201
Views
11
CrossRef citations to date
0
Altmetric
Review

Gremlin – a putative pathogenic player in progressive renal disease

, , , &
Pages 523-526 | Published online: 02 Mar 2005

Bibliography

  • PETERS H, NOBLE NA, BORDER WA: Transforming growth factor-I 3 in human glomerular injury. Cun: Opin. Nephrol. Hypertens. (1997) 6(4):389–393.
  • CLARKSON MR, GUPTA S, MURPHY M, MARTIN F, GODSON C, BRADY HR: Connective tissue growth factor: a potential stimulus for glomerulosclerosis and tubulointerstitial fibrosis in progressive renal disease. Cun: Opin. Nephrol. Hypertens. (1999) 8(5):543–548.
  • STRUTZ E ZEISBERG M, ZIYADEH FN etal.: Role of basic fibroblast growth factor-2 in epithelial-mesenchymal transformation. Kidney Int. (2002) 61(5):1714–1728.
  • DOLAN, V, HENSEY C, BRADY HR: Diabetic nephropathy: renal development gone awry? Pediatr. Nephrol. (2003) 18(2):75–84.
  • LAPPIN DW, HENSEY C, MCMAHON R, GODSON C, BRADY HR: Gremlins, glomeruli and diabetic nephropathy. Curr. Opin. Nephrol. Hypertens. (2000) 9(5):469–472.
  • HSU DR, ECONOMIDES AN, WANG X, EIMON PM, HARLAND RM: The Xeriopus dorsalizing factor Gremlin identifies a novel family of secreted proteins that antagonize BMP activities. Mai Cell (1998) 1(5):673–683.
  • •The first description of gremlin in development.
  • MERINO R, RODRIGUEZ-LEON J, MACIAS D, GANAN Y, ECONOMIDES AN, HURLE JM: The BMP antagonist Gremlin regulates outgrowth, chondrogenesis and programmed cell death in the developing limb. Development (1999) 126(23):5515–5522.
  • TOPOL LZ, MARX M, LAUGIER D: Identification of drm, a novel gene whose expression is suppressed in transformed cells and which can inhibit growth of normal but not transformed cells in culture. Mel. Cell. Biol. (1997) 17(8):4801–4810.
  • •The first description of drm/gremlin and an insight into its role in the cell cycle.
  • MCMAHON R, MURPHY M, CLARKSON M et al.: IHG-2, a mesangial cell gene induced by high glucose, is human gremlin. Regulation by extracellular glucose concentration, cyclic mechanical strain, and transforming growth factor-I31. j. Biol. Chem. (2000) 275(14):9901–9904.
  • ••Describes gremlin induction by high glucose, TGF-I3 and cyclical mechanical strain in vifro, as well as raised levels in the diabetic kidney in vivo.
  • BALEMANS W, VAN HUL W: Extracellular regulation of BMP signaling in vertebrates: a cocktail of modulators. Dev. Biol. (2002) 250(2):231–250.
  • ••Describes the mechanisms of BMP regulation in a variety of systems.
  • SHI W, ZHAO J, ANDERSON KD etal.: Gremlin negatively modulates BMP-4 induction of embryonic mouse lung branching morphogenesis. Am. j Physiol. Lung Cell. Mol. Physiol (2001) 280(5):1030–1039.
  • LU MM, YANG H, ZHANG L, SHU W BLAIR DG, MORRISEY EE: The bone morphogenic protein antagonist gremlin regulates proximal-distal patterning of the lung. Dev. Dpi. (2001) 222(4):667–680.
  • ZUNIGA A, HARAMIS AP, MCMAHON AP, ZELLER R: Signal relay by BMP antagonism controls the SHH/FGF4 feedback loop in vertebrate limb buds. Nature (1999) 401(6753):598–602.
  • ••Outlines the FGF/SHH pathway andpotential roles and regulators of gremlin.
  • MASS RL, ZELLER R, WOYCHIK RP, VOGT TF, LEDER P: Disruption of formin-encoding transcripts in two mutant limb deformity alleles. Nature (1990) 346(6287):853–855.
  • DUDLEY AT, LYONS KM, ROBERTSON EJ: A requirement for bone morphogenetic protein-7 during development of the mammalian kidney and eye. Genes Dev. (1995) 9(22):2795–2807.
  • •Illustrates the importance of BMP-7 in renal development by describing the knockout mouse.
  • DUDLEY AT, GODIN RE, ROBERTSON EJ: Interaction between FGF and BMP signaling pathways regulates development of metanephric mesenchyme. Genes Dev. (1999) 13(12):1601–1613.
  • KARSENTY G, LUO G, HOFMANN C, BRADLEY A: BMP 7 is required for nephrogenesis, eye development, and skeletal patterning. Ann. NY Acad. Sci. (1996) 785:98–107.
  • MIYAZAKI Y, OSHIMA K, FOGO A, HOGAN BL, ICHIKAWA I: Bone morphogenetic protein 4 regulates the budding site and elongation of the mouse ureter. j OM. Invest. (2000) 105 (7):863–873.
  • PISCIONE TD, YAGER TD, GUPTA IR et al: BMP-2 and OP-1 exert direct and opposite effects on renal branching morphogenesis. Am. I Physiol (1997) 273(6 Pt 2):F961–F975.
  • DUNN NR, WINNIER GE, HARGETT LK, SCHRICK JJ, FOGO AB, HOGAN BL: Haploinsufficient phenotypes in Bmp4 heterozygous null mice and modification by mutations in Gli3 and Alx4. Dev. Biol. (1997) 188(2):235–247.
  • DOLAN V, HENSEY C, MARTIN F, BRADY HR: Gremlin and the developing xerropus pronephros. j Am. Soc. Nephrol (2002) 13(SA-FC124).
  • MURPHY M, MACMAHON R, CLARKSON M et al: Induction of gremlin expression in the remnant kidney in vivo and during TGF-induced epithelial mesenchymal transformation in vitro. Am. Soc. Nephrol (2000) 11(3298A).
  • SIMON M, MARESH JG, HARRIS SE et al.: Expression of bone morphogenetic protein-7 mRNA in normal and ischemic adult rat kidney. Am. J Physiol (1999) 276(3 Pt 2):F382–F389.
  • WANG SN, LAPAGE J, HIRSCHBERG R: Loss of tubular bone morphogenetic protein-7 in diabetic nephropathy. J. Am. Soc Nephrol. (2001) 12(11):2392–2399.
  • ••Outlines the changes in gremlin and itstarget BMP-7 in an animal model of diabetic nephropathy.
  • ALMANZAR MM, FRAZIER KS, DUBE PH etal.: Osteogenic protein-1 mRNA expression is selectively modulated after acute ischemic renal injury. I Am. Soc. Nephrol (1998) 9(8):1456–1463.
  • HRUSKA KA, GUO G, WOZNIAK M et al.: Osteogenic protein-1 prevents renal fibrogenesis associated with ureteral obstruction. Am. j Physiol. Rena] Physiol (2000) 279(1):F130–F143.
  • •Comparison of the effects BMP-7 and ACE inhibitor treatment in a model of acute renal failure.
  • MORRISSEY J, HRUSKA K, GUO G, WANG S, CHEN Q, KLAHR S: Bone morphogenetic protein-7 improves renal fibrosis and accelerates the return of renal function. I Am. Soc. Nephrol. (2002) 13\(Suppl. 1):514–521.
  • GOULD SE, DAY M, JONES SS, DORAI H: BMP-7 regulates chemokine, cytokine, and hemodynamic gene expression in proximal tubule cells. Kidney Int. (2002) 61(1):51–60.
  • MURPHY M, GODSON C, CANNON S et al.: Suppression subtractive hybridization identifies high glucose levels as a stimulus for expression of connective tissue growth factor and other genes in human mesangial cells. Biol. Chem. (1999) 274(9):5830–5834.
  • •Original description of the upregulation of gremlin (IHG-2) by high glucose levels.
  • WANG SN, LAPAGE J, HIRSCHBERG R:Role of glomerular ultrafiltration of growth factors in progressive interstitial fibrosis in diabetic nephropathy. Kidney Int. (2000) 57(3):1002–1014.
  • SHARMA K, ZIYADEH FN: Hyperglycemia and diabetic kidney disease. The case for transforming growth factor-I3 as a key mediator. Diabetes (1995) 44(10):1139–1146.
  • RISER BL, LADSON-WOFFORD S, SHARBA A etal.: TGF-I3 receptor expression and binding in rat mesangial cells: modulation by glucose and cyclic mechanical strain. Kidney Int. (1999) 56(2):428–439.
  • TOPOL LZ, BARDOT B, ZHANG Q et al: Biosynthesis, post-translation modification, and functional characterization of DrmiGremlin. Biol. Chem. (2000) 275(12):8785–8793.
  • CHEN B, ATHANASIOU M, GU Q, BLAIR DG: Drm/Gremlin transcriptionally activates p21(Cipl) via a novel mechanism and inhibits neoplastic transformation. Biochem. Biophys. Res. Commun. (2002) 295(5):1135–1141.
  • MONKAWA T, HIROMURA K, WOLF G, SHANKLAND SJ: The hypertrophic effect of transforming growth factor-I3 is reduced in the absence of cyclin-dependent kinase-inhibitors p21 and p27. jAm. Soc. Nephrol. (2002) 13(5):1172–1178. Affiliation

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.