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BMC Nephrology
Published in: BMC Nephrology 1/2012

Open Access 01-12-2012 | Research article

Identification of nephropathy candidate genes by comparing sclerosis-prone and sclerosis-resistant mouse strain kidney transcriptomes

Authors: Ashraf El-Meanawy, Jeffery R Schelling, Sudha K Iyengar, Patrick Hayden, Shrinath Barathan, Katrina Goddard, Fatima Pozuelo, Essam Elashi, Viji Nair, Matthias Kretzler, John R Sedor

Published in: BMC Nephrology | Issue 1/2012

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Abstract

Background

The genetic architecture responsible for chronic kidney disease (CKD) remains incompletely described. The Oligosyndactyly (Os) mouse models focal and segmental glomerulosclerosis (FSGS), which is associated with reduced nephron number caused by the Os mutation. The Os mutation leads to FSGS in multiple strains including the ROP-Os/+. However, on the C57Bl/6J background the mutation does not cause FSGS, although nephron number in these mice are equivalent to those in ROP-Os/+ mice. We exploited this phenotypic variation to identify genes that potentially contribute to glomerulosclerosis.

Methods

To identify such novel genes, which regulate susceptibility or resistance to renal disease progression, we generated and compared the renal transcriptomes using serial analysis of gene expression (SAGE) from the sclerosis-prone ROP-Os/+ and sclerosis resistant C57-Os/+ mouse kidneys. We confirmed the validity of the differential gene expression using multiple approaches. We also used an Ingenuity Pathway Analysis engine to assemble differentially regulated molecular networks. Cell culture techniques were employed to confirm functional relevance of selected genes.

Results

A comparative analysis of the kidney transcriptomes revealed multiple genes, with expression levels that were statistically different. These novel, candidate, renal disease susceptibility/resistance genes included neuropilin2 (Nrp2), glutathione-S-transferase theta (Gstt1) and itchy (Itch). Of 34 genes with the most robust statistical difference in expression levels between ROP-Os/+ and C57-Os/+ mice, 13 and 3 transcripts localized to glomerular and tubulointerstitial compartments, respectively, from micro-dissected human FSGS biopsies. Network analysis of all significantly differentially expressed genes identified 13 connectivity networks. The most highly scored network highlighted the roles for oxidative stress and mitochondrial dysfunction pathways. Functional analyses of these networks provided evidence for activation of transforming growth factor beta (TGFβ) signaling in ROP-Os/+ kidneys despite similar expression of the TGFβ ligand between the tested strains.

Conclusions

These data demonstrate the complex dysregulation of normal cellular functions in this animal model of FSGS and suggest that therapies directed at multiple levels will be needed to effectively treat human kidney diseases.
Appendix
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Literature
1.
Chun MJ, Korbet SM, Schwartz MM, Lewis EJ: Focal segmental glomerulosclerosis in nephrotic adults: Presentation, prognosis, and response to therapy of the histologic variants. J Am Soc Nephrol. 2004, 15: 2169-2177. 10.1097/01.ASN.0000135051.62500.97.CrossRefPubMed
2.
Bakir AA, Bazilinski NG, Rhee HL, Ainis H, Dunea G: Focal segmental glomerulosclerosis. A common entity in nephrotic black adults. Arch Intern Med. 1989, 149: 1802-1804. 10.1001/archinte.1989.00390080072016.CrossRefPubMed
3.
Bakir AA, Share DS, Levy PS, Arruda JAL, Dunea G: Focal segmental glomerulosclerosis in adult African Americans. Clin Nephrol. 1996, 46: 306-311.PubMed
4.
Bonilla-Felix M, Parra C, Dajani T, Ferris M, Swinford RD, Portman RJ, et al: Changing patterns in the histopathology of idiopathic nephrotic syndrome in children. Kidney Int. 1999, 55: 1885-1890. 10.1046/j.1523-1755.1999.00408.x.CrossRefPubMed
5.
Gulati S, Sharma AP, Sharma RK, Gupta A: Changing trends of histopathology in childhood nephrotic syndrome. Amer J Kidney Dis. 1999, 34: 646-650. 10.1016/S0272-6386(99)70388-4.CrossRef
6.
Gipson DS, Trachtman H, Kaskel FJ, Greene TH, Radeva MK, Gassman JJ, et al: Clinical trial of focal segmental glomerulosclerosis in children and young adults. Kidney Int. 2011, 80: 868-878. 10.1038/ki.2011.195.CrossRefPubMedPubMedCentral
7.
Fencl F, Simkova E, Vondrak K, Janda J, Chadimova M, Stejskal J, et al: Recurrence of nephrotic proteinuria in children with focal segmental glomerulosclerosis after renal transplantation treated with plasmapheresis and immunoadsorption: case reports. Transplant Proc. 2007, 39: 3488-3490. 10.1016/j.transproceed.2007.09.045.CrossRefPubMed
8.
Fine RN: Recurrence of nephrotic syndrome/focal segmental glomerulosclerosis following renal transplantation in children. Pediatr Nephrol. 2007, 22: 496-502. 10.1007/s00467-006-0361-6.CrossRefPubMed
9.
Itami N, Akutus Y, Hattori M, Itoh K: Recurrence of nephrotic syndrome in focal segmental glomerulosclerosis after transplantation. Pediatr Nephrol. 1990, 4: 298-299.PubMed
10.
Kaplan JM, Kim SH, North KN, Rennke H, Correia LA, Tong HQ, et al: Mutations in ACTN4, encoding à-actinin-4, cause familial focal segmental glomerulosclerosis. Nat Genet. 2000, 24: 251-256. 10.1038/73456.CrossRefPubMed
11.
Winn MP, Conlon PJ, Lynn KL, Farrington MK, Creazzo T, Hawkins AF, et al: A Mutation in the TRPC6 Cation Channel Causes Familial Focal Segmental Glomerulosclerosis. Science. 2005, 308: 1801-1804. 10.1126/science.1106215.CrossRefPubMed
12.
Reiser J, Polu KR, Moller CC, Kenlan P, Altintas MM, Wei C, et al: TRPC6 is a glomerular slit diaphragm-associated channel required for normal renal function. Nat Genet. 2005, 37: 739-744. 10.1038/ng1592.CrossRefPubMedPubMedCentral
13.
Kopp JB: Gene expression in kidney using transgenic approaches. Exp Nephrol. 1997, 5: 157-167.PubMed
14.
Kao WH, Klag MJ, Meoni LA, Reich D, Berthier-Schaad Y, Li M, et al: MYH9 is associated with nondiabetic end-stage renal disease in African Americans. Nat Genet. 2008, 40: 1185-1192. 10.1038/ng.232.CrossRefPubMed
15.
Genovese G, Friedman DJ, Ross MD, Lecordier L, Uzureau P, Freedman BI, et al: Association of trypanolytic ApoL1 variants with kidney disease in African Americans. Science. 2010, 329: 841-845. 10.1126/science.1193032.CrossRefPubMedPubMedCentral
16.
Tzur S, Rosset S, Shemer R, Yudkovsky G, Selig S, Tarekegn A, et al: Missense mutations in the APOL1 gene are highly associated with end stage kidney disease risk previously attributed to the MYH9 gene. Hum Genet. 2010, 128: 345-350. 10.1007/s00439-010-0861-0.CrossRefPubMedPubMedCentral
17.
Butkus DE: Familial clustering of end-stage renal disease in Mississippi. J Miss State Med Assoc. 2002, 43: 71-77.PubMed
18.
Magnuson T, Epstein CJ: Oligosyndactyly: a lethal mutation in the mouse that results in mitotic arrest very early in development. Cell. 1984, 38: 823-833. 10.1016/0092-8674(84)90277-0.CrossRefPubMed
19.
Stewart AD, Stewart J: Studies on syndrome of diabetes insipidus associated with oligosyndactyly in mice. Am J Physiol. 1969, 217: 1191-1198.PubMed
20.
He C, Zalups RK, Henderson DA, Striker GE, Striker LJ: Molecular analysis of spontaneous glomerulosclerosis in Os/+ mice, a model with reduced nephron mass. Am J Physiol. 1995, 269: F266-F273.PubMed
21.
Zalups RK: The Os/+ mouse: a genetic animal model of reduced renal mass. Am J Physiol. 1993, 264: F53-F60.PubMed
22.
Esposito C, He CJ, Striker GE, Zalups RK, Striker LJ: Nature and severity of the glomerular response to nephron reduction is strain-dependent in mice. Am J Pathol. 1999, 154: 891-897. 10.1016/S0002-9440(10)65336-9.CrossRefPubMedPubMedCentral
23.
Lenz O, Zheng F, Vilar J, Doublier S, Lupia E, Schwedler S, et al: The inheritance of glomerulosclerosis in mice is controlled by multiple quantitative trait loci. Nephrol Dial Transplant. 1998, 13: 3074-3078. 10.1093/ndt/13.12.3074.CrossRefPubMed
24.
Wang Y, Heilig KO, Minto AW, Chen S, Xiang M, Dean DA, et al: Nephron-deficient Fvb mice develop rapidly progressive renal failure and heavy albuminuria involving excess glomerular GLUT1 and VEGF. Lab Invest. 2009, 90: 83-97.CrossRefPubMedPubMedCentral
25.
Velculescu VE, Zhang L, Vogelstein B, Kinzler KW: Serial analysis of gene expression. Science. 1995, 270: 484-487. 10.1126/science.270.5235.484.CrossRefPubMed
26.
Velculescu VE, Madden SL, Zhang L, Lash AE, Yu J, Rago C, et al: Analysis of human transcriptomes. Nat Genet. 1999, 23: 387-388.CrossRefPubMed
27.
Velculescu VE, Zhang L, Zhou W, Vogelstein J, Basrai MA, Bassett DE, et al: Characterization of the yeast transcriptome. Cell. 1997, 88: 243-251. 10.1016/S0092-8674(00)81845-0.CrossRefPubMed
28.
El-Meanawy MA, Schelling JR, Barathan S, Iyengar SK, Sedor JR: Serial analysis of gene expression (SAGE). Methods in Molecular Medicine: Renal Disease. Guide to Technical Approaches. Volume 86. Edited by: Goligorsky MS. 2003, The Humana Press, Totowa, 1
29.
El-Meanawy MA, Schelling JR, Pozuelo F, Churpek MM, Ficker EK, Iyengar S, et al: Use of serial analysis of gene expression to generate kidney expression libraries. Am J Physiol Renal Physiol. 2000, 279: F383-F392.PubMed
30.
He CJ, Esposito C, Phillips C, Zalups RK, Henderson DA, Striker GE, et al: Dissociation of glomerular hypertrophy, cell proliferation, and glomerulosclerosis in mouse strains heterozygous for a mutation (Os) which induces a 50% reduction in nephron number. J Clin Invest. 1996, 97: 1242-1249. 10.1172/JCI118539.CrossRefPubMedPubMedCentral
31.
Kaufman JM, Hardy R, Hayslett JP: Age-dependent characteristics of compensatory renal growth. Kidney Int. 1975, 8: 21-26. 10.1038/ki.1975.72.CrossRefPubMed
32.
Sambrook J, Fritsch EF, Maniatis T: Molecular cloning: a laboratory manual. 1989, Cold Springs Harbor, Cold Springs Harbor, 2
33.
Cooper GF, Herskovits E: A Bayesian method for the induction of probabilistic networks from data. Mach Learn. 1992, 9: 309-347.
34.
Schoenberg BS: Calculating Confidence Intervals for Rates and Ratios. Neuroepidemiology. 1983, 2: 257-265. 10.1159/000110529.CrossRef
35.
van Kampen AH, van Schaik BD, Pauws E, Michiels EM, Ruijter JM, Caron HN, et al: USAGE: a web-based approach towards the analysis of SAGE data. Serial Analysis of Gene Expression. Bioinformatics. 2000, 16: 899-905. 10.1093/bioinformatics/16.10.899.CrossRefPubMed
36.
Kal AJ, van Zonneveld AJ, Benes V, van den Berg M, Koerkamp MG, Albermann K, et al: Dynamics of gene expression revealed by comparison of serial analysis of gene expression transcript profiles from yeast grown on two different carbon sources [In Process Citation]. MolBiol Cell. 1999, 10: 1859-1872.
37.
Laemmli EK: Cleavage of structural proteins during the assembly of the head of bacteriophage T4. Nature. 1970, 227: 680-685. 10.1038/227680a0.CrossRefPubMed
38.
Abe M, Harpel JG, Metz CN, Nunes I, Loskutoff DJ, Rifkin DB: An Assay for Transforming Growth Factor-β Using Cells Transfected with a Plasminogen Activator Inhibitor-1 Promoter-Luciferase Construct. Anal Biochem. 1994, 216: 276-284. 10.1006/abio.1994.1042.CrossRefPubMed
39.
Khan S, Lakhe-Reddy S, McCarty JH, Sorenson CM, Sheibani N, Reichardt LF, et al: Mesangial Cell Integrin [alpha]v[beta]8 Provides Glomerular Endothelial Cell Cytoprotection by Sequestering TGF-[beta] and Regulating PECAM-1. Am J Pathol. 2011, 178: 609-620. 10.1016/j.ajpath.2010.10.031.CrossRefPubMedPubMedCentral
40.
Berthier CC, Zhang H, Schin M, Henger A, Nelson RG, Yee B, et al: Enhanced expression of Janus kinase-signal transducer and activator of transcription pathway members in human diabetic nephropathy. Diabetes. 2009, 58: 469-477.CrossRefPubMedPubMedCentral
41.
Tusher VG, Tibshirani R, Chu G: Significance analysis of microarrays applied to the ionizing radiation response. Proc Natl Acad Sci USA. 2001, 98: 5116-5121. 10.1073/pnas.091062498.CrossRefPubMedPubMedCentral
42.
He L, Sun Y, Patrakka J, Mostad P, Norlin J, Xiao Z, et al: Glomerulus-specific mRNA transcripts and proteins identified through kidney expressed sequence tag database analysis. Kidney Int. 2007, 71: 889-900. 10.1038/sj.ki.5002158.CrossRefPubMed
43.
Nystrom J, Fierlbeck W, Granqvist A, Kulak SC, Ballermann BJ: A human glomerular SAGE transcriptome database. BMC Nephrol. 2009, 10: 13-27. 10.1186/1471-2369-10-13.CrossRefPubMedPubMedCentral
44.
Margulies EH, Kardia SL, Innis JW: Identification and prevention of a GC content bias in SAGE libraries. Nucleic Acids Res. 2001, 29: E60-10.1093/nar/29.12.e60.CrossRefPubMedPubMedCentral
45.
Bennett MR, Czech KA, Arend LJ, Witte DP, Devarajan P, Potter SS: Laser Capture Microdissection-Microarray Analysis of Focal Segmental Glomerulosclerosis Glomeruli. Nephron Exp Nephrol. 2007, 107: e30-e40. 10.1159/000106775.CrossRefPubMed
46.
Pergola PE, Krauth M, Huff JW, Ferguson DA, Ruiz S, Meyer CJ, et al: Effect of bardoxolone methyl on kidney function in patients with T2D and Stage 3b-4 CKD. Am J Nephrol. 2011, 33: 469-476. 10.1159/000327599.CrossRefPubMed
47.
Bai Y, Yang C, Hu K, Elly C, Liu YC: Itch E3 ligase-mediated regulation of TGF-beta signaling by modulating smad2 phosphorylation. Mol Cell. 2004, 15: 825-831. 10.1016/j.molcel.2004.07.021.CrossRefPubMed
48.
Reich HN, Tritchler D, Cattran DC, Herzenberg AM, Eichinger F, Boucherot A, et al: A Molecular Signature of Proteinuria in Glomerulonephritis. PLoS One. 2010, 5: e13451-10.1371/journal.pone.0013451.CrossRefPubMedPubMedCentral
49.
Kaplan J, Pollak MR: Familial focal segmental glomerulosclerosis. Curr Opin Nephrol Hypertens. 2001, 10: 183-187. 10.1097/00041552-200103000-00005.CrossRefPubMed
50.
Striker LJ: Nephron reduction in man–lessons from the Os mouse. Nephrol Dial Transplant. 1998, 13: 543-545. 10.1093/ndt/13.3.543.CrossRefPubMed
51.
Barathan S, Konieczkowski M, El-Meanawy MA, Khan S, Wang B, Dodig T, et al: Expression analysis demonstrates the cell guidance signal neuropilin 2b is reduced in sclerosis-prone ROP-Os/+ but not sclerosis-resistant C57-Os/+ mouse kidneys. J Am Soc Nephrol. 2001, 12: 809A-Ref Type: Abstract
52.
Gluzman-Poltorak Z, Cohen T, Herzog Y, Neufeld G: Neuropilin-2 is a receptor for the vascular endothelial growth factor (VEGF) forms VEGF-145 and VEGF-165. J BiolChem. 2000, 275: 29922-
53.
Bock BC, Tagscherer KE, Fassl A, Kr+ñmer A, Oehme I, Zentgraf HW, et al: The PEA-15 Protein Regulates Autophagy via Activation of JNK. J BiolChem. 2010, 285: 21644-21654.
54.
Oriente F, Iovino S, Cassese A, Romano C, Miele C, Troncone G, et al: Overproduction of phosphoprotein enriched in diabetes (PED) induces mesangial expansion and upregulates protein kinase C-beta activity and TGF-beta1 expression. Diabetologia. 2009, 52: 2642-2652. 10.1007/s00125-009-1528-z.CrossRefPubMed
55.
Condorelli G, Vigliotta G, Iavarone C, Caruso M, Tocchetti CG, Andreozzi F, et al: PED/PEA-15 gene controls glucose transport and is overexpressed in type 2 diabetes mellitus. EMBO J. 1998, 17: 3858-3866. 10.1093/emboj/17.14.3858.CrossRefPubMedPubMedCentral
56.
Omerovic J, Santangelo L, Puggioni EM-R, Marrocco J: Dall'Armi C, Palumbo C et al.: The E3 ligase Aip4/Itch ubiquitinates and targets ErbB-4 for degradation. The. FASEB J. 2007, 21: 2849-2862. 10.1096/fj.06-7925com.CrossRefPubMed
57.
Azakir BA, Angers A: Reciprocal regulation of the ubiquitin ligase Itch and the epidermal growth factor receptor signaling. Cell Signal. 2009, 21: 1326-1336. 10.1016/j.cellsig.2009.03.020.CrossRefPubMed
58.
Lallemand F, Seo SR, Ferrand N, Pessah M, L'Hoste S, Rawadi G, et al: AIP4 restricts transforming growth factor-beta signaling through a ubiquitination-independent mechanism. J BiolChem. 2005, 280: 27645-27653.
59.
Yang C, Zhou W, Jeon MS, Demydenko D, Harada Y, Zhou H, et al: Negative regulation of the E3 ubiquitin ligase itch via Fyn-mediated tyrosine phosphorylation. Mol Cell. 2006, 21: 135-141. 10.1016/j.molcel.2005.11.014.CrossRefPubMed
60.
Magnifico A, Ettenberg S, Yang C, Mariano J, Tiwari S, Fang S, et al: WW domain HECT E3s target Cbl RING finger E3s for proteasomal degradation. J BiolChem. 2003, 278: 43169-43177.
61.
Verma R, Wharram B, Kovari I, Kunkel R, Nihalani D, Wary KK, et al: Fyn binds to and phosphorylates the kidney slit diaphragm component nephrin. J BiolChem. 2003, 278: 20716-20723.
62.
Azhibekov TA, Wu Z, Padiyar A, Bruggeman LA, Simske JS: TM4SF10 and ADAP interaction in podocytes: role in Fyn activity and nephrin phosphorylation. Am J Physiol Cell Physiol. 2011, 301: C1351-C1359. 10.1152/ajpcell.00166.2011.CrossRefPubMedPubMedCentral
63.
Huber TB, Kwoh C, Wu H, Asanuma K, Godel M, Hartleben B, et al: Bigenic mouse models of focal segmental glomerulosclerosis involving pairwise interaction of CD2AP, Fyn, and synaptopodin. J Clin Invest. 2006, 116: 1337-1345. 10.1172/JCI27400.CrossRefPubMedPubMedCentral
64.
Thiele BJ, Doller A, Kahne T, Pregla R, Hetzer R, Regitz-Zagrosek V: RNA-binding proteins heterogeneous nuclear ribonucleoprotein A1, E1, and K are involved in post-transcriptional control of collagen I and III synthesis. Circ Res. 2004, 95: 1058-1066. 10.1161/01.RES.0000149166.33833.08.CrossRefPubMed
65.
Nkova-Kostova AT, Liby KT, Stephenson KK, Holtzclaw WD, Gao X, Suh N, et al: Extremely potent triterpenoid inducers of the phase 2 response: correlations of protection against oxidant and inflammatory stress. Proc Natl Acad Sci USA. 2005, 102: 4584-4589. 10.1073/pnas.0500815102.CrossRef
66.
Yang Y, Kao MT, Chang CC, Chung SY, Chen CM, Tsai JJ, et al: Glutathione S-transferase T1 deletion is a risk factor for developing end-stage renal disease in diabetic patients. Int J Mol Med. 2004, 14: 855-859.PubMed
67.
Turk T, Leeuwis JW, Gray J, Torti SV, Lyons KM, Nguyen TQ, et al: BMP Signaling and Podocyte Markers Are Decreased in Human Diabetic Nephropathy in Association With CTGF Overexpression. J HistochemCytochem. 2009, 57: 623-631.
68.
Mason RM: Connective tissue growth factor(CCN2), a pathogenic factor in diabetic nephropathy. What does it do? How does it do it?. J Cell Commun Signal. 2009, 3: 95-104. 10.1007/s12079-009-0038-6.CrossRefPubMedPubMedCentral
69.
Umezono T, Toyoda M, Kato M, Miyauchi M, Kimura M, Maruyama M, et al: Glomerular expression of CTGF, TGF-beta 1 and type IV collagen in diabetic nephropathy. J Nephrol. 2006, 19: 751-757.PubMed
70.
Hudkins KL, Giachelli CM, Eitner F, Couser WG, Johnson RJ, Alpers CE: Osteopontin expression in human crescentic glomerulonephritis. Kidney Int. 2000, 57: 105-116.CrossRefPubMed
71.
Pichler R, Giachelli CM, Lombardi D, Pippin J, Gordon K, Alpers CE, et al: Tubulointerstitial disease in glomerulonephritis: Potential role of osteopontin (uropontin). Am J Pathol. 1994, 144: 915-926.PubMedPubMedCentral
72.
Mooney A, Jackson K, Bacon R, Streuli C, Edwards G, Bassuk J, et al: Type IV collagen and laminin regulate glomerular mesangial cell susceptibility to apoptosis via beta(1) integrin-mediated survival signals. Am J Pathol. 1999, 155: 599-606. 10.1016/S0002-9440(10)65155-3.CrossRefPubMedPubMedCentral
73.
Brera-Abeleda MA, Nishimura C, Smith JL, Sethi S, McRae JL, Murphy BF, et al: Variations in the complement regulatory genes factor H (CFH) and factor H related 5 (CFHR5) are associated with membranoproliferative glomerulonephritis type II (dense deposit disease). J Med Genet. 2006, 43: 582-589.CrossRef
74.
Matsuda J, Kido M, Tadano-Aritomi K, Ishizuka I, Tominaga K, Toida K, et al: Mutation in saposin D domain of sphingolipid activator protein gene causes urinary system defects and cerebellar Purkinje cell degeneration with accumulation of hydroxy fatty acid-containing ceramide in mouse. Hum Mol Genet. 2004, 13: 2709-2723. 10.1093/hmg/ddh281.CrossRefPubMed
75.
Lindenmeyer MT, Eichinger F, Sen K, Anders HJ, Edenhofer I, Mattinzoli D, et al: Systematic analysis of a novel human renal glomerulus-enriched gene expression dataset. PLoS One. 2010, 5: e11545-10.1371/journal.pone.0011545.CrossRefPubMedPubMedCentral
Metadata
Title
Identification of nephropathy candidate genes by comparing sclerosis-prone and sclerosis-resistant mouse strain kidney transcriptomes
Authors
Ashraf El-Meanawy
Jeffery R Schelling
Sudha K Iyengar
Patrick Hayden
Shrinath Barathan
Katrina Goddard
Fatima Pozuelo
Essam Elashi
Viji Nair
Matthias Kretzler
John R Sedor
Publication date
01-12-2012
Publisher
BioMed Central
Published in
BMC Nephrology / Issue 1/2012
Electronic ISSN: 1471-2369
DOI
https://doi.org/10.1186/1471-2369-13-61

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