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Retinal regeneration requires dynamic notch signaling

Neural Regeneration Research 2022年第6期17卷 1199-1209页

作者： Leah J.Campbell Jaclyn L.Levendusky Shannon A.Steines David R.Hyde Department of Biological Sciences Center for Zebrafish ResearchCenter for Stem Cells and Regenerative MedicineUniversity of Notre DameNotre DameINUSA

Retinal damage in the adult zebrafish induces Müller glia reprogramming to produce neuronal progenitor cells that proliferate and differentiate into retinal *** signaling,which is a fundamental mechanism known to drive cell-cell communication,is required to maintain Müller glia in a quiescent state in the undamaged retina,and repression of notch signaling is necessary for Müller glia to reenter the cell *** dynamic regulation of notch signaling following retinal damage also directs proliferation and neurogenesis of the Müller glia-derived progenitor cells in a robust regeneration *** contrast,mammalian Müller glia respond to retinal damage by entering a prolonged gliotic state that leads to additional neuronal death and permanent vision *** the dynamic regulation of notch signaling in the zebrafish retina may aid efforts to stimulate Müller glia reprogramming for regeneration of the diseased human *** findings identified DeltaB and notch3 as the ligand-receptor pair that serves as the principal regulators of zebrafish Müller glia *** addition,multi-omics datasets and functional studies indicate that additional notch receptors,ligands,and target genes regulate cell proliferation and neurogenesis during the regeneration time ***,our understanding of notch signaling during retinal regeneration is *** fully appreciate the complex regulation of notch signaling that is required for successful retinal regeneration,investigation of additional aspects of the pathway,such as post-translational modification of the receptors,ligand endocytosis,and interactions with other fundamental pathways is *** we review various modes of notch signaling regulation in the context of the vertebrate retina to put recent research in perspective and to identify open areas of inquiry.

关键词： differentiation gliosis Müller glia neuronal progenitor cell notch signaling proliferation quiescence retinal development retinal regeneration zebrafish

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MicroRNA miR-252-5p regulates the notch signaling pathway by targeting Rab6 in Drosophila wing development

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Insect Science 2023年第5期30卷 1431-1444页

作者： Do-Hwan Lim Min-Seok Choi Ji Won Jeon Young Sik Lee School of Systems Biomedical Science Soongsil UniversitySeoulRepublic of Korea College of Life Sciences and Biotechnology Korea UniversitySeoulRepublic of Korea Institute of Animal Molecular Biotechnology Korea UniversitySeoulRepublic of Korea

The notch signaling pathway plays a central role in the development of various ***,dysregulation of microRNAs(miRNAs),which are crucial regulators of gene expression,can disrupt signaling pathways at all stages of *** notch signaling is involved in wing development in Drosophila,the mechanism underlying miRNA-based regulation of the notch signaling pathway is ***,we report that loss of Drosophila miR-252 increases the size of adult wings,whereas the overexpression of miR-252 in specific compartments of larval wing discs leads to patterning defects in the adult *** miR-252 overexpression-induced wing phenotypes were caused by aberrant notch signaling with intracellular accumulation of the full-length notch receptor during development,which could be due to defects in intracellular notch trafficking associated with its recycling to the plasma membrane and autophagy-mediated ***,we identified Rab6 as a direct target of miR-252-5p;Rab6 encodes a small Ras-like GTPase that regulates endosomal trafficking *** with this finding,RNAi-mediated downregulation of Rab6 led to similar defects in both wing patterning and notch ***,co-overexpression of Rab6 completely rescued the wing phenotype associated with miR-252 overexpression,further supporting that Rab6 is a biologically relevant target of miR-252-5p in the context of wing ***,our data indicate that the miR-252-5p-Rab6 regulatory axis is involved in Drosophila wing development by controlling the notch signaling pathway.

关键词： Drosophila miR-252-5p notch signaling Rab6 wing development

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The Role of notch signaling in Genetic Reticular Pigmentary Disorders

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International Journal of Dermatology and Venereology 2023年第3期6卷 163-167页

作者： Wei-Xue Jia Ling-Ling Luo Wen-Rui Li Yuan-Yuan Zhang Ping Cheng Cheng-Rang Li Department of Dermatology Hospital for Skin Diseases(Institue of Dermatology)Chinese Academy of Medical Sciences and Peking Union Medical CollegeNanjingJiangsu 210042China

notch signaling is an essential conserved mechanism through local cell *** regulates cell differentiation,proliferation,and apoptotic,influencing organ formation and *** signaling plays a vital role in both development of melanocyte during embryogenesis and maintenance of melanocyte stem ***1,POGLUT1,ADAM10,presenilin enhancer-2,and nicastrin genes are pathogenic genes of genetic reticular pigmentation diseases Dowling-Degos disease,reticulate acropigmentation of Kitamura,and acne inversa with pigment abnormalities *** they are all vital genes in notch signaling *** group of pigmentary diseases have similarities and overlaps in clinical manifestations and pathological *** review the essential role of notch signaling in genetic reticular pigmentary disorders,and discuss the underlying mechanisms behind dysfunction of melanocyte induced by gene mutations in notch signaling.

关键词： genetic melanocyte notch signaling pigmentary disorder

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notch signaling regulates expression of Mcl-1 andapoptosis in PPD-treated macrophages

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Cellular & Molecular Immunology 2013年第5期10卷 444-452页

作者： Tanapat P alaga Siriluk Ratanabunyong Thitiporn Pattarakankul Naunpun Sangphech Wipawee Wongchana Yukihiro Hadae Patipark Kueanjinda Department of Microbiology Faculty of Science Chulalongkorn University Bangkok 10330 Thailand Interdisciplinary Program in Medical Microbiology Graduate School Chulalongkorn University Bangkok 10330 Thailand Graduate Program in Industrial Microbiology Faculty of Science Chulalongkorn University Bangkok 10330 Thailand Graduate Program in Biotechnology Faculty of Science Chulalongkorn University Bangkok 10330 Thailand International Center for Biotechnology Osaka University Osaka 565-0871 Japan

Macrophages are cellular targets for infection by bacteria and viruses. The fate of infected macrophages plays a key role in determining the outcome of the host immune response. Apoptotic cell death of macrophages is considered to be a protective host defense that eliminates pathogens and infected cells. In this study, we investigated the involvement of notch signaling in regulating apoptosis in macrophages treated with tuberculin purified protein derivative （PPD）. Murine bone marrow-derived macrophages （BMMs） treated with PPD or infected with Mycobacterium bovis Bacillus Calmette-Guerin （BCG） induced upregulation of notch1. This upregulation correlated well with the upregulation of the anti-apoptotic gene mcl-1 both at the transcriptional and translational levels. Decreased levels of notch I and Mcl- 1 were observed in BMM treated with PPD when a gamma secretase inhibitor （GSI）, which inhibits the processing of notch receptors, was used. Moreover, silencing notch1 in the macrophage-like cell line RAW264.7 decreased Mcl-1 protein expression, suggesting that notch1 is critical for Mcl-1 expression in macrophages. A significant increase in apoptotic cells was observed upon treatment of BMM with PPD in the presence of GSI compared to the vehicle-control treated cells. Finally, analysis of the mcl-1 promoter in humans and mice revealed a conserved potential CSURBP-Jκ binding site. The association of notch I with the mcl-1 promoter was confirmed by chromatin immunoprecipitation. Taken together, these results indicate that notch I inhibits apoptosis of macrophages stimulated with PPD by directly controlling the mcl-1 promoter.

关键词： apoptosis BCG macrophage Mcl-1 notch signaling PPD

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notch signaling： a novel regulating differentiation mechanism of human umbilical cord blood-derived mesenchymal stem cells into insulin-producing cells in vitro

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Chinese Medical Journal 2010年第5期123卷 606-614页

作者： HU Yan-hua WU De-quan GAO Feng LI Guo-dong ZHANG Xin-chen Department of General Surgery Second Affiliated Hospital of Harbin Medical University Harbin Heilongjiang 150086 China

Background Human umbilical cord blood-derived mesenchymal stem cells （UCB-MSCs） could be induced to differentiate into insulin producing cells （IPCs） in vitro, which have good application potential in the cell replacement treatment of type-1 diabetes. However, the mechanisms regulating this differentiation have remained largely unknown. notch signaling is critical in cell differentiation. This study investigated whether notch signaling could regulate the IPCs differentiation of human UCB-MSCs. Methods Using an interfering notch signaling protocol in vitro, we studied the role of notch signaling in differentiation of human UCB-MSCs into IPCs. In a control group the induction took place without interfering notch signaling. Results Human UCB-MSCs expressed the genes of notch receptors （notch 1 and notch 2） and ligands （Jagged 1 and Deltalike 1）. Human UCB-MSCs with over-expressing notch signaling in differentiation resulted in the down-regulation of insulin gene level, proinsulin protein expression, and insulin-positive cells percentage compared with the control group. These results showed that over-expressing notch signaling inhibited IPCs differentiation. Conversely, when notch signaling was attenuated by receptor inhibitor, the induced cells increased on average by 3.06-fold （n=-4, P 〈0.001） in insulin gene level, 2.60-fold （n=-3, P 〈0.02） in proinsulin protein expression, and 1.62-fold （n=-6, P 〈0.001） in the rate of IPCs compared with the control group. notch signaling inhibition significantly promoted IPCs differentiation with about 40% of human UCB-MSCs that converted to IPCs, but these IPCs were not responsive to glucose challenge very well both in vitro and in vivo. Hence, further research has to be carried out in the future. Conclusions notch signaling may be an important mechanism regulating IPCs differentiation of human LICB-MSCs in vitro and notch signaling inhibition may be an efficient way to increase the number of IPCs, which may resolve the shortage of

关键词： notch signaling mesenchymal stem cells differentiation insulin producing cells diabetes

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notch signaling and its emerging role in autoimmunity

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Frontiers in Biology 2013年第3期8卷 279-294页

作者： Tanapat PALAGA Lisa M. MINTER Department of Microbiology Faculty of Science Medical Microbiology Interdisciplinary Program Graduate School ChulalongkornUniversity Pathumwan Bangkok 10330 Thailand Program in Molecular and Cellular Biology University of Massachusetts Amherst MA 01003 USA Department of Veterinary & Animal Sciences University of Massachusetts Amherst MA 01003 USA

Studies of notch signaling in immune cells have uncovered critical roles for this pathway both during the differentiation and effector function phases of immune responses. Cells of the myeloid lineage, including macrophages and dendritic cells, function as key components of innate immune defense against infection and, by acting as antigen presenting cells, can instruct cells of the adaptive immune response, specifically CD4 and CD8 T cells. Tight regulation of this functional interaction is needed to ensure a well-balanced immune response and its dysregulation may indirectly or directly cause the tissue damage characteristic of autoimmune diseases. In this review, the focus will be placed on those recent findings which support a role for notch signaling in inflammatory responses mediated by macrophages and other myeloid lineage cells, as well as peripheral T cells, and their relevance to inflammatory and autoimmne diseases.

关键词： notch signaling inflammation autoimmunity

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notch signaling in female cancers: a multifaceted node to overcome drug resistance

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Cancer Drug Resistance 2021年第4期4卷 805-836页

作者： Maria V.Giuli Angelica Mancusi Eugenia Giuliani Isabella Screpanti Saula Checquolo Laboratory of Molecular Pathology Department of Molecular MedicineSapienza UniversityRome 00161Italy Scientific Direction San Gallicano Dermatological Institute IRCCSRome 00144Italy Department of Medico-Surgical Sciences and Biotechnology Sapienza UniversityLatina 04100Italy Center for Life Nano Science@Sapienza Istituto Italiano di TecnologiaRome 00161Italy

Drug resistance is one of the main challenges in cancer therapy,including in the treatment of female-specific malignancies,which account for more than 60%of cancer cases among ***,elucidating the underlying molecular mechanisms is an urgent need in gynecological cancers to foster novel therapeutic ***,notch signaling,including either receptors or ligands,has emerged as a promising candidate given its multifaceted role in almost all of the hallmarks of *** the connection between notch pathway and drug resistance in the afore-mentioned tumor contexts,several studies focused on the notch-dependent regulation of the cancer stem cell(CSC)subpopulation or the induction of the epithelial-to-mesenchymal transition(EMT),both features implicated in either intrinsic or acquired ***,the present review provides an up-to-date overview of the published results on notch signaling and EMT-or CSC-driven drug ***,other drug resistance-related mechanisms are examined such as the involvement of the notch pathway in drug efflux and tumor ***,there is a long way to go before every facet will be fully understood;nevertheless,some small pieces are falling neatly into ***,the main aim of this review is to provide strong evidence in support of notch signaling inhibition as an effective strategy to evade or reverse resistance in female-specific cancers.

关键词： notch signaling drug resistance female-specific cancers cancer stem cells epithelial-to-mesenchymal transition drug efflux tumor microenvironment

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dBrms1 Acts as a Positive Regulator of notch signaling in Drosophila Wing

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Journal of Genetics and Genomics 2014年第6期41卷 317-325页

作者： Qinghai Zhang Yan Zhang Longfei Wu Yongfei Yang Xue Li Lei Gao Xiaomeng Hou Yihui Wu Guoli Hou Zhouhua Li Xinhua Lin State Key Laboratory of Biomembrane and Membrane Biotechnology Institute of Zoology Chinese Academy of Sciences University of Chinese Academy of Sciences School of Life Sciences Capital Normal University Division of Developmental Biology Cincinnati Children’s Hospital Medical Center

The highly conserved notch signaling is precisely regulated at different steps in a series of developmental events. However, little is known about the regulation of notch receptor at transcriptional level. Here, we demonstrate that dBrmsl is involved in regulating notch signaling in Drosophila wing. We show that knockdown of dBrmsl by RNA interference （RNAi） in wing disc suppresses the expression of notch signaling target genes wingless （wg）, cut and Enhancer of split m8 [E（spl）m8]. Consistently, the levels of Wg and Cut are reduced in the dBrmsl mutant clones. Importantly, loss of dBrmsl leads to significant reduction of notch proteins. Furthermore, depletion of dBrmsl results in apparent downregulation of notch transcription in the wing disc. Moreover, we find that dBrmsl is functionally conserved with human Breast cancer metastasis suppressor 1 like （hBRMSIL） in the modulation of notch signaling. Taken together, our data provide important insights into the biological function of dBrmsl in regulating notch signaling.

关键词： notch signaling Drosophila Wing disc notch transcription dBrmsl

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Direct regulation of interleukin-6 expression by notch signaling in macrophages

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Cellular & Molecular Immunology 2012年第2期9卷 155-162页

作者： Wipawee Wongchana Tanapat Palaga Graduate Program in Biotechnology Faculty of Science Chulalongkorn University Bangkok Thailand Department of Microbiology Faculty of Science Chulalongkorn University Bangkok Thailand

Interleukin-6 （IL-6） is a pleiotropic, pro-inflammatory cytokine produced by various types of cells, including macrophages. Within the IL-6 gene promoter region, the signature binding motif of CBFI/Su（H）/Lag-1 （CSL）, a key DNA-binding protein in the notch signaling pathway, was identified and found to overlap with a consensus nuclear factor （NF）-κB-binding site. notch signaling is highly conserved and is involved in the regulation of biological functions in immune cells. In this study, we investigated the role of notch signaling in the regulation of the IL-6transcript in murine macrophages. The upregulation of notch1 protein levels and the appearance of cleaved notch1 （Va11744） correlated well with the increased IL-6 mRNA expression levels in murine primary bone marrow-derived macrophages （BMMφ） after activation by lipopolysaccharide （LPS） together with interferon-gamma （IFN-γ）. Treatment of BMMφ with the γ-secretase inhibitor IL-CHO to suppress the transduction of notch signaling resulted in a partial decrease in the level of IL-6mRNA and the amount of I L-6 protein produced. In contrast, the overexpression of a constitutively activated intracellular notch I protein （N^IC） in the RAW264.7 macrophage-like cell line resulted in significantly higher IL-6transcript expression levels than in cells transfected with the empty vector control. The NF-κB inhibitor completely abrogated IL-6 mRNA expression induced by the overexpression of N^IC. Chromatin immunoprecipitation （CHIP） using an anti-notch1 antibody demonstrated that notch 1 is associated with the IL-6promoter in RAW264.7 cells activated by LPS/IFN-γ but not in unstimulated cells. Taken together, these results strongly suggest that notch 1 positively regulates IL-6 expression via NF-κB in activated macrophages.

关键词： CSL interleukin-6 macrophages NF-κB notch signaling

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The notch signaling pathway in retinal dysplasia and retina vascular homeostasis

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Journal of Genetics and Genomics 2010年第9期37卷 573-582页

作者： Minhua Zheng Zifeng Zhang Xingcheng Zhao Yuqiang Ding Hua Han Department of Medical Genetics and Developmental Biology Fourth Military Medical University Xi'an 710032 China Department of Ophthalmology Xifing Hospital Fourth Military Medical University Xi' an 710032 China Department of Anatomy and Neurobiology Tongji University School of Medicine Shanghai 200092 China

The retina is one of the most essential elements of vision pathway in vertebrate. The dysplasia of retina cause congenital blindness or vision disability in individuals, and the misbalance in adult retinal vascular homeostasis leads to neo adults, such as diabetic retinopathy or age-related macular degeneration. Many developmental signaling pathways are involved in the process of retinal development and vascular homeostasis. Among them, notch signaling pathway has long been studied, and notch signaling-interfered mouse models show both neural retina dysplasia and vascular abnormality. In this review, we discuss the roles of notch signaling in the maintenance of retinal progenitor cells, specification of retinal neurons and glial cells, and the sustaining of retina vascular homeostasis, especially from the aspects of conditional knockout mouse models. The potential of notch signal manipulation may provide a powerful cell fate- and neovascularization-controUing tool that could have important applications in treatment of retinal diseases.

关键词： notch signaling retinal dysplasia vascular homeostasis neovascularization knockout mice

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