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        當前位置:首頁技術文章Probetex,Inc 腎炎模型誘導試劑一級代理

        Probetex,Inc 腎炎模型誘導試劑一級代理

        更新時間:2019-11-28點擊次數:2345

        Probetex,Inc公司成立于1997年,是一家為生物科研研究提供服務的CRO 公司。公司專注于6個研究領域:1)成人和胚胎腎細胞系的細胞庫2)生產和銷售綿羊腎毒性抗體以誘導抗腎小球基底膜(抗GBM)腎小球腎炎,膜性(抗Fx1A)腎病和系膜增生性(抗Thy1)腎小球腎炎。3)腎病模型研究的組織產品4)組織病理學服務,提供常規組織學,免疫組織化學,電子顯微鏡和圖像分析; 5)提供以上腎病以及20多種急性、慢性實驗性腎病、心腦血管和肺病的其他模型的構建服務。6)其他研究領域,比如:再生醫學、血管炎新模型以及其他罕見疾病模型的構建和評價服務。

        特色產品:

        綿羊抗大鼠腎小球基底膜血清(PTX-001AGBM

        Sheep Anti Rat Glomerular Basement Membrane (GBM) Serum

        --GBM型腎炎模型誘導

         

        產品名稱

        Sheep Anti Rat Glomerular Basement Membrane (GBM) Serum

        貨號

        PTX-001AGBM

        規格

        25ml

        保存

        -20

        說明

        產品經56℃熱處理30min,請避免反復凍融。解凍后會有輕微沉淀,注射前3000-5000rmp 離心30min。

        注:只做過大鼠炎癥,沒有做過小鼠驗證。

        應用說明:(實驗前請仔細閱讀實驗流程)

        每瓶血清含有足夠的抗體用于誘導至少25只大鼠*175-200 g體重)被動抗GBM腎炎模型。

        免疫抗GMB血清麻醉大鼠,尾靜脈注射抗GMB血清超過15秒,疾病的產生依賴于免疫劑量,依照免疫劑量*打入體內很關鍵(推薦用量:0.4-0.5ml/100g體重)。由于不同批次抗血清差異,大鼠來源,以及實驗要求的不同,我們建議進行劑量-反應研究,具體的免疫劑量和疾病的嚴重程度,需要根據每個不同批次血清和產生疾病的嚴重程度,選擇合適的免疫劑量。

        腎病研究:

        1)異源性疾病:免疫抗GBM (anti GBM)3-5天后,免疫熒光檢測顯示綿羊IgG在腎小球基底膜內呈線狀沉積。大鼠c3也呈線性分布,24小時后出現蛋白尿。

        2)自身疾病免疫GBM抗體8-10天后,檢測大鼠蛋白尿增加,同時大鼠腎小球IgG(自身抗體) 呈線狀沉積,自體疾病變得明顯。(自體)免疫組化呈線性模式的IgG(圖1)。到3周時,蛋白尿有望達到200毫克/24小時,腎小球病變(圖2)明顯,隨著時間的推移,嚴重程度增加,導致腎小球硬化。

        1.免疫熒光檢測顯示免疫抗GBM3周后腎小球毛細血管壁大鼠IgG免疫沉積的。

        2.免疫組化染色顯示免疫抗GBM 3周后新月體形成、系膜細胞增生、毛細血管變形。

        相關產品:

         

        貨號

        產品名稱

        規格

        腎炎模型

        PTX-001AGBM

        Sheep Anti-Rat GBM Serum 

        25ml

        PTX-002S

        Sheep Anti-Rat Fx1A Serum

        25ml

        PTX-003S

        Sheep Anti-Rat Thy-1 Serum

        20ml

        PTX-000S

        Sheep Non-Immune Serum

        25ml

        組織產品(動物疾病模型組織、切片、血漿、尿液)

        PTX-001

        Anti-GBM (Immune-mediated Glomerulonephritis)

        -

        PTX-002

        Anti-Fx1A (Heymann Nephritis, Membranous Nephritis)

        -

        PTX-003.

        Anti-Thy-1 (Mesangial Proliferative Glomerulonephritis) 

        -

        PTX-004

        Diabetic nephropathy (streptozotocin- Type I Diabetes) 

        -

        PTX-005

        Control (Normal) Kidney

        -

        PTX-006

        Sheep Kidney Section(anti-GBM and Fx1A membranous nephropathy

        -

        細胞

        CRGMes-1

        Rat Glomerular Mesangial Cells

        1x106

        CRGEp-1

        Rat Glomerular Epithelial Cells

        1x106

        CBGEn-1

        Bovine Glomerular Endothelial Cells

        1x106

        CMUB-1

        Mouse Ureteric Bud Cells

        1x106

        CMMM-1

        Mouse Metanephric Mesynchymal Cells

        1x106

        CRMM-1

        Rat Metanephric Mesynchymal Cells

        1x106

        抗體

        BS-001GBM

        FITC- Sheep Anti-Glomerular Basement Membrane IgG

        0.5ml

        BS-002ECM

        FITC- Sheep Anti-Extracellular Matrix (ECM) IgG

        0.5ml

        參考文獻:

        1.McIntosh LM, Barnes JL, Barnes VL, McDonald JR. Selective CCR2-targeted macrophage depletion ameliorates experimental mesangioproliferative glomerulonephritis. Clin Exp Immunol 155:295-303, 2009. Osprey Pharma, Probetex, Inc. (Contract Research, Pre-Clinical Testing, Histopathology)

        2.Velagapudi C, Nilsson R-P, Barnes VL, Arar M, Abboud HE, Barnes JL. Reciprocal induction of simple organogenesis by mouse kidney progenitor cells in three-dimensional co-culture. Am J Pathol 180:819-830, 2012. Link (Cover Photo, February Issue). Probetex, Inc, Univ TX Hlth Sci Ctr, San Antonio, TX.  (CMMM-1 and CMUB-1: Mouse Kidney Primordial Cells).

        3.Riser BL, Najmabadi F, Garchow K, Barnes JL, Peterson DR, Sukowski EJ: Treatment with matricellular protein CCN3 blocks and/or reverses fibrosis development in obesity with diabetic nephropathy. Am J Pathol 184:2908–2921, 2014. Rosalind Franklin University of Medicine and Science, Baxter Healthcare, Probetex, Inc. (Histopathology, Image Analysis).

        4.Sun H, Olsen HS, Merigeon EY, So E, Burch E, Kinsey S, Papadimitriou JC, Drachenberg CB, Bentzen SM, Block DS, Strome SE, Zhang X: Recombinant human IgG1 based Fc multimers, with limited FcR bindng capacity, can effectively inhibit complement-mediated disease. J Autoimmun 84: 87-98, 2017. (rats) University of Maryland School of Medicine, Gliknik, Inc., Chengdu Military General Hospital China.

        5.Patel M, Velagapudi C, Burns HS, Doss R, Lee, MJ, Mariappan M, Wagner B, Arar M, Barnes VL, Abboud HE, Barnes JL. Mouse metanephric mesenchymal cell-derived angioblasts undergo vasculogenesis in three-dimensional culture. Am J Pathol 188: 768-784, 2018. Probetex, Inc, Univ TX Hlth Sci Ctr, San Antonio, TX. (CMMM-1 and CMUB-1: Mouse Kidney Primordial Cells).

        6.Rufanova VA, Lianos E, Alexanian A, Sorokina E, Sharma M, McGinty A, Sorokin A: G3G overexpression in glomerular epithelial cells during anti-GBM-induced glomerulonephritis. Kidney Int 75:31-40, 2009. (mice) (Medical College of Wisconsin).

        7.Lichtnekert J, Kulkarni OP, Mulay SR, Rupanagudi KV, Ryu M, Allam R, Vielhauer V, Muruve D, Lindenmeyer MT, Cohen CD, Anders H-J. Anti-GBM glomerulonephritis involves IL-1 but is independent of NLRP3/ASC inflammasome-mediated activation of caspase-1. PLoS ONE 6(10): e26778. doi:10.1371/journal.pone.0026778. October 2011. (mice) (Ludwig-Maximillians-Univeristy of Munich).

        8.Schwarz M, Taubitz A, Eltrich N, Mulay SR, Allam R, Vielhauer V: Analysis of TNF-mediated recruitment and activation of glomerular dendritic cells in mouse kidneys by compartment-specific flow cytometry. Kidney Int 84: 116-129, 2013. (mice) (Ludwig-Maximillians-Univeristy of Munich).

        9.Kim J, Imig JD, Yang J, Hammock BD, Padanilam BJ: Inhibition of soluble epoxide hydrolase prevents renal interstitial fibrosis and inflammation. Am J Physiol Renal Physiol 307: F971-F980, 2014. (mice). (University of Nebraska USA).

        10.Zheng W, Warner R, Ruggeri R, Su C, Cortes C, Skoura A, Ward J, Ahn K, Kalgutkar A, Sun D, Maurer TS, Bonin PD, Okerberg C, Bobrowski W, Kawabe T, Zhang Y, Coskran T, Bell S, Kapoor B, Johnson K, Buckbinder L. PF-1355, a mechanism-based myeloperoxidase inhibitor, prevents immune complex vasculitis and anti–glomerular basement membrane glomerulonephritis. J Pharmacol Exp Ther 353:288–298, 2015. (mice). Pfizer and University of Michigan.

        11.Pavkovic M, Riefke B, Frisk AL, Gröticke I, Ellinger-Ziegelbauer H. Glomerulonephritis-induced changes in urinary and kidney MicroRNA profiles in rats. Toxicol Sci. 145(2), 348–359, 2015. (Rats). Bayer Pharma AG and Harvard Medical School.

        12.Kumar SV, Kulkarni OP, Mulay SR, Darisipudi MN, Romoli S, Thomasova D, Scherbaum CR, Hohenstein B, Hugo C, Müller S, Liapis H, Anders HJ. Neutrophil Extracellular Trap-Related Extracellular Histones Cause Vascular Necrosis in Severe GN. J Am Soc Nephrol. 26 (10):2399-2413, 2015 (mice) (Ludwig-Maximilians-University of Munich, Munich).

        13.Bosma M, Gerling M, Pasto J, Georgiadi A, Graham E, Shilkova O, Iwata Y, Almer S, Soderman J, Toftgard R, Wermeling F, Bostrom EA, Bostrom PA. FNDC4 acts as an anti-inflammatory factor on macrophages and improves colitis in mice. Nature Commun 7: 11314. Apr 12 2016. (mice) Karolinska Institute, Stockholm Sweden

        14.Mulay SR, Romoli S, Desai J, Honarpischeh, MM, Kumar SV, Anders H-J. Murine double minute-2 inhibition ameliorates established crescentic glomerulonephritis. Am J Pathol. 186: 1442-153, 2016. (mice) Medizinische Klinik und Poliklinik University Hoispital of Ludwig-Maximillians-University , Munich, Germany.

        15.Hachmo Y, Kalechman Y, Skornick I, Gafter U, Caspi RR, and Sredni B: The small tellurium compound AS101 ameliorates rat crescentic glomerulonephritis: association with inhibition of macrophage caspase-1 activity via very late antigen-4 inactivation. Front Immunol. 8: 240-, 2017. doi: 10.3389/immu.2017.00240 PMCID: PMC5339302. (Rats) C.A.I.R. Institute, The Safdiè AIDS and Immunology Research Center; Laboratory of Immunology, National Eye Institute, National

        Institutes of Health, Bethesda, MD, USA

        16.Hsu M-F, Betaieb A, Ito Y, Graham J, Havel PJ, Haj FG. Protein tyrosine phosphatase Shp2 deficiency in podocytes attenuates lipopolysaccharide-induced proteinuria. Scientific Reports 7: 461 2017. (mice). UC-Davis Univ Tennessee-Knoxville Tennessee, USA.

        17.Velez JCQ, Arif E, Rodgers J, Hicks MP, Arthur JM, Nihalani D, Bruner ET, Budisavljevic MN, Atkinson C, Fitzgibbon WR, Janech MG. Deficiency of the angiotensinase aminopeptidase A increases susceptibility to glomerular injury. J Am Soc Nephrol: 28(7):2119-2132, 2017. (mice). Ochsner Clinic Foundation, New Orleans, LA, Medical University of South Carolina, Charleston, SC, Augusta University, Augusta, GA, University of Arkansas for Medical Sciences, Little

        Rock, AR

        18.Bettaieb A, Koike S, Chahed S, Zhao Y, Bachaalany S, Hashoush N, Graham J, Fatima H, Havel PJ, Gruzdev A, Zeldin DC, Hammock BD, Haj FG. Podocyte-specific soluble epoxide hydrolase deficiency in mice attenuates acute kidney injury. FEBS J. 284(13):1970-1986, 2017.(mice). UC Davis, Univ of Tenn-Knoxville, NIEHS PMCID:

        19.Wen Y, Lu X, Ren J, Privratsky JR, Yang B, Rudemiller NP, Zhang J, Griffiths R, Jain MK, Nedospasov SA, Liu BC, Crowley SD. KLF4 in macrophages attenuates TNFα-mediated kidney injury and fibrosis. J Am Soc Nephrol.  30:1925-1938, 2019. (mice). Duke University Medical Center, Duke-National University of Singapore, Durham Veterans Affairs Medical Center.

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