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Could autophagy dysregulation link neurotropic viruses to Alzheimer’s disease?

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Neural Regeneration Research 2019年第9期14卷 1503-1506页

作者： Maria Anele Romeo Alberto Faggioni Mara Cirone Department of experimental Medicine Sapienza University of Rome Laboratory Affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti

Neurotropic herpesviruses have been associated with the onset and progression of Alzheimer’s disease,a common form of dementia that afflicts a large percentage of elderly individuals.Interestingly,among the neurotropic herpesviruses,herpes simplex virus-1,human herpesvirus-6A,and human herpesvirus-6B have been reported to infect several cell types present in the central nervous system and to dysregulate autophagy,a process required for homeostasis of cells,especially neurons.Indeed autophagosome accumulation,indicating an unbalance between autophagosome formation and autophagosome degradation,has been observed in neurons of Alzheimer’s disease patients and may play a role in the intracellular and extracellular accumulation of amyloidβand in the altered protein tau metabolism.Moreover,herpesvirus infection of central nervous system cells such as glia and microglia can increase the production of oxidant species through the alteration of mitochondrial dynamics and promote inflammation,another hallmark of Alzheimer’s disease.This evidence suggests that it is worth further investigating the role of neurotropic herpesviruses,particularly human herpesvirus-6A/B,in the etiopathogenesis of Alzheimer’s disease.

关键词： Alzheimer’s disease autophagy HHV-6A HHV-6B HSV-1 neurotropic viruses amyloidβ tau protein reactive oxygen species inflammation AD

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细胞间线粒体成分转移触发缺血性心肌纤维化

Science Bulletin 2023年第16期68卷 1784-1799,M0004页

作者：张婵郝好王一石穆楠姜文华张子绘殷玥余璐张家毓马恒 Xi’an Key laboratory of Stem Cell and Regenerative Medicine Institute of Medical ResearchNorthwestern Polytechnical UniversityXi’an 710072China Department of Physiology and pathophysiology School of Basic MedicineFourth Military Medical UniversityXi’an 710032China Department of Cardiology and Shanghai Institute of Precision Medicine Ninth People’s HospitalShanghai Jiao Tong University School of MedicineShanghai 211125China Department of Pathology Xijing HospitalFourth Military Medical UniversityXi’an 710032China

心肌纤维化是引发心源性猝死的重要原因.心肌缺血/再灌注(MI/R)损伤可导致心肌细胞损伤甚至死亡,而成纤维细胞却出现激活并导致纤维化.目前,导致这一矛盾现象的细胞间通讯机制仍不清楚.小细胞外囊泡(small extracellular vesicles,sEVs... 详细信息

心肌纤维化是引发心源性猝死的重要原因.心肌缺血/再灌注(MI/R)损伤可导致心肌细胞损伤甚至死亡,而成纤维细胞却出现激活并导致纤维化.目前,导致这一矛盾现象的细胞间通讯机制仍不清楚.小细胞外囊泡(small extracellular vesicles,sEVs)在细胞间通讯中起重要作用.但是,sEVs是否介导以及如何介导MI/R后心肌细胞和成纤维细胞间的通讯尚不清楚.本研究通过在体MI/R模型和细胞学实验发现,MI/R损伤情况下存在一种心肌细胞来源的sEV(Myo-sEV^(I/R)),其内容物富含线粒体成分.Myo-sEV^(I/R)被成纤维细胞摄取并触发纤维化.通过生物信息学筛选和实验验证,新发现Ambra1是Myo-sEV^(I/R)中的关键组分和潜在标志物.并且证实,Ambra1+-Myo-sEVs的释放是由MI/R损伤后心肌细胞的分泌型自噬所驱动,而不是经典的降解型自噬.在缺血和缺血周边区域,Ambra1^(+)-Myo-sEVs被成纤维细胞内吞导致跨细胞线粒体成分传递;线粒体DNA(mtDNA)激活cGAS-STING通路,促进成纤维细胞的活化和增殖.此外,数据显示,Ambral定位于Myo-sEV^(I/R)表面,心脏特异性的下调Ambral可抑制Ambral^(+)-Myo-sEVs的释放和成纤维细胞摄取,有效抑制缺血后心肌纤维化.本研究新证实了心肌分泌型自噬可介导缺血后心肌纤维化发生过程中的细胞间通讯.Ambral是Myo-sEVs的潜在标志物和特征分子,并具有重要的生物活性.本研究为缺血后心脏重塑提供了新的治疗靶点.

关键词：心肌缺血/再灌注心源性猝死细胞间通讯成纤维细胞细胞线粒体细胞学实验心肌细胞矛盾现象

Effect of temperature on the standard metabolic rates of juvenile and adult Exopalaemon carinicauda

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Chinese Journal of Oceanology and Limnology 2015年第2期33卷 381-388页

作者：张成松李富花相建海 Key laboratory of experimental Marine Biology Institute of OceanologyChinese Academy of Sciences

Ridgetail white prawn(E xopalaemon carinicauda) are of significant economic importance in China where they are widely cultured. However,there is little information on the basic biology of this species. We evaluated the effect of temperature(16,19,22,25,28,31,and 34°C) on the standard metabolic rates(SMRs) of juvenile and adult E. carinicauda in the laboratory under static conditions. The oxygen consumption rate(OCR),ammonia-Nexcretion rate(AER),and atomic ratio of oxygen consumed to nitrogen consumed(O:N ratio) of juvenile and adult E. carinicauda were significantly influenced by temperature( P0.05). The O:N ratio in juveniles was significantly higher than that in the adults over the entire temperature range(P <0.05). The temperature coefficient(Q 10) of OCR and AER ranged from 5.03 to 0.86 and 6.30 to 0.85 for the adults,respectively,and from 6.09–1.03 and 3.66–1.80 for the juveniles,respectively. The optimal temperature range for growth of the juvenile and adult shrimp was from 28 to 31°C,based on Q 10 and SMR values. Results from the present study may be used to guide pond culture production of E. carinicauda.

关键词：标准代谢率温度升高脊尾白虾生物学基础氨氮排泄率温度范围池塘培养小型反应堆

Targeting the Transnitrosylation Cascade Provides a Novel Therapeutic Strategy for Alzheimer’s Disease

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Neuroscience Bulletin 2021年第9期37卷 1373-1376页

作者： Yi Liu Gang Wu Xiji Shu Xiaochuan Wang Department of pathophysiology School of Basic MedicineKey Laboratory of Education Ministry of China for Neurological DisordersTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China Department of Pathology and pathophysiology School of MedicineJianghan UniversityWuhan 430056China Co-innovation Center of Neuroregeneration Nantong UniversityNantong 226001China

As a major public health problem in modern society,Alzheimer’s disease(AD)is currently the most widely prevalent neurodegenerative disease,which will indubitably increase dramatically in the coming years,unless drugs that can prevent or cure the disease become available.Because AD is characterized histopathologically by extracellular deposition of amyloid beta(Aβ)surrounded by dystrophic neuritis forming senile plaques(SPs).

关键词： Alzheimer drugs Aβ

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细胞休眠在肿瘤耐药和复发中的作用（英文）

生物化学与生物物理进展 2018年第4期45卷 460-470页

作者：代亚非向娟娟 Institute of pathophysiology School of Basic Medical Sciences Lanzhou University Cancer Research Institute Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education Key Laboratory of Carcinogenesis of Ministry of Health Central South University

Despite progresses achieved in the therapy of tumors, the prognosis of patients is still limited by reccurence of residual tumor cells. Cancer cell dormancy plays a pivotal role in cancer relapse and drug resistance. In recent years, tumor cells undergoing EMT(epithelial-mesenchymal transition), CSCs(cancer stem cells) and CTCs(circulating tumor cells) are proved to share some common characteristics and show a cell cycle arrest phenotype. Thus, understanding the dormant stage of tumor cells could facilitate us in discovering ways to accelerate the development of tumor therapy and prevent its reccurence. In this review, we summarize the specific process of tumor cell dormancy induced by pharmacotherapy, and consider that dormancy is an initiative response rather than a passive defense to cytotoxicity. Besides, we probe into the mechanisms of tumor cell dormancy-mediated drug resistance, anticipating paving a way to target dormant tumor cells and result in better clinical outcomes.

关键词：癌细胞肿瘤治疗方法医学研究

Cold-induced Yes-associated-protein expression through miR-429 mediates the browning of white adipose tissue

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Science China(Life Sciences) 2021年第3期64卷 404-418页

作者： Chenji Ye Jinjie Duan Xuejiao Zhang Liu Yao Yayue Song Guangyan Wang Qi Li Biqing Wang Ding Ai Chunjiong Wang Yi Zhu Tianjin Key laboratory of Metabolic Diseases Department of Physiology and PathophysiologyCollaborative Innovation Center of Tianjin for Medical EpigeneticsTianjin Medical UniversityTianjin 300070China Tianjin Key laboratory of Medical Epigenetics Tianjin Medical UniversityTianjin 300070China

Targeting the white-to-brown fat conversion is important for developing potential strategies to counteract metabolic diseases;yet the mechanisms are not fully understood.Yes-associated-protein(YAP),a transcription co-activator,was demonstrated to regulate adipose tissue functions;however,its effects on browning of subcutaneous white adipose tissue(sWAT)are unclear.We demonstrated that YAP was highly expressed in cold-induced beige fat.Mechanistically,YAP was found as a target gene of miR-429,which downregulated YAP expression in vivo and in vitro.In addition,miR-429 level was decreased in cold-induced beige fat.Additionally,pharmacological inhibition of the interaction between YAP and transcriptional enhanced associate domains by verteporfin dampened the browning of sWAT.Although adipose tissue-specific YAP overexpression increased energy expenditure with increased basal uncoupling protein 1 expression,it had no additional effects on the browning of sWAT in young mice.However,we found age-related impairment of sWAT browning along with decreased YAP expression.Under these circumstances,YAP overexpression significantly improved the impaired WAT browning in middle-aged mice.In conclusion,YAP as a regulator of sWAT browning,was upregulated by lowering miR-429 level in cold-induced beige fat.Targeting the miR-429-YAP pathway could be exploited for therapeutic strategies for age-related impairment of sWAT browning.

关键词： aging browning miR-429 UCP1 YAP

Tau-Induced Ca^(2+)/Calmodulin-Dependent Protein Kinase-IV Activation Aggravates Nuclear Tau Hyperphosphorylation

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Neuroscience Bulletin 2018年第2期34卷 261-269页

作者： Yu-Ping Wei Jin-Wang Ye Xiong Wang Li-Ping Zhu Qing-Hua Hu Qun Wang Dan Ke Qing Tian Jian-Zhi Wang pathophysiology Department Tongji Medical CollegeHuazhong University of Science and Technology Key laboratory of Ministry of Education for Neurological Disorders and Hubei Provincial Key laboratory for Neurological Disorders Tongji Medical College Huazhong University of Science and Technology

Hyperphosphorylated tau is the major protein component of neurofibrillary tangles in the brains of patients with Alzheimer’s disease(AD). However, the mechanism underlying tau hyperphosphorylation is not fully understood. Here, we demonstrated that exogenously expressed wild-type human tau40 was detectable in the phosphorylated form at multiple AD-associated sites in cytoplasmic and nuclear fractions from HEK293 cells.Among these sites, tau phosphorylated at Thr205 and Ser214 was almost exclusively found in the nuclear fraction at the conditions used in the present study. With the intracellular tau accumulation, the Ca2+concentration was significantly increased in both cytoplasmic and nuclear fractions. Further studies using site-specific mutagenesis and pharmacological treatment demonstrated that phosphorylation of tau at Thr205 increased nuclear Ca2+concentration with a simultaneous increase in the phosphorylation of Ca2+/calmodulin-dependent protein kinase IV(Ca MKIV) at Ser196. On the other hand, phosphorylation of tau at Ser214 did not significantly change the nuclear Ca2+/Ca MKIV signaling. Finally, expressing calmodulin-binding protein-4 that disrupts formation ofthe Ca2+/calmodulin complex abolished the okadaic acidinduced tau hyperphosphorylation in the nuclear fraction.We conclude that the intracellular accumulation of phosphorylated tau, as detected in the brains of AD patients, can trigger nuclear Ca2+/Ca MKIV signaling, which in turn aggravates tau hyperphosphorylation. Our findings provide new insights for tauopathies: hyperphosphorylation of intracellular tau and an increased Ca2+concentration may induce a self-perpetuating harmful loop to promote neurodegeneration.

关键词： Alzheimer’s disease Tau Phosphorylation Nuclear calcium signal CaMKIV

Circulating predictive and diagnostic biomarkers for hepatitis B virus-associated hepatocellular carcinoma

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World Journal of Gastroenterology 2016年第37期22卷 8271-8282页

作者： Stijn Van Hees Peter Michielsen Thomas Vanwolleghem Department of Gastroenterology and Hepatology Antwerp University Hospital laboratory of experimental Medicine and Pediatrics University of Antwerp

Chronic hepatitis B virus(HBV) infected patients have an almost 100-fold increased risk to develop hepatocellular carcinoma(HCC). HCC is the fifth most common and third most deadly cancer worldwide. Up to 50% of newly diagnosed HCC cases are attributed to HBV infection. Early detection improves survival and can be achieved through regular screening. Six-monthly abdominal ultrasound, either alone or in combination with alphafetoprotein serum levels, has been widely endorsed for this purpose. Both techniques however yield limited diagnostic accuracy, which is not improved when they are combined. Alternative circulating or histological markers to predict or diagnose HCC are therefore urgently needed. Recent advances in systems biology technologies have enabled the identification of several new putative circulating biomarkers. Although results from studies assessing combinations of these biomarkers are promising, evidence for their clinical utility remains low. In addition, most of the studies conducted so far show limitations in design. Attention must be paid for instance to different ethnicities and different etiologies when studying biomarkers for hepatocellular carcinoma. This review provides an overview on the current understandings and recent progress in the field of diagnostic and predictive circulating biomarkers for hepatocellular carcinoma in chronically infected HBV patients and discusses the future prospects.

关键词： Hepatocellular carcinoma Hepatitis B virus infection Biomarkers Predictive Diagnostic Alphafetoprotein Validation Limitations MicroR NA

Skull and vertebral bone marrow in central nervous system inflammation

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Fundamental Research 2024年第2期4卷 246-250页

作者： Honglei Ren Qiang Liu Department of Neurology Tianjin Neurological InstituteTianjin Institute of ImmunologyState Key Laboratory of Experimental HematologyInternational Joint Laboratory of Ocular DiseasesMinistry of EducationHaihe Laboratory of Cell EcosystemTianjin Medical University General HospitalTianjin 300052China

Emerging evidence has highlighted the capacity of hematogenous cells in skull and vertebral bone marrow to enter the meningeal borders via ossified vascular channels and maintain immune homeostasis in the central nervous system(CNS).CNS-adjacent skull and vertebral bone marrow comprises hematopoietic niches that can sense CNS injury and supply specialized immune cells to fine-tune inflammatory responses.Here,we review recent advances in our understanding of skull and vertebral bone marrow-derived immune cells in homeostasis and inflammatory CNS diseases.Further,we discuss the implications for future development of therapies to mitigate CNS inflammation and its detrimental sequelae in neurological disorders.

关键词： Central nervous system Bone marrow Hematopoiesis Immune cells Neuroinflammation Stroke Multiple sclerosis