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Antiapoptotic activity of 30 kDa lipoproteins family from fat body tissue of silkworm, Bombyx moil

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Insect Science 2015年第5期22卷 629-638页

作者： Britto Cathrin Pakkianathan Nitin Kumar Singh Simone Konig Muthukalingan Krishnan Department of Environmental Biotechnology Bharathidasan University Tiruchirappalli India and Integrated Functional genomics Interdisciplinary Center for Clinical Research University of MEmster Germany

The family of 30kDa lipoproteins （LP1-5） is abundant in silkworm pupa fat body （FB） and hemolymph. One of its members, the 29 kDa protein decreased in concentration from peripheral （PP） FB tissue but was sustained in perivisceral （PV） FB tissue at the time of apoptosis. This study investigated the correlation of the 30kDa proteins with FB apoptosis. Two protein fractions were purified, a 29 and a 30/31 kDa protein fraction, and they were used to test for activity against actinomycin D-induced apoptosis in the FB tissues. Concentrations as little as 50/zg/mL of the 29 kDa protein fraction efficiently inhibited apoptosis. Less antiapoptotie activity was detected for the higher MW fraction; DNA fragmentation was observed in FB tissue treated with 50 #g/mL of the 30/31 kDa fraction. The viability of the cells in the 29 kDa protein-supplemented culture was 40% higher than in the 31 kDa protein-supplemented culture. However, the 30 kDa lipoproteins were not able to prevent scheduled FB degeneration during silkworm metamorphosis. Thus, it is hypothesized that the antiapoptotic 29 kDa protein needs to be proteolytically degraded by a regulatory mechanism to allow programmed cell death of FB tissue.

关键词： actinomycin D apoptosis Bombyx mori fat body tissue 30 kDa proteins

Blood F_2-isoprostanes are significantly associated with abnormalities of lipid status in rats with steatosis

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World Journal of Gastroenterology 2008年第29期14卷 4677-4683页

作者： Man-Jie Zhu Li-Juan Sun Yue-Qin Liu Yan-Ling Feng Hai-Tao Tong Ying-He Hu Zheng Zhao Laboratory of Pharmacology Institute of Brain Functional Genomics East China Normal University Key Laboratory of Brain Functional Genomics MOE & STCSM Shanghai 200062 China Department of Pathology Shanghai Public Health Clinical Center Fudan University Shanghai 201508 China

AIM: To investigate oxidative stress and lipid peroxi-dation in hepatic steatosis and the underlying implica-tions in pathological mechanisms of non-alcoholic fatty liver disease (NAFLD). METHODS: F_2-isoprostanes (iPF2α-) in blood and liver samples from steatotic (n = 9) and control (n = 7) rats were measured as in vivo marker of lipid peroxida-tion by a mass spectrometric approach. The lipid pro-fi le and endogenous antioxidant status (SOD and CAT) in the rats were also analyzed. RESULTS: Signifi cantly higher levels of iPF2α-(mean 3.47 vs 2.40 pmol/mg tissue, P = 0.004) and lower activities of SOD (mean 1.26 U vs 1.40 U, P < 0.001) and CAT (mean 1026.36 U/mg vs 1149.68 U/mg pro-tein, without signifi cance) were observed in the livers of steatotic rats. Plasma total iPF2α-was signifi cantly correlated with the abnormalities of blood lipids as well as alanine aminotransferase (ALT) levels in the rats with simple steatosis, whereas no similar tendencies were observed in the control rats. CONCLUSION: Enhancement of hepatic oxidative imbalance occurring at the steatotic stage of NAFLD suggests a possibility that manifestation of the local ⅢⅢⅢoxidative damage precedes that of systemic oxidative imbalance. Predominant metabolic features of the in-creased lipid peroxidation further suggest a close asso-ciation of the oxidative imbalance and the dyslipidemia with functional deterioration of the steatotic liver. The fi ndings need to be further evaluated, especially in hu-man studies.

关键词： Isoprostanes Oxidative stress Lipid per-oxidation Steatosis Non-alcoholic fatty liver disease

Identification of genomic features associated with immunotherapy response in gastrointestinal cancers

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World Journal of Gastrointestinal Oncology 2019年第4期11卷 270-280页

作者： Yin He Zhi-Xian Liu Ze-Hang Jiang Xiao-Sheng Wang Biomedical Informatics Research Lab School of Basic Medicine and Clinical Pharmacy Cancer genomics Research Center School of Basic Medicine and Clinical Pharmacy Big Data Research Institute China Pharmaceutical University

Gastrointestinal(GI) cancers prevail and account for an extremely high number of cancer deaths worldwide. The traditional treatment strategies, including surgery, chemotherapy, radiotherapy, and targeted therapy, have a limited therapeutic effect for advanced GI cancers. Recently, immunotherapy has shown promise in treating various refractory malignancies, including the GI cancers with mismatch repair deficiency(dMMR) or microsatellite instability(MSI). Thus,immunotherapy could be a promising treatment approach for GI ***, only a small proportion of GI cancer patients currently respond to immunotherapy. Therefore, it is important to discover predictive biomarkers for stratifying GI cancer patients response to immunotherapy. Certain genomic features, such as dMMR/MSI, tumor mutation burden(TMB), and tumor aneuploidy have been associated with tumor immunity and im-munotherapy response and may serve as predictive biomarkers for cancer immunotherapy. In this review, we examined the correlations between tumor immunity and three genomic features: dMMR/MSI, TMB, and tumor aneuploidy. We also explored their correlations using The Cancer Genome Atlas data and confirmed that the dMMR/MSI status, high TMB, and low tumor aneuploidy are associated with elevated tumor immunity in GI cancers. To improve the immunotherapeutic potential in GI cancers, more genetic or genomic features associated with tumor immune response need to be identified. Furthermore, it is worth exploring the combination of different immunotherapeutic methods and the combination of immunotherapy with other therapeutic approaches for cancer therapy.

关键词： Gastrointestinal cancer Tumor immunity Tumor immunotherapy DNA mismatch repair Tumor mutation burden Tumor aneuploidy

Unraveling brain aging through the lens of oral microbiota

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Neural Regeneration Research 2025年第7期20卷 1930-1943页

作者： Qinchao Hu Si Wang Weiqi Zhang Jing Qu Guang-Hui Liu State Key Laboratory of Membrane Biology Institute of ZoologyChinese Academy of SciencesBeijingChina Hospital of Stomatology Guanghua School of StomatologyGuangdong Provincial Key Laboratory of StomatologySun Yat-sen UniversityGuangzhouGuangdong ProvinceChina Advanced Innovation Center for Human Brain Protection and National clinical Research Center for Geriatric Disorders Xuanwu HospitalCapital Medical UniversityBeijingChina Aging Translational Medicine Center International Center for Aging and CancerBeijing Municipal Geriatric Medical Research CenterXuanwu HospitalCapital Medical UniversityBeijingChina CAS Key Laboratory of Genomic and Precision Medicine Beijing Institute of GenomicsChinese Academy of Sciences and China National Center for BioinformationBeijingChina University of Chinese Academy of Sciences BeijingChina Institute for Stem Cell and Regeneration Chinese Academy of SciencesBeijingChina Aging Biomarker Consortium BeijingChina State Key Laboratory of Stem Cell and Reproductive Biology Institute of ZoologyChinese Academy of SciencesBeijingChina Beijing Institute for Stem Cell and Regenerative Medicine BeijingChina

The oral cavity is a complex physiological community encompassing a wide range of *** of oral microbiota can lead to various oral infectious diseases,such as periodontitis and tooth decay,and even affect systemic health,including brain aging and neurodegenerative *** studies have highlighted how oral microbes might be involved in brain aging and neurodegeneration,indicating potential avenues for intervention *** this review,we summarize clinical evidence demonstrating a link between oral microbes/oral infectious diseases and brain aging/neurodegenerative diseases,and dissect potential mechanisms by which oral microbes contribute to brain aging and *** also highlight advances in therapeutic development grounded in the realm of oral microbes,with the goal of advancing brain health and promoting healthy aging.

关键词： Alzheimer's disease brain aging multiple sclerosis neurodegeneration neurodegenerative diseases oral microbiota Parkinson's disease periodontitis bacteria Porphyromonas gingivalis

Now and future of mouse mutagenesis for human disease models

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Journal of Genetics and genomics 2010年第9期37卷 559-572页

作者： Yoichi Gondo Mutagenesis and genomics Team RIKEN Bio Resource Center

One of the major objectives of the Human Genome Project is to understand the biological function of the gene and genome as well as to develop clinical applications for human diseases. For this purpose, the experimental validations and preclinical trails by using animal models are indispensable. The mouse （Mus musculus） is one of the best animal models because genetics is well established in the mouse and embryonic manipulation technologies are also well developed. Large-scale mouse mutagenesis projects have been conducted to develop various mouse models since 1997. Originally, the phenotype-driven mutagenesis with N-ethyl-N-nitrosourea （ENU） has been the major efforts internationally then knockout/conditional mouse projects and gene-driven mutagenesis have been following. At the beginning, simple monogenic traits in the experimental condition have been elucidated. Then, more complex traits with variety of environmental interactions and gene-to-gene interactions （epistasis） have been challenged with mutant mice. In addition, chromosomal substitution strains and collaborative cross strains are also available to elucidate the complex traits in the mouse. Altogether, mouse models with mutagenesis and various laboratory strains will accelerate the studies of functional genomics in the mouse as well as in human.

关键词： mutagenesis functional genomics reverse genetics model animal quantitative trait epistasis

Microbiome and pancreatic cancer: A comprehensive topic review of literature

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World Journal of Gastroenterology 2017年第10期23卷 1899-1908页

作者： Natalie Ertz-Archambault Paul Keim Daniel Von Hoff Department of Internal Medicine Mayo School of Graduate Medical EducationMayo Clinic Arizona genomics Division Translational Genomics Institute and Regents Northern Arizona University Translational genomics Institute(TGen) Mayo Clinic Arizona

To review microbiome alterations associated with pancreatic cancer, its potential utility in diagnostics, risk assessment, and influence on disease *** comprehensive literature review was conducted by all-inclusive topic review from PubMed, MEDLINE, and Web of Science. The last search was performed in October *** microbiome alterations exist among several body sites including oral, gut, and pancreatic tissue, in patients with pancreatic cancer compared to healthy *** study successes in non-invasive screening strategies warrant further investigation for future translational application in early diagnostics and to learn modifiable risk factors relevant to disease prevention. Pre-clinical investigations exist in other tumor types that suggest microbiome manipulation provides opportunity to favorably transform cancer response to existing treatment protocols and improve survival.

关键词： Pancreatic Cancer Human microbiome Biomarkers cancer Cancer screening tests Treatment effectiveness

The role of mitochondria in osteogenic, adipogenic and chondrogenic differentiation of mesenchymal stem cells

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Protein & Cell 2017年第6期8卷 439-445页

作者： Qianqian Li Zewen Gao Ye Chen Min-Xin Guan Division of clinical Genetics and genomics The Children's Hospital Zhejiang University School of MedicineHangzhou 310058 China Institute of Genetics Zhejiang University and Department of Genetics Zhejiang University School of MedicineHangzhou 310058 China

Mesenchymal stem cells （MSCs） are progenitors of con- nective tissues, which have emerged as important tools for tissue engineering due to their differentiation potential along various cell types. In recent years, accumulating evidence has suggested that the regulation of mitochon- dria dynamics and function is essential for successful dif- ferentiation of MSCs. In this paper, we review and provide an integrated view on the role of mitochondria in MSC dif- ferentiation. The mitochondria are maintained at a relatively low activity level in MSCs, and upon induction, mtDNA copy number, protein levels of respiratory enzymes, the oxygen consumption rate, mRNA levels of mitochondrial biogene- sis-associated genes, and intracellular ATP content are increased. The regulated level of mitochondrial ROS is found not only to influence differentiation but also to con- tribute to the direction determination of differentiation. Understanding the roles of mitochondrial dynamics during MSC differentiation will facilitate the optimization of differ- entiation protocols by adjusting biochemical properties, such as energy production or the redox status of stem cells, and ultimately, benefit the development of new pharmacologic strategies in regenerative medicine.

关键词： mesenchymal stem cells mitochondria,differentiation

Mitochondrial DNA mutations associated with aminoglycoside induced ototoxicity

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Journal of Otology 2017年第1期12卷 1-8页

作者： Zewen Gao Ye Chen Min-Xin Guan Division of clinical Genetics and genomics The Children's HospitalZhejiang University School of Medicine Institute of Genetics Zhejiang University and Department of GeneticsZhejiang University School of Medicine

Aminoglycosides(Am An) are widely used for their great efficiency against gram-negative bacterial infections. However, they can also induce ototoxic hearing loss, which has affected millions of people around the world. As previously reported, individuals bearing mitochondrial DNA mutations in the 12 S rRNA gene, such as m.1555A>G and m.1494C>T, are more prone to Am An-induced ototoxicity. These mutations cause human mitochondrial ribosomes to more closely resemble bacterial ribosomes and enable a stronger aminoglycoside interaction. Consequently,exposure to Am An can induce or worsen hearing loss in these individuals. Furthermore, a wide range of severity and penetrance of hearing loss was observed among families carrying these mutations. Studies have revealed that these mitochondria mutations are the primary molecular mechanism of genetic susceptibility to Am An ototoxicity, though nuclear modifier genes and mitochondrial haplotypes are known to modulate the phenotypic manifestation.

关键词： Aminoglycosides ototoxicity Genetic susceptibility Mitochondrial DNA mutations

Disease Biomarkers for Precision Medicine:Challenges and Future Opportunities

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genomics, Proteomics & Bioinformatics 2017年第2期15卷 57-58页

作者： Edwin Wang William C.S.Cho S.C.Cesar Wong Siqi Liu Center for Health genomics and Informatics University of Calgary Cumming School of Medicine Department of clinical Oncology Queen Elizabeth Hospital Department of Health Technology and Informatics Faculty of Health and Social Sciences Hong Kong Polytechnic University CAS Key Laboratory of Genome Sciences and Information Beijing Institute of Genomics Chinese Academy of Sciences

Most of the human diseases are complex diseases,which could be caused by many genetic *** means that for a given phenotype(i.e.,a complex disease),there are multiple potential genes which could be genomically or epigenetically changed(i.e.,mutations,copy number variations,epigenetic modifications,and so on).Therefore,it is understandable that different individuals who share the same phenotype/diseases may have different causal genes and thus,may have different drug *** example,mutated genes are rarely common between the cancer patients of the same cancer type[1];furthermore,for a given drug,only 10%-30% of the patients

关键词： data Disease Biomarkers for Precision Medicine:Challenges and Future Opportunities