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NAC Transcription Factor ORE1 and senescence- Induced BIFUNCTIONAL NUCLEASE1 （BFN1） Constitute a Regulatory Cascade in Arabidopsis

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Molecular Plant 2013年第5期6卷 1438-1452页

作者： Lilian R Matallana-Ramirez Mamoona Rauf Sarit Farage-Barhom Hakan Dortay Gang-Ping Xue Wolfgang Droge-Laser Amnon Lers Salma Balazadeh Bernd Mueller-Roeber University of Potsdam Institute of Biochemistry and Biology KarI-Liebknecht-Straβe 24-25 14476 Potsdam-Golm Germany Department of Postharvest Science of Fresh Produce. Volcani Center Agricultural Research Organization Israel CSIRO Plant Industry Brisbane Australia University of Wurzburg Julius-von-Sachs Institute Julius-von-Sachs Platz 2 97082 Wurzburg Germany Max-Planck Institute of Molecular Plant Physiology 14476 Potsdam-Golm Germany

senescence is a highly regulated process that involves the action of a large number of transcription factors. The NAC transcription factor ORE1 （ANAC092） has recently been shown to play a critical role in positively controlling senescence in Arabidopsis thaliana; however, no direct target gene through which it exerts its molecular function has been identified previously. Here, we report that BIFUNCTIONAL NUCLEASE1 （BFN1）, a well-known senescence-enhanced gene, is directly regulated by ORE1. We detected elevated expression of BFN1 already 2 h after induction of ORE1 in estradiol-inducible ORE1 overexpression lines and 6 h after transfection of Arabidopsis mesophyll cell protoplasts with a 35S：ORE1 construct, ORE1 and BFN1 expression patterns largely overlap, as shown by promoter-reporter gene （GUS） fusions, while BFN1 expression in senescent leaves and the abscission zones of maturing flower organs was virtually absent in ore1 mutant background. In vitro binding site assays revealed a bipartite ORE1 binding site, similar to that of ORS1, a paralog of ORE1. A bipartite ORE1 binding site was identified in the BFN1 promoter; mutating the cis-element within the context of the full-length BFN1 promoter drastically reduced OREl-mediated transactivation capacity in tran- siently transfected Arabidopsis mesophyll cell protoplasts. Furthermore, chromatin immunoprecipitation （CHIP） demon- strates in vivo binding of ORE1 to the BFN1 promoter. We also demonstrate binding of ORE1 in vivo to the promoters of two other senescence-associated genes, namely SAG29/SWEET15 and SINA1, supporting the central role of ORE1 during senescence.

关键词： Arabidopsis thaliana senescence transcription factor ORE1 BFN1 promoter.

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Preventive effect of Shenkang injection against high glucose-induced senescence of renal tubular cells

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Frontiers of Medicine 2019年第2期13卷 267-276页

作者： Biqiong Fu Jie Yang Jia Chen Lirong Lin Kehong Chen Weiwei Zhang Jianguo Zhang Yani He Department of Nephrology Daping HospitalArmy Medical UniversityChongqing 400042China

Shenkang injection (SKI) is a classic prescription composed of Radix Astragali, rhubarb, Astragalus, Safflower, and Salvia. This treatment was approved by the State Food and Drug Administration of China in 1999 for treatment of chronic kidney diseases based on good efficacy and safety. This study aimed to investigate the protective effect of SKI against high glucose (HG)-induced renal tubular cell senescence and its underlying mechanism. Primary renal proximal tubule epithelial cells were cultured in (1) control medium (control group), medium containing 5 mmol/L glucose;(2) mannitol medium (mannitol group), medium containing 5 mmol/L glucose, and 25 mmol/L mannitol;(3) HG medium (HG group) containing 30 mmol/L glucose;(4) SKI treatment at high (200 mg/L), medium (100 mg/L), or low (50 mg/L) concentration in HG medium (HG+ SKI group);or (5) 200 mg/L SKI treatment in control medium (control+ SKI group) for 72 h. HG-induced senescent cells showed the emergence of senescence associated heterochromatin foci, up-regulation of P16INK4 and cyclin D1, increased senescence-associated β-galactosidase activity, and elevated expression of membrane decoy receptor 2. SKI treatment potently prevented these changes in a dose-independent manner. SKI treatment prevented HG-induced up-regulation of pro-senescence molecule mammalian target of rapamycin and p66Shc and down-regulation of anti-senescence molecules klotho, sirt1, and peroxisome proliferator-activated receptor-g in renal tubular epithelial cells. SKI may be a novel strategy for protecting against HG-induced renal tubular cell senescence in treatment of diabetic nephropathy.

关键词： Shenkang injection senescence renal tubular epithelial cells diabetic nephropathy

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Amyloid 13 Protein Aggravates Neuronal senescence an, d Cognitive Deficits in 5XFAD Mouse Model of Alzheimer s Disease

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Chinese Medical Journal 2016年第15期129卷 1835-1844页

作者： Zhen Wei Xiao-Chun Chen Yue Song Xiao-Dong Pan Xiao-Man Dai Jing Zhang Xiao-Li CUI Xi-Lin Wu Yuan-Gui Zhu Department of Neurology Fujian Medical University Union Hospital Fuzhou Fujian 350001 China Fujian Institute of Geriatrics Fujian Medical University Union Hospital Fuzhou Fujian 350001 China Key Laboratory of Brain Aging and NeurodegenerativeDiseases Fujian KeyLaboratory of Molecular Neurology Fujian Medical University Fuzhou Fujian 350001 China

Background： Amyloid β （Aβ） has been established as a key factor for the pathological changes in the brains of patients with Alzheimer＇s disease （AD）, and cellular senescence is closely associated with aging and cognitive impairment. However, it remains blurred whether, in theAD brains, Aβ accelerates the neuronal senescence and whether this senescence, in turn, impairs the cognitive function. This study aimed to explore the expression of senescence-associated genes in the hippocampal tissue from young to aged 5XFAD mice and their age-matched wild type （WT） mice to determine whether senescent neurons are present in the transgenic AD mouse model. Methods： The 5XFAD mice and age-matched wild type mice, both raised from 1 to 18 months, were enrolled in the study. The senescence-associated genes in the hippocampus were analyzed and differentially expressed genes （DEGs） were screened by quantitative real-time polymerase chain reaction. Cognitive perfom3ance of the mice was evaluated by Y-maze and Morris water maze tests. Oligomeric Aβ（oAβ）（1-42） was applied to culture primary neurons to simulate the in vivo manifestation. Aging-related proteins were detected by Western blotting analysis and immunofluorescence. Results： In 5XFAD mice, of all the DEGs, the senescence-associated marker p16 was most significantly increased, even at the early age. It was mainly localized in neurons, with a marginal expression in astrocytes （labeled as glutamine synthetase）, nil expression in activated microglia （labeled as lba1）, and negatively correlated with the spatial cognitive impairments of 5XFAD mice. oAβ （1-42） induced the production of senescence-related protein p1 6, but not p53 in vitro, which was in line with the in vivo manifestation. Conclusions： oAβ-accelerated neuronal senescence may be associated with the cognitive impairment in 5XFAD mice. senescence-associated marker p16 can serve as an indicator to estimate the cognitive prognosis for A D population.

关键词： Alzheimer＇s Disease Amyloid β Cognition P 16 senescence

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Quantitative Trait Loci Mapping of Dark-Induced senescence in Winter Wheat(Triticum aestivum)

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Journal of Integrative Plant Biology 2012年第1期54卷 33-44页

作者： Hongwei Li Fanyun Lin Gui Wang Ruilian Jing Qi Zheng Bin Li Zhensheng Li State Key Laboratory of Plant Cell and Chromosome Engineering Institute of Genetics and Developmental Biology the Chinese Academyof Sciences Beijing 100101 China Institute of Crop Sciences the Chinese Academy of Agricultural Sciences Beijing 100081 China

In order to explore the genetics of dark-induced senescence in winter wheat （Triticum aestivum L.）, a quantitative trait loci （QTL） analysis was carried out in a doubled haploid population developed from a cross between the varieties Hanxuan 10 （HX） and Lumai 14 （LM）. The senescence parameters chlorophyll content （Chl a＋b, Chl a, and Chl b）, original fluorescence （Fo）, maximum fluorescence level （Fm）, maximum photochemical efficiency （FvlFm）, and ratio of variable fluorescence to original fluorescence （FvlFo） were evaluated in the second leaf of whole three-leaf seedlings subjected to 7 d of darkness. A total of 43 QTLs were identified that were associated with dark-induced senescence using composite interval mapping. These QTLs were mapped to 20 loci distributed on 11 chromosomes： 1B, 1D, 2A, 2B, 3B, 3D, 5D, 6A, 6B, 7A, and 7B. The phenotypic variation explained by each QTL ranged from 7.5% to 19.4%. Eleven loci coincided with two or more of the analyzed parameters. In addition, 14 loci co-located or were linked with previously reported QTLs regulating flag leaf senescence, tolerance to high light stress, and grain protein content （Gpc）, separately.

关键词： chlorophyll content photosynthetic efficiency senescence Triticum aestivum.

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E2FBP1 antagonizes the p16^(INK4A)-Rb tumor suppressor machinery for growth suppression and cellular senescence by regulating promyelocytic leukemia protein stability

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International Journal of Oral Science 2011年第4期3卷 200-208页

作者： Yayoi Fukuyo Akiko Takahashi Eiji Hara Nobuo Horikoshi Tej K. Pandita Takuma Nakajima Department of Immunology Tulane National Primate Research Center Section of Bacterial Pathogenesis Graduate School Tokyo Medical and Dental University Division of Cancer Biology The Cancer Institute Japanese Foundation for Cancer Research Division of Molecular Radiation Biology Department of Radiation Oncology University of Texas Southwestern Medical Center

Cellular senescence is an irreversible cell cycle arrest triggered by the activation of oncogenes or mitogenic signaling as well as the enforced expression of tumor suppressors such as p53, p16INK4A and promyelocytic leukemia protein （PML） in normal cells. E2F-binding protein 1 （E2FBP1）, a transcription regulator for E2F, induces PML reduction and suppresses the formation of PML-nuclear bodies, whereas the down-regulation of E2FBP1 provokes the PML-dependent premature senescence in human normal fibroblasts. Here we report that the depletion of E2FBP1 induces the accumulation of PML through the Ras-dependent activation of MAP kinase signaling. The cellular levels of p16INK4A and p53 are elevated during premature senescence induced by depletion of E2FBP1, and the depletion of p16INK4A, but not p53 rescued senescent cells from growth arrest. Therefore, the premature senescence induced by E2FBP1 depletion is achieved through the pl6INK4A-Rb pathway. Similar to human normal fibroblasts, the growth inhibition induced by E2FBP1 depletion is also observed in human tumor cells with intact p16INK4A and Rb. These results suggest that E2FBP1 functions as a critical antagonist to the pI6INK4A-Rb tumor suppressor machinery by regulating PML stability.

关键词： E2F-binding protein 1 senescence cell cycle ubiquitin promyelocytic leukemia protein

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TGF-beta receptor mediated telomerase inhibition, telomere shortening and breast cancer cell senescence

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Protein & Cell 2017年第1期8卷 39-54页

作者： Lucy Cassar Craig Nicholls Alex R. Pinto Ruping Chen Lihui Wang He Li Jun-Ping Liu Molecular Signaling Laboratory Department of Immunology Central Eastern Clinical School Monash University Prahran VIC 3181 Australia Institute of Aging Research Hangzhou Normal University School of Medicine Hangzhou 311121 Zhejiang Province China

Human telomerase reverse transcriptase （hTERT） plays a central role in telomere lengthening for continuous cell proliferation, but it remains unclear how extracellular cues regulate telomerase lengthening of telomeres. Here we report that the cytokine bone morphogenetic protein-7 （BMP7） induces the hTERT gene repression in a BMPRII receptor- and Smad3-dependent manner in human breast cancer cells. Chonic exposure of human breast cancer cells to BMP7 results in short telomeres, cell senescence and apoptosis. Mutation of the BMPRII receptor, but not TGFbRII, ACTRIIA or ACTRIIB receptor, inhibits BMP7-induced repression of the hTERT gene promoter activity, leading to increased telomerase activity, lengthened telomeres and continued cell proliferation. Expression of hTERT prevents BMP7-induced breast cancer cell senescence and apoptosis. Thus, our data suggest that BMP7 induces breast cancer cell aging by a mechanism involving BMPRII receptor- and Smad3-mediated repression of the hTERT gene.

关键词： BMPRII TGFbeta hTERT telomerase telomeres senescence breast cancer cells

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Correlation of Twist upregulation and senescence bypass during the progression and metastasis of cervical cancer

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Frontiers of Medicine 2014年第1期8卷 106-112页

作者： Tian Wang Yan Li Abidan Tuerhanjiang Wenwen Wang Zhangying Wu Ming Yuan Shixuan Wang Department of Obstetrics and Gynecology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan430030 China

Cervical carcinoma is associated with high propensity for local invasion and lymph node metastasis. However, the molecular alterations that drive progression and metastasis of cervical cancer remain unclear. Cellular senescence has been proposed as the mechanism that protects an organism against cancer progression and metastasis. In addition, Twist, a basic helix-loop-helix transcription factor, has been suggested as an oncogene because it is overexpressed in many types of human cancer. This gene also exhibits a positive function in regulating invasion and metastasis. In this study, Twist was strongly and positively expressed in normal tissue, squamous cell carcinoma （SCC） IA-IIA, and SCC IIB-IIIB （4.3%, 44%, and 88.9%, respectively）. The strong positive expressions of the senescence marker CBX3 were 39.1%, 32%, and 15.6%, respectively. The strong positive expressions of Twist in the SCC groups with or without lymph node metastasis were 80.8% and 50%. For CBX3, such expressions were 7.7% and 29.5%, respectively. Results also showed that the expression of Twist was inversely correlated with that of CBX3. Moreover, the knockdown of Twist with target siRNA in SiHa triggered the induction of the chromatin marker of the cellular senescence CBX3 and senescence-associated p-galactosidase activity. Our results suggested that the expression of Twist increased during the progression and metastasis of cervical cancer. Furthermore, Twist-induced senescence bypass is important in this process.

关键词： cervical cancer senescence Twist CBX3 lymph node metastasis

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Exhaustion and senescence: two crucial dysfunctional states of T cells in the tumor microenvironment

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Cellular & Molecular Immunology 2020年第1期17卷 27-35页

作者： Yangjing Zhao Qixiang Shao Guangyong Peng Division of Infectious Diseases Allergy&Immunology and Department of Internal MedicineSaint Louis University School of MedicineSaint LouisMO 63104USA Department of Immunology Key Laboratory of Medical Science and Laboratory Medicine of Jiangsu ProvinceSchool of MedicineJiangsu UniversityZhenjiang 212013P.R.China Department of Molecular Microbiology&Immunology Saint Louis University School of MedicineSt.LouisMO 63104USA

The failure of a massive influx of tumor-infiltrating T lymphocytes to eradicate tumor cells in the tumor microenvironment is mainly due to the dysfunction of T cells hyporesponsive to tumors.T-cell exhaustion and senescence induced by malignant tumors are two important dysfunctional states that coexist in cancer patients,hindering effective antitumor immunity and immunotherapy and sustaining the suppressive tumor microenvironment.Although exhausted and senescent T cells share a similar dysfunctional role in antitumor immunity,they are distinctly different in terms of generation,development,and metabolic and molecular regulation during tumor progression.Here,we discuss the unique phenotypic and functional characteristics of these two types of dysfunctional T cells and their roles in tumor development and progression.In addition,we further discuss the potential molecular and metabolic signaling pathways responsible for the control of T-cell exhaustion and senescence in the suppressive tumor microenvironment.Understanding these critical and fundamental features should facilitate rethinking the unresponsiveness to current immunotherapies in clinical patients and lead to further development of novel and effective strategies that target different types of dysfunctional T cells to enhance cancer immunotherapy.

关键词： T-cell dysfunction Exhaustion senescence Tumor microenvironment Inhibitory receptor Metabolism Checkpoint blockade

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Cellular senescence:from anti-cancer weapon to anti-aging target

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Science China(Life Sciences) 2020年第3期63卷 332-342页

作者： Lifeng Yuan Peter BAlexander Xiao-Fan Wang Program in Cellular and Molecular Medicine Boston Children’s HospitalBostonMA 02115USA Department of Genetics Harvard Medical SchoolBostonMA 02115USA Duke University Medical Center DurhamNC 27710USA

Cellular senescence(CS)is a state of stable cell cycle arrest characterized by the production and secretion of inflammatory molecules.Early studies described oncogene-induced senescence(OIS)as a barrier to tumorigenesis,such that the therapeutic induction of CS might represent a rational anti-cancer strategy.Indeed,the validity of this approach has been borne out by the development and approval of the cyclin-dependent kinase(CDK)inhibitor palbociclib for the treatment of breast cancer.Apart from tumors,senescent cells have also been shown to accumulate during natural mammalian aging,where they produce detrimental effects on the physiology of surrounding tissues.Thus,pharmacological senescent cell depletion has been proposed as an approach to delay age-related functional decline;this has been formally demonstrated in animal models.In this review article,we describe the current mechanistic understanding of cellular senescence at the molecular level and how it informs the development of new therapeutic strategies to combat cancer and aging.

关键词： cellular senescence cancer healthy aging pro-senescence cancer therapy senolytic therapies

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Interactions Between Temperature and Sugars in the Regulation of Leaf senescence in the Perennial Herb Arabis alpina L.

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Journal of Integrative Plant Biology 2012年第8期54卷 595-605页

作者： Astrid Wingler Emma Josefine Stangberg Triambak Saxena Rupal Mistry Research Department of Genetics Evolution and EnvironmentUniversity College LondonGower StreetLondon WC1E 6BTUnited Kingdom

Annual plants usually flower and set seed once before senescence results in the death of the whole plant （monocarpic senescence）. Leaf senescence also occurs in polycarpic perennials; even in ＂evergreen＂ species individual leaves senesce. In the annual model Arabidopsis thaliana sugars accumulate in the senescent leaves and senescence is accelerated by high sugar availability. Similar to A. thaliana, sugar contents increased with leaf age in the perennial Arabis alpina grown under warm conditions （22℃ day/18 night）. At 5℃, sugar contents in non-senescent leaves were higher than at a warm temperature, but dependent on the accession, either sugars did not accumulate or their contents decreased in old leaves. In A. alpina plants grown in their natural habitat in the Alps, sugar contents declined with leaf age. Growth at a cold temperature slightly delayed senescence in A. alpina. In both warm and cold conditions, an external glucose supply accelerated senescence, but natural variation was found in this response. In conclusion, sugar accumulation under warm conditions could accelerate leaf senescence in A. alpina plants, but genotype-specific responses and interactions with growth temperature are likely to influence senescence under natural conditions.

关键词： Perennial polycarpic senescence sugar signaling.

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