« Previous
Next »
Human Pathology
Volume 41, Issue 12
, Pages 1682-1693
, December 2010
Activation of the transcription factor c-Jun in acute cellular and antibody-mediated rejection after kidney transplantation
References
- Transcription factor Ets-1 is essential for mesangial matrix remodeling. Kidney Int. 2006;70:298–305
- . Suppression of NF-kappa B and AP-1 activation by glucocorticoids in experimental glomerulonephritis in rats: molecular mechanisms of anti-nephritic action. Biochim Biophys Acta. 1997;1362:252–262
- . Chronic inhibition of nuclear factor-kappaB attenuates renal injury in the 5/6 renal ablation model. Am J Physiol Renal Physiol. 2007;292:F92–F99
- . In situ non-radioactive detection of nuclear factors in paraffin sections by Southwestern histochemistry. Kidney Int. 1999;55:209–214
- . The regulation of AP-1 activity by mitogen-activated protein kinases. J Biol Chem. 1995;270:16483–16486
- . Ap-1 function and regulation. Curr Opin Cell Biol. 1997;9:240–246
- . Oncogenic and transcriptional cooperation with Ha-Ras requires phosphorylation of c-Jun on serines 63 and 73. Nature. 1991;354:494–496
- JNK1: a protein kinase stimulated by UV light and Ha-Ras that binds and phosphorylates the c-Jun activation domain. Cell. 1994;76:1025–1037
- Activation and cellular localization of the p38 and JNK MAPK pathways in rat crescentic glomerulonephritis. Kidney Int. 2003;64:2121–2132
- . Cell-type-specific activation of mitogen-activated protein kinases in PAN-induced progressive renal disease in rats. Biochem Biophys Res Commun. 2004;323:1–8
- A pathogenic role for c-Jun amino-terminal kinase signaling in renal fibrosis and tubular cell apoptosis. J Am Soc Nephrol. 2007;18:472–484
- Glomerular and tubular induction of the transcription factor c-Jun in human renal disease. J Pathol. 2007;213:219–228
- A pathogenic role for JNK signaling in experimental anti-GBM glomerulonephritis. Kidney Int. 2007;72:698–708
- Suppression of alloreactivity and allograft rejection by SP600125, a small molecule inhibitor of c-Jun N-terminal kinase. Transplantation. 2007;83:1358–1364
- Banff '05 Meeting Report: differential diagnosis of chronic allograft injury and elimination of chronic allograft nephropathy (‘CAN’). Am J Transplant. 2007;7:518–526
- . Insights into acute and chronic rejection. Transplant Proc. 1996;28:2081–2084
- . New insights into mechanisms of allograft rejection. Am J Med Sci. 1997;313:257–263
- JNK is required for effector T-cell function but not for T-cell activation. Nature. 2000;405:91–94
- . c-Jun N-terminal kinases as potential therapeutic targets. Expert Opin Ther Targets. 2007;11:1339–1353
- . c-Jun NH(2)-terminal kinase (JNK)1 and JNK2 signaling pathways have divergent roles in CD8(+) T cell-mediated antiviral immunity. J Exp Med. 2002;195:801–810
- . Pathologic features of acute renal allograft rejection associated with donor-specific antibody. Analysis using the Banff grading schema. Transplantation. 1996;61:1586–1592
- Acute humoral rejection in kidney transplantation: II. Morphology, immunopathology, and pathologic classification. J Am Soc Nephrol. 2002;13:779–787
- Endothelial C4d deposition is associated with inferior kidney allograft outcome independently of cellular rejection. Nephrol Dial Transplant. 2001;16:2058–2066
- . Infiltrating cell types in transplant glomerulitis: relationship to peritubular capillary C4d deposition. Am J Kidney Dis. 2005;45:1084–1089
- . Monocytes and peritubular capillary C4d deposition in acute renal allograft rejection. Kidney Int. 2003;63:1888–1893
- Relationship between macrophage infiltration of renal allografts and chronic renal impairment. Transplant Proc. 1997;29:2783–2786
- . Complement activates the c-Jun N-terminal kinase/stress-activated protein kinase in glomerular epithelial cells. J Immunol. 2002;169:2594–2601
- . Endoplasmic reticulum stress in the kidney. Clin Exp Nephrol. 2008;12:317–325
- . Adenovirus-mediated overexpression of c-Jun and c-Fos induces intercellular adhesion molecule-1 and monocyte chemoattractant protein-1 in human endothelial cells. Arterioscler Thromb Vasc Biol. 1999;19:2078–2084
- Effects of glucocorticoids on activation of c-jun N-terminal, extracellular signal-regulated, and p38 MAP kinases in human pulmonary endothelial cells. Biochem Pharmacol. 2001;62:1719–1724
- . N-Acetyl cysteine ameliorates ischemic renal failure. Am J Physiol. 1997;272:F292–F298
- . The stress-activated protein kinases are major c-Jun amino-terminal kinases activated by ischemia and reperfusion. J Biol Chem. 1994;269:26546–26551
- . Inhibition of c-Jun N-terminal kinase ameliorates apoptosis induced by hydrogen peroxide in the kidney tubule epithelial cells (NRK-52E). Nephron. 2002;91:142–147
- . Epithelial to mesenchymal transition during late deterioration of human kidney transplants: the role of tubular cells in fibrogenesis. Am J Transplant. 2005;5:1367–1374
- . Blockade of the c-Jun amino terminal kinase prevents crescent formation and halts established anti-GBM glomerulonephritis in the rat. Lab Invest. 2009;89:470–484
☆ This work had no funding support and the authors report no conflict of interest.
PII: S0046-8177(10)00166-8
doi: 10.1016/j.humpath.2010.04.016
© 2010 Elsevier Inc. All rights reserved.
« Previous
Next »
Human Pathology
Volume 41, Issue 12
, Pages 1682-1693
, December 2010
