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| 1 | Intravenous immune globulin suppresses angiogenesis in mice and humans显示文摘Human intravenous immune globulin(IVIg),a purified IgG fraction composed of~60%IgG1 and obtained from the pooled plasma of thousands of donors,is clinically used for a wide range of diseases.The biological actions of IVIg are incompletely understood and have been attributed both to the polyclonal antibodies therein and also to their IgG(IgG)Fc regions.Recently,we demonstrated that multiple therapeutic human IgG1 antibodies suppress angiogenesis in a target-independent manner via FcγRI,a high-affinity receptor for IgG1.Here we show that IVIg possesses similar anti-angiogenic activity and inhibited blood vessel growth in five different mouse models of prevalent human diseases,namely,neovascular age-related macular degeneration,corneal neovascularization,colorectal cancer,fibrosarcoma and peripheral arterial ischemic disease.Angioinhibition was mediated by the Fc region of IVIg,required FcγRI and had similar potency in transgenic mice expressing human FcγRs.Finally,IVIg therapy administered to humans for the treatment of inflammatory or autoimmune diseases reduced kidney and muscle blood vessel densities.These data place IVIg,an agent approved by the US Food and Drug Administration,as a novel angioinhibitory drug in doses that are currently administered in the clinical setting.In addition,they raise the possibility of an unintended effect of IVIg on blood vessels. | Reo Yasuma Valeria Cicatiello Takeshi Mizutani Laura Tudisco Younghee Kim Valeria Tarallo Sasha Bogdanovich Yoshio Hirano Nagaraj Kerur Shengjian Li Tetsuhiro Yasuma Benjamin J Fowler Charles B Wright Ivana Apicella Adelaide Greco Arturo Brunetti Balamurali K Ambati Sevim Barbasso Helmers Ingrid E Lundberg Ondrej Viklicky Jeanette HW Leusen J Sjef Verbeek Bradley D Gelfand Ana Bastos-Carvalho Sandro De Falco Jayakrishna Ambati | 2016 | Signal Transduction and Targeted Therapy2016，1，1： | 3 |
| 2 | Age-Related Macular degeneration: etiology pathogenesis and the repeutic strategies 显示文摘 | Jayakrishna A Balamurali KA | 2003 | SurvOpthalmol2003，48，： | 1 |
| 3 | Age-Related Macular Degeneration: etiology, pathogenesis, and therapertic Strategies显示文摘 | Jayakrishna A Balamurali KA | 2003 | Sur of Ophthalmol2003，48，： | 1 |
| 4 | Age-Related Macular Degeneration: Etiology, Pathogenesis, and Therapeutic Strategies显示文摘 | Jayakrishna Ambati Balamurali K Ambati Sonia H Yoo Sean Ianchulev Anthony P Adamis | 2003 | Survey of Ophthalmology2003，，3： | 1 |
| 5 | Environmental impact minimisation in an automotive component using alternative materials and manufacturing processes显示文摘 | Vinodh S Jayakrishna K | | 0，，10： | 1 |
| 6 | Molecular docking and analysis of interactions between vascular endothelial growth factor (VEGF) and SPARC protein显示文摘 | Vasu C Jayakrishna A Balamurali K | 2007 | Molecular Graphics Modelling2007，26，： | 1 |
| 7 | Age-Related Macular degeneration : etiol- ogy pathogenesis and the repeutic stratehies 显示文摘 | Jayakrishna A BalamurMi KA | 2003 | Sure Opthalmol2003，48，： | 1 |
| 8 | Targeting the m6A mRNA demethylase FTO suppresses vascular endothelial growth factor release and choroidal neovascularization显示文摘Dear Editor,Vascular endothelial growth factor-A(VEGFA,also known as VEGF)is a critical angiogenic factor that regulates the physiological and pathological blood vessel growth.1 Increased abundance of VEGF in the eye underlies many forms of aberrant ocular angiogenesis and resultant vision loss,including in neovascular age-related macular degeneration(nvAMD),proliferative diabetic retinopathy(PDR). | Shao-bin Wang Yosuke Nagasaka Dionne Argyle Ayami Nagasaka Praveen Yerramothu Bradley DGelfand Jayakrishna Ambati | 2023 | Signal Transduction and Targeted Therapy2023，8，3： | 0 |
| 9 | Nucleoside reverse transcriptase inhibitors and Kamuvudines inhibit amyloid-βinduced retinal pigmented epithelium degeneration显示文摘Nonfibrillar amyloid-βoligomers(AβOs)are a major component of drusen,the sub-retinal pigmented epithelium(RPE)extracellular deposits characteristic of age-related macular degeneration(AMD),a common cause of global blindness.We report that AβOs induce RPE degeneration,a clinical hallmark of geographic atrophy(GA),a vision-threatening late stage of AMD that is currently untreatable.We demonstrate that AβOs induce activation of the NLRP3 inflammasome in the mouse RPE in vivo and that RPE expression of the purinergic ATP receptor P2RX7,an upstream mediator of NLRP3 inflammasome activation,is required for AβO-induced RPE degeneration.Two classes of small molecule inflammasome inhibitors—nucleoside reverse transcriptase inhibitors(NRTIs)and their antiretrovirally inert modified analog Kamuvudines—both inhibit AβOs-induced RPE degeneration.These findings crystallize the importance of P2RX7 and NLRP3 in a disease-relevant model of AMD and identify inflammasome inhibitors as potential treatments for GA. | Siddharth Narendran Felipe Pereira Praveen Yerramothu Ivana Apicella Shao-bin Wang Kameshwari Ambati Shuichiro Hirahara Younghee Kim Meenakshi Ambati Vidya L.Ambati Peirong Huang Akhil Varshney Yosuke Nagasaka Shinichi Fukuda Kirstie L.Baker Kenneth M.Marion Jan M.Deussing Srinivas R.Sadda Bradley D.Gelfand Jayakrishna Ambati | 2021 | Signal Transduction and Targeted Therapy2021，6，5： | 0 |
| 10 | Human IgG1 antibodies suppress angiogenesis in a target-independent manner显示文摘Aberrant angiogenesis is implicated in diseases affecting nearly 10%of the world’s population.The most widely used antiangiogenic drug is bevacizumab,a humanized IgG1 monoclonal antibody that targets human VEGFA.Although bevacizumab does not recognize mouse Vegfa,it inhibits angiogenesis in mice.Here we show bevacizumab suppressed angiogenesis in three mouse models not via Vegfa blockade but rather Fc-mediated signaling through FcγRI(CD64)and c-Cbl,impairing macrophage migration.Other approved humanized or human IgG1 antibodies without mouse targets(adalimumab,alemtuzumab,ofatumumab,omalizumab,palivizumab and tocilizumab),mouse IgG2a,and overexpression of human IgG1-Fc or mouse IgG2a-Fc,also inhibited angiogenesis in wild-type and FcγR humanized mice.This anti-angiogenic effect was abolished by Fcgr1 ablation or knockdown,Fc cleavage,IgG-Fc inhibition,disruption of Fc-FcγR interaction,or elimination of FcRγ-initated signaling.Furthermore,bevacizumab’s Fc region potentiated its anti-angiogenic activity in humanized VEGFA mice.Finally,mice deficient in FcγRI exhibited increased developmental and pathological angiogenesis.These findings reveal an unexpected anti-angiogenic function for FcγRI and a potentially concerning off-target effect of hIgG1 therapies. | Sasha Bogdanovich Younghee Kim Takeshi Mizutani Reo Yasuma Laura Tudisco Valeria Cicatiello Ana Bastos-Carvalho Nagaraj Kerur Yoshio Hirano Judit Z Baffi Valeria Tarallo Shengjian Li Tetsuhiro Yasuma Parthasarathy Arpitha Benjamin J Fowler Charles B Wright Ivana Apicella Adelaide Greco Arturo Brunetti Menotti Ruvo Annamaria Sandomenico Miho Nozaki Ryo Ijima Hiroki Kaneko Yuichiro Ogura Hiroko Terasaki Balamurali K Ambati Jeanette HW Leusen Wallace Y Langdon Michael R Clark Kathryn L Armour Pierre Bruhns J Sjef Verbeek Bradley D Gelfand Sandro De Falco Jayakrishna Ambati | 2016 | Signal Transduction and Targeted Therapy2016，1，1： | 0 |
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