestibule that opens to the cytosol with variable *** acid(C26:0)-CoA substrate binds to the transmembrane domains(TMDs)and stimulates the ATPase activity of the nucleotide-binding domains(NBDs).W339 from the transmembrane helix 5(TM5)is essential for binding substrate and stimulating ATP hydrolysis by ***1 has a unique C-terminal coiled-coil domain that negatively modulates the ATPase activity of the ***,the structure of ABCD1 in the outward-facing state indicates that ATP molecules pull the two NBDs together and open the TMDs to the peroxisomal lumen for substrate *** five structures provide a view of the substrate transport cycle and mechanistic implication for disease-causing mutations.

关键词： starting hydrolysis insight

Brain-derived neurotrophic factor and its related enzymes and receptors play important roles after hypoxic-ischemic brain damage

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Neural Regeneration Research 2021年第8期16卷 1453-1459页

作者： Liu-Lin Xiong Jie Chen Ruo-Lan Du Jia Liu Yan-Jun Chen Mohammed Al Hawwas Xin-Fu Zhou ting-hua wang Si-Jin Yang Xue Bai National Traditional Chinese Medicine Clinical Research Base and Western Medicine Translational Medicine Research Center Department of Cardiovascular DiseaseAffiliated Traditional Chinese Medicine HospitalSouthwest Medical UniversityLuzhouSichuan ProvinceChina Cinical and Health Sciences University of South AustraliaAdelaideAustralia Animal Zoology Department Institute of NeuroscienceKunming Medical UniversityKunmingYunnan ProvinceChina Institute of Neurological Disease Translational Neuroscience CenterWest China HospitalSichuan UniversityChengduSichuan ProvinceChina

Brain-derived neurotrophic factor(BDNF) regulates many neurological functions and plays a vital role during the recovery from central nervous system injuries. However, the changes in BDNF expression and associated factors following hypoxia-ischemia induced neonatal brain damage, and the significance of these changes are not fully understood. In the present study, a rat model of hypoxic-ischemic brain damage was established through the occlusion of the right common carotid artery, followed by 2 hours in a hypoxic-ischemic environment. Rats with hypoxic-ischemic brain damage presented deficits in both sensory and motor functions, and obvious pathological changes could be detected in brain tissues. The m RNA expression levels of BDNF and its processing enzymes and receptors(Furin, matrix metallopeptidase 9, tissuetype plasminogen activator, tyrosine Kinase receptor B, plasminogen activator inhibitor-1, and Sortilin) were upregulated in the ipsilateral hippocampus and cerebral cortex 6 hours after injury;however, the expression levels of these m RNAs were found to be downregulated in the contralateral hippocampus and cerebral cortex. These findings suggest that BDNF and its processing enzymes and receptors may play important roles in the pathogenesis and recovery from neonatal hypoxic-ischemic brain damage. This study was approved by the Animal Ethics Committee of the University of South Australia(approval No. U12-18) on July 30, 2018.

关键词： brain injury brain-derived neurotrophic factor enzyme hypoxia-ischemia receptors recovery repair