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Probetex动物造模PTX-001AGBM绵羊抗大鼠肾小球基底膜(anti-GBM)血清
肾小球基底膜肾炎造模血清
Sheep Anti-Rat Isolated Glomerular Basement Membrane (Anti-GBM) Serum for the Induction of Immune-Mediated Glomerulonephritis
  • 产品编号: PTX-001AGBM

  • 相关CAS号:

  • 分子式:

  • 分子量:

订货号 规格 价格 库存 数量 购买
PTX-001AGBM 25mL ¥ 14100.00元 1

两种广泛用于研究涉及肾小球毛细血管免疫沉积物的免疫性肾小球肾炎机制的大鼠模型是抗 GBM 肾炎和被动 Heymann 肾炎 (PHN)。 GBM 中免疫复合物的位置决定了由此产生的肾小球损伤和肾综合征。倾向于在内皮细胞表面和内皮下间隙沿肾小球毛细血管壁内表面积累的免疫复合物(如抗 GBM 抗体和抗原抗体复合物)可直接接触到循环炎症细胞和介质,并且通常与新月体形成有关 。随之而来的补体激活、炎性细胞浸润和细胞因子、生长因子和氧化剂的释放是对肾小球毛细血管的损伤和增生性肾小球肾炎、通透性屏障改变和新月体发育。倾向于定位于上皮下区域的免疫复合物,远离毛细血管腔(如在 AntiFx1A、PHN 中)导致最小的浸润和增殖 ,而是导致肾小球上皮损伤和蛋白尿。


Probetex 提供独特的肾毒性抗血清(抗 GBM、抗 Fx1A 和抗 Thy-1)来源,以诱导经典的肾病免疫模型。 免疫介导的新月体肾小球肾炎,被动膜性(Heymann 肾炎,系膜增生性 GN)

一瓶25ml的抗血清足以在至少 25 只大鼠中诱发疾病。其用于学术和制药行业! 在未经 Probetex 验证但已被该物种的多个研究人员成功使用的小鼠中使用。Sheep Anti-Rat Isolated Glomerular Basement Membrane (Anti-GBM) Serum绵羊抗大鼠离体肾小球基底膜(抗 GBM)血清,用于诱导免疫介导的肾小球肾炎。病理表现如下:

* 系膜增生

* 炎性细胞血管炎

* 肾小球硬化

* 肾纤维化

1. 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).

2. 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).

3. 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).

4. 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).

5. 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. Link

6. 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.

7. 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). Link

8. 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. Link

9. 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. Link

10. 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. Link

11. 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. Link

12. 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. Link
 
13. 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:

14. Unnersjo-Jess D, Scott L, Sevilla SZ, Patrakka J, Blom H, Brismar H. Confocal super-resolution imaging of the glomerular filtration barrier enabled by tissue expansion. Kidney Int. 93:1008-1013, 2018. (mice). Royal Institute of Technology, Karolinska Institutet, Stockholm, Sweden.

15. Ougaard MKE, Kvist PH, Jensen HE, Hess C, Rune I, Sondergaard H. Murine nephrotoxic nephritis as a model of chronic kidney disease. Int J Nephrol Article ID 8424502 pg 1-12, 2018. (mice) Novo Nordisk, Univ Copenhagen, Denmark.

16. Pagan JD, Kitaoka M, Anthony RM. Engineered sialylation of pathogenic antibodies in vivo attenuates autoimmune disease. Cell. 172(3):564-577, 2018. (Mice) Massachusetts General Hospital and Harvard Medical School, Boston, MA.
Featured in "Research Highlights" McHugh J. Autoimmunity: Glycoengineering has therapeutic potential. Nat Rev Rheumatol. 14(3):121, 2018. Commentary

17. Zambrano S, Rodriguez PQ, Guo J, Möller-Hackbarth K, Schwarz A, Patrakka J. FYVE domain-containing protein ZFYVE28 regulates EGFR-signaling in podocytes but is not critical for the function of filtration barrier in mice. Sci Rep. 16;8(1):4712-. 2018. (Mice). Karolinska Institutet at Karolinska University Hospital Huddinge, Stockholm, Sweden.
 
18. Bideak A, Blaut A, Hoppe JM, Müller MB, Federico G, Eltrich N, Gröne HJ, Locati M, Vielhauer V. The atypical chemokine receptor 2 limits renal inflammation and fibrosis in murine progressive immune complex glomerulonephritis. Kidney Int. 93(4):826-841, 2018. (Mice). Ludwig-Maximilians-University Munich, Munich, Germany, German Cancer Research Center, Heidelberg, Germany, Humanitas Clinical and Research Center, Rozzano, Italy, Università degli Studi di Milano, Milan, Italy.
See Commentary:
Eller K, Rosenkranz AR. Atypical chemokine receptors—“chemokine PACMANs” as new therapeutic targets in glomerulonephritis Kidney Int. 93 (4): 774-775, 2018. Abstract

19. Ougaard ME, Jensen HE, Thuen ID, Petersen EG, Kvist PH. Inhibitors of the renin-angiotensin system ameliorates clinical and pathological aspects of experimentally induced nephrotoxic serum nephritis. Ren Fail. 40:640-648, 2018. (Mice) Novo Nordisk and University of Copenhagen , Frederiksberg , Denmark.

20. Ougaard ME, Sembach FE, Kvist PH, Tonnesen M, Frederiksen KS, Egfjord M, Jensen HE, Galsgaard ED. Temporal regulation of glomerular and cortical tubulointerstitial genes involved in the development of nephrotoxic serum nephritis. Nephron. 140(3):218-230, 2018.  (mice). Novo Nordisk A/S and University of Copenhagen, Copenhagen, Denmark.

21. Kim EY, Shotorbani PY, Dryer SE. TRPC6 inactivation does not affect loss of renal function in nephrotoxic serum glomerulonephritis in rats, but reduces severity of glomerular lesions. Biochem Biophys Rep. 17:139-150, 2019. (Rats) University of Houston and Baylor University, Houston, TX. Link
 
22. Gualdani R, Seghers F, Yerna X, Schakman O, Tajeddine N, Achouri Y, Tissir F, Devuyst O, Gailly P Mechanical activation of TRPV4 channels controls albumin reabsorption by proximal tubule cells. bioRxiv preprint posted online Feb. 1, 2019; doi: http://dx.doi.org/10.1101/537944.(mice). Université catholique de Louvain, University of Zurich

23. Arif E, et al. The motor protein Myo1c regulates transforming growth factor-β-signaling and fibrosis in podocytes. Kidney Intl, 96(1):139-158, 2019. (mice). Medical University of South Carolina, Charleston, University of Pennsylvania, TU Dresden, College of Charleston, Augusta University, GA. Research Gate Post

24. Müller MB, Hoppe JM, Bideak A, Lux M, Lindenmeyer MT, Müller S, Eltrich N, Ryffel B, et al. Exclusive expression of transmembrane TNF aggravates acute glomerulonephritis despite reduced leukocyte infiltration and inflammation. Kidney Int, 95: 75–93, 2019. (mice) Universität München, Ludwig-Maximilians-Universität München, Munich, Germany

25. Arif E, Solanki AK, Srivastava P, Rahman B, Fitzgibbon WR, Deng P, Budisavljevic MN, Baicu CF, Zile MR, Megyesi J, Janech MG, Kwon SH, Collier J, Schnellmann RG, Nihalani D. Mitochondrial biogenesis induced by the β2-adrenergic receptor agonist formoterol accelerates podocyte recovery from glomerular injury. Kidney Int. S0085-2538(19)30458-2. doi: 10.1016/j.kint.2019.03.023. [Epub ahead of print]2019 pii: (mice). Medical University of South Carolina, Ralph H. Johnson VA Medical Center, John C McClelland VA Hospital, College of Charleston, Augusta University, University of Arizona, Southern Arizona VA Health Care System.

26. 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

27. Solanki AK, Srivastava P, Rahman B, Lipschutz JH, Nihalani D, Arif E. The use of high-throughput transcriptomics to identify pathways with therapeutic significance in podocytes.  Int. J. Mol. Sci. 21: 274, 2020. (mice). Medical University of South Carolina

28. Wen Y, Rudemiller NP, Zhang J, et al. TNF-α in T lymphocytes attenuates renal injury and fibrosis during nephrotoxic nephritis.  Am J Physiol Renal Physiol.;318(1):F107-F116, 2020. (mice).  Durham Veterans Affairs and Duke University Medical Center, Durham, North Carolina.

29. Dylewski J, Tonsawan P, Garcia G, Lewis L, Blaine J.  Podocyte-specific knockout of the neonatal Fc receptor (FcRn) results in differential protection depending on the model of immune-mediated kidney disease. bioRxiv 2020.03.02.972851 (mice). University of Colorado Denver, Anschutz Medical Campus 

30. Liu F, Dai S, Feng D, et al. Distinct fate, dynamics and niches of renal macrophages of bone marrow or embryonic origins. Nat Commun. 2020;11(1):2280. Published 2020 May 8. doi:10.1038/s41467-020-16158-z. (mice). Tulane University School of Medicine, Brigham and Women’s Hospital and Harvard Medical School,Temple University Lewis Katz School of Medicine.

31. Jing C,  Castro-Dopico T,  Richoz N, et al. Macrophage metabolic reprogramming presents a therapeutic target in lupus nephritis. PNAS 117 (26):15160-15171, 2020. (mice). University of Cambridge, National Institute of Arthritis and Musculoskeletal and Skin Disease.

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