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Acta Biochimica et Biophysica Sinica 2005年第8期37卷 507-514页

作者： Qiu-Ling FAN~(1,2) Cai-Guo HUANG~(2*) Yan JIN~2 Bo FENG~2 Hui-Nan MIAO~2 Wen-Jie LI~2 Bing-Hua JIAO~2 Qin-Sheng YUAN~(1*) ~1 State Key Laboratory of Bioreactor Engineering.East China University of Science and Techology,Shanghai 200237.China ~2 Department of Biochemistry and Molecular Biology,Second Military Medical University.Shanghai 200433.China State Key Laboratory of Bioreactor Engineering East China University of Science and TechnologyShanghai 200237 China Department of Biochemistry and Molecular Biology Second Military Medical UniversityShanghai 200433 China

This study was carried out to investigate whether shark hepatic stimulator substance(HSS)can prevent acute liver injury and affect mitochondrial function and antioxidant defenses in a rat model ofthioacetamide(TAA)-induced liver injury.The acute liver injury was induced by two intraperitoneal injectionsof TAA(400 mg/kg)in a 24 h interval.In the TAA plus shark HSS group,rats were treated with shark HSS(80 mg/kg)I h prior to each TAA injection.In this group,serum liver enzyme activities were significantlylower than those in the TAA group.The mitochondrial respiratory control ratio was improved,and themitochondrial respiratory enzyme activities were increased in the TAA plus shark HSS group.The mitochondrialantioxidant enzyme activities and glutathione level were higher in the TAA plus shark HSS group than in theTAA group.These results suggest that the protective effect of shark HSS against TAA-induced acute liverinjury may be a result of the restoration of the mitochondrial respiratory function and antioxidant defensesand decreased oxygen stress.

关键词： shark hepatic stimulator substance acute liver injury mitochondrion respiratory function antioxidant capacity

Identification of Target Genes and Transcription Factors Implicated in Translation-Dependent Retrograde Sig- naling in Arabidopsis

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Molecular Plant 2014年第7期7卷 1228-1247页

作者： Dario Leister Isidora Romani Lukas Mittermayr Francesca Paieri Elena Fenino Tatjana Kleine Plant Molecular Biology (Botany) Department Biology I Ludwig-Maximilians-University Munich Gro0haderner Str. 2 D-82152Martinsried Germany

Changes in organellar gene expression （OGE） trigger retrograde signaling. The molecular dissection of OGE-dependent retrograde signaling based on analyses of mutants with altered OGE is complicated by compensatory responses that mask the primary signaling defect and by secondary effects that influence other retrograde signaling pathways. Therefore, to identify the earliest effects of altered OGE on nuclear transcript accumulation, we have induced OGE defects in adult plants by ethanol-dependent repression of PRORS1, which encodes a prolyl-tRNA synthetase located in chloroplasts and mitochondria. After 32 h of PRORS1 repression, the translational capacity of chloroplasts was reduced, and this effect subsequently intensified, while basic photosynthetic parameters were still unchanged at 51 h. Analysis of changes in whole-genome transcriptomes during exposure to ethanol revealed that induced PRORS1 silencing affects the expression of 1020 genes in all. Some of these encode photosynthesis-related proteins, including several down-regulated light-harvesting chlorophyll a/b binding （LHC） proteins. Interestingly, genes for presumptive endoplasmic reticulum pro- teins are transiently up-regulated. Furthermore, several NAC-domain-containing proteins are among the transcription factors regulated. Candidate cis-acting elements which may coordinate the transcriptional co-regulation of genes sets include both G-box variants and sequence motifs with no similarity to known plant c/s-elements.

关键词： Arabidopsis chloroplast mitochondrion retrograde signaling target genes transcription factors cis-elements.

Mechanisms of secondary degeneration after partial optic nerve transection

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Neural Regeneration Research 2014年第6期9卷 565-574页

作者： Hong-Ying Li Yi-Wen Ruan Chao-Ran Ren Qi Cui Kwok-Fai So Department of Ophthalmology the University of Hong Kong State Key Laboratory of Brain and Cognitive Science the University of Hong Kong GHM Institute of CNS Regeneration Jinan University Guangdong Key Laboratory of Brain Function and Diseases Jinan University

Secondary degeneration occurs commonly in the central nervous system after traumatic injuries and following acute and chronic diseases, including glaucoma. A constellation of mechanisms have been shown to be associated with secondary degeneration including apoptosis, necrosis, autophagy, oxidative stress, excitotoxicity, derangements in ionic homeostasis and calcium influx. Glial cells, such as microglia, astrocytes and oligodendrocytes, have also been demon- strated to take part in the process of secondary injury. Partial optic nerve transection is a useful model which was established about 13 years ago. The merit of this model compared with other optic nerve injury models used for glaucoma study, including complete optic nerve transection model and optic nerve crush model, is the possibility to separate primary degeneration from secondary degeneration in location. Therefore, it provides a good tool for the study of secondary degeneration. This review will focus on the research progress of the mechanisms of secondary degeneration using partial optic nerve transection model.

关键词： secondary degeneration partial injury optic nerve oxidative stress excitotoxicity calci-um overload mitochondrion macrophage astrocyte oligodendrocyte

Genistein suppresses the mitochondrial apoptotic pathway in hippocampal neurons in rats with Alzheimer's disease

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Neural Regeneration Research 2016年第7期11卷 1153-1158页

作者： Yan Wang Biao Cai Jing Sha Ting-ting Wang Run-ze Cai Chang-ju Ma Tao Han Jun Du School of Integrated Chinese and Western Medicine Anhui University of Chinese Medicine Hefei Anhui Province China Institute of Integrated Chinese and Western Medicine Anhui Academy of Chinese Medicine Hefei Anhui Province China

Genistein is effective against amyloid-β toxicity, but the underlying mechanisms are unclear. We hypothesized that genistein may protect neurons by inhibiting the mitochondrial apoptotic pathway, and thereby play a role in the prevention of Alzheimer＇s disease. A rat model of Alzheimer＇s disease was established by intraperitoneal injection of D-galactose and intracerebral injection of amyloid-β peptide （25-35）. In the genistein treatment groups, a 7-day pretreatment with genistein （10, 30, 90 mg/kg） was given prior to establishing Alzheimer＇s disease model, for 49 consecutive days. Terminal deoxyribonucleotidyl transferase-mediated dUTP nick end labeling assay demonstrated a reduction in apoptosis in the hippocampus of rats treated with genistein. Western blot analysis showed that expression levels of capase-3, Bax and cytochrome c were decreased compared with the model group. Furthermore, immunohistochemical staining revealed reductions in cytochrome c and Bax immunoreactivity in these rats. Morris water maze revealed a substantial shortening of escape latency by genistein in Alzheimer＇s disease rats. These findings suggest that genistein decreases neuronal loss in the hippocampus, and improves learning and memory ability. The neuroprotective effects of genistein are associated with the inhibition of the mitochondrial apoptotic pathway, as shown by its ability to reduce levels of caspase-3, Bax and cytochrome c.

关键词： nerve regeneration genistein Alzheimer＇s disease mitochondrion apoptosis hippocampus Bax cytochrorne c caspase-3 learning memory neural regeneration

Three-dimensional structure of axonal mitochondria reflects the age of drosophila

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Neural Regeneration Research 2013年第7期8卷 616-621页

作者： Honglian Zhu Xiaojiang Sun Department of Neurology Sixth People's Hospital of Shanghai Jiao Tong University Department of Geriatrics Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine

This study aimed to reconstruct a three-dimensional map of axonal mitochondria using Fiji and Neurolucida software, and to observe directly the morphology and distribution of mitochondria in axons of motor neurons in dorsal longitudinal flight muscles of drosophila aged 5 days and 20 days, using electron microscopy. Results indicated that there was no difference in the total area and volume of mitochondria between 5-day-old drosophila and 20-day-old drosophila in all sections, but the ratio of mitochondrial total areas to axon total areas, as well as mitochondrial density of 20-day-old drosophila, was lower than that of 5-day-old drosophila. The number of mitochondria, whose volume was less than 1 000 000 IJm3, and between 1 000 000 pm3 and 10 000 000 pm3, was higher in 20-day-old drosophila than that in 5-day-old drosophila. The number of mitochondria with a volume between 1 000 000 pm3 and 100 000 000 IJm3 was apparently higher than those with a volume less than 1 000 000 t.lm3 or larger than 100 000 000 IJm3. In addition, the number of mitochondria with a volume more than 100 000 000 tJm3 was small; however, the volume was nearly 70% of the total volume in both 5-day-old and 20-day-old drosophila. In contrast, the number of mitochondria with a volume between 1 000 000 t.Jm3 and 10 000 000 IJm3 was large, but the volume was less than 30% of the total volume. These experimental findings suggest that changes in mitochondrial morphology and number in motor neurons from the dorsal longitudinal muscle of drosophila are present during different ages.

关键词： neural regeneration neurodegenerative diseases neurogenesis mitochondrion drosophila axon three-dimensional model electron microscopy age-related neurodegenerative diseases mitochondrial morphology cell microstructure photographs-containing paper neuroregeneration

The Association between the C5263T Mutation in the Mitochondrial ND2 Gene and Coronary Heart Disease among Young Chinese Han People

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Biomedical and Environmental Sciences 2017年第4期30卷 280-287页

作者： HAN Guo Xin XIA Lei LI Shuo Shuo JIN Qin Hua SONG Yang SHEN Hong WANG Li Li KONG Ling Jie LI Tan Shi ZHU Hai Yan Emergency Department General Hospital of Chinese PLABeijing 100853China Medical Support Department General Hospital of Chinese PLABeijing 100853China Cardiology Department of Chinese PLA Beijing 100853China

Objective This study aimed to investigate the genetic background of mitochondrial genes in young patients with Coronary heart disease （CHD） to provide a foundation for the early prevention of young patients with CHD. Methods 115 cases of young （〈 45 years） CHD Chinese Han patients （case group）, 100 cases of older （〉 45 years） Chinese Hart CHD patients （experimental group） hospitalized and 100 cases of healthy people through physical examination （control group） at the General Hospital of PLA between January 2014 and December 2015 were selected. General information, clinical assessment, pedigree analysis, and mitochondrial full sequence scanning were performed. The pedigrees of one patient harbouring the C5263T mutation were recruited. Mitochondrial functional analysis including cellular reactive oxygen species （ROS） levels and mitochondrial membrane potential （MMP） were performed on pedigrees with the C5263T mutation （mutation group） and without the mutation （non-mutation group）. Results The differences in biochemical tests （P 〉 0.05） between the case group and experimental group were not significant. The C5263T single-nucleotide mutation of the mitochondrial ND2 gene was observed in 2 young CHD patients in the case group. The premature CHD of these 2 patients followed a pattern of maternal inheritance. The mutation group （11, 112） had higher ROS levels （4750.82±1045.55 vs. 3888.58 ± 487.60, P= 0.022） and lower MMP levels （P= 0.045） than the non-mutation group （II1, III1, III2）. Conclusion We speculated that the mitochondrial C5263T mutation might be associated with the occurrence CHD in Chinese Hart young people.

关键词： mitochondrion Coronary heart disease Young

Evidence on neuroprotective properties of coenzyme Q10 in the treatment of glaucoma

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Neural Regeneration Research 2019年第2期14卷 197-200页

作者： Alessio Martucci Carlo Nucci Ophthalmology Unit Department of Experimental Medicine University of Rome Tor Vergata

Glaucoma, the leading cause of visual impairment and irreversible blindness worldwide, is a multifactorial, progressive optic neuropathy characterized by loss of retinal ganglion cells, alterations of the optic nerve head, and specific visual field defects. Clinical evidence shows that intraocular pressure is the major risk factor of the treatable disease. However, in some patients, glaucoma develops and continues to progress despite normal intraocular pressure values, suggesting that other risk factors are involved in the disease. Consequently, neuroprotective treatments, focused on preventing retinal ganglion cells death by acting on different therapeutic strategies but not focused on intraocular pressure reduction, has therefore become of great interest. In this contest, coenzyme Q10, showing evidence in slowing or reversing pathological changes typical of the disease, has been proposed as a potential neuroprotective agent in glaucoma. In this review, we describe the possible mechanisms of action of coenzyme Q10 and the recent evidence in literature regarding the neuroprotective activity of the molecule.

关键词： glaucoma neuroprotection retinal ganglion cells coenzyme Q10 intraocular pressure mitochondrion oral administration neurodegenerative diseases

Proteomic profiling of early degenerative retina of RCS rats

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International Journal of Ophthalmology(English edition) 2017年第6期10卷 878-889页

作者： Zhi-Hong Zhu Yan Fu Chuan-Huang Weng Cong-Jian Zhao Zheng-Qin Yin Southwest Hospital/Southwest Eye Hospital Third Military Medical University Key Lab of Visual Damage and Regeneration & Restoration of Chongqing

AIM： To identify the underlying cellular and molecular changes in retinitis pigmentosa （RP）. METHODS： Label-free quantification-based proteomics analysis, with its advantages of being more economic and consisting of simpler procedures, has been used with increasing frequency in modern biological research. Dystrophic RCS rats, the first laboratory animal model for the study of RP, possess a similar pathological course as human beings with the diseases. Thus, we employed a comparative proteomics analysis approach for in-depth proteome profiling of retinas from dystrophic RCS rats and non-dystrophic congenic controls through Linear Trap Quadrupole - orbitrap MS/MS, to identify the significant differentially expressed proteins （DEPs）. Bioinformatics analyses, including Gene ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway annotation and upstream regulatory analysis, were then performed on these retina proteins. Finally, a Western blotting experiment was carried out to verify the difference in the abundance of transcript factor E2F1. RESULTS： In this study, we identified a total of 2375 protein groups from the retinal protein samples of RCS rats and non-dystrophic congenic controls. Four hundred thirty-four significantly DEPs were selected by Student＇s t-test. Based on the results of the bioinformatics analysis, we identified mitochondrial dysfunction and transcription factor E2F1 as the key initiation factors in early retinal degenerative process. CONCLUSION： We showed that the mitochondrial dysfunction and the transcription factor E2F1 substantially contribute to the disease etiology of RP. The results provide a new potential therapeutic approach for this retinal degenerative disease.

关键词： retinal degeneration proteomics mitochondrion E2F1 MaxQuant RCS rat

Targeting cancer stem cells in drug discovery: Current state and future perspectives

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World Journal of Stem Cells 2019年第7期11卷 398-420页

作者： Fang-Yu Du Qi-Fan Zhou Wen-Jiao Sun Guo-Liang Chen Key Laboratory of Structure-Based Drug Design and Discovery of Ministry of Education Shenyang Pharmaceutical University

In recent decades,cancer stem cells(CSCs)have been increasingly identified in many malignancies.CSC-related signaling pathways and their functions provide new strategies for treating cancer.The aberrant activation of related signaling pathways(e.g.,Wnt,Notch,and Hedgehog pathways)has been linked to multiple types of malignant tumors,which makes these pathways attractive targets for cancer therapy.CSCs display many characteristic features,such as self-renewal,differentiation,high tumorigenicity,and drug resistance.Therefore,there is an urgent need to develop new therapeutic strategies to target these pathways to control stem cell replication,survival,and differentiation.Notable crosstalk occurs among different signaling pathways and potentially leads to compensatory escape.Therefore,multitarget inhibitors will be one of the main methods to overcome the drug resistance of CSCs.Many small molecule inhibitors of components of signaling pathways in CSCs have entered clinical trials,and some inhibitors,such as vismodegib,sonidegib,and glasdegib,have been approved.Tumor cells are susceptible to sonidegib and vismodegib resistance due to mutations in the Smo protein.The signal transducers and activators of transcription 3(STAT3)inhibitor BBI608 is being evaluated in a phase III trial for a variety of cancers.Structural derivatives of BBI608 are the main focus of STAT3 inhibitor development,which is another strategy for CSC therapy.In addition to the potential pharmacological inhibitors targeting CSCrelated signaling pathways,other methods of targeting CSCs are available,such as nano-drug delivery systems,mitochondrion targeting,autophagy,hyperthermia,immunotherapy,and CSC microenvironment targeting.In addition,we summarize the latest advances in the clinical development of agents targeting CSC-related signaling pathways and other methods of targeting CSCs.

关键词： Cancer stem cells Cancer stem cell-related signaling pathways Nano-drug delivery system Immunotherapy mitochondrion Cancer stem cell

Late-onset multiple acyl-CoA dehydrogenase deficiency with cardiac syncope: A case report

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World Journal of Clinical Cases 2020年第5期8卷 995-1001页

作者： Xue-Qi Pan Xue-Li Chang Wei Zhang Hua-Xing Meng Jing Zhang Jia-Ying Shi Jun-Hong Guo Department of Neurology Frist Hospital of Shanxi Medical University

BACKGROUND Multiple acyl-CoA dehydrogenase deficiency(MADD)is an uncommon autosomal recessive disorder of mitochondrial fatty acid beta-oxidation.Syncope is a transient loss of consciousness due to acute global cerebral hypoperfusion.Late-onset MADD with syncope has not been reported previously.CASE SUMMARY We report a 17-year-old girl with exercise intolerance and muscle weakness.She felt palpitation and shortness of breath after short bouts of exercise.She also suffered from a transient loss of consciousness many times.Muscle biopsy showed lipid storage.Genetic mutation analysis indicated a compound heterozygous mutation c.250G>A(p.A84T)and c.872T>G(p.V291G)in the ETFDH gene.The results of Holter electrocardiogram monitoring showed supraventricular tachycardia when the patient experienced a loss of consciousness.After treatment with riboflavin and carnitine,muscle weakness and palpitation symptoms improved rapidly.No loss of consciousness occurred,and the Holter electrocardiogram monitoring was normal.CONCLUSION Late-onset MADD with supraventricular tachycardia can cause cardiac syncope.Carnitine and riboflavin supplement were beneficial for treating the late-onset MADD with cardiac syncope.Attention should be paid to the prevention of cardiac syncope when diagnosing late-onset MADD.

关键词： Late-onset multiple acyl-CoA dehydrogenase deficiency ETFDH Cardiac syncope Supraventricular tachycardia mitochondrion Carnitine Case report