Ekspresi dan Aktivasi Sub Unit p65 NF-κB pada Sel Mononuklear Penderita Sindrom Nefrotik Resisten Steroid Anak
DOI:
https://doi.org/10.21776/ub.jkb.2009.025.03.7Abstract
Resitance  to  steroid  therapy  is  a  poor  prognosis  sign  for  nephrotic  syndrome,  but  this  mechanism is  still unclear. NF-κB has been reported to affect the glucocorticoid at the T cell through the transrepression in  the glucocorticoid  receptor .  Until  know,  this  study  was  still  limited.  The  aim  of  this  study  was  to  show  the  difference expression  and  activation  of  NF-κB  p65  subunit  between  childhood  SRNS  and  SSNS  patient.  Cross  sectional study  was  conducted  during  January  2009  to  December  2009  in  the  Saiful Anwar  General  Hospital  and Biomedic  Laboratory  Brawijaya  University.  Expression  and  activation  of  NF-κB  p65  subunit  were  determine  by immunochemistry  staining  by  counting  the  amount  of  lymphocyte  that  express  and  activate  NF-κB  p65  subunit among  200  lymphocytes  under  light  microscope  with  1000  magnification.  Results  was  analyzed  by independent  t  test  with  95%  CI  (p<0,05)  and  Pearson  correlation.  The  result  of  this  study  revealed  no significant  difference  of  expression  of  NF-κB p65  subunit  between  SRNS and  SSNS  (p=0,153),  but  there  was an increase activation of NF-κB p65 subunit in the SRNS patients (p=0,000).Downloads
References
Bagga A, Mantan M. Nephrotic syndrome in children. Indian J Med Res. 2005;122:13-28.
UKK Nefrologi. Konsensus Tata Laksana Sindrom Nefrotik Idiopatik pada Anak. Jakarta:2008
Orth S, Ritz E. The Nephrotic Syndrome. NEJM. 1998;23:1202-11.
Cho, Hong EH, Lee TH, Ko CW. Pathophysiology of minimal change nephrotic syndrome and focal segmental glomerulosclerosis. Nephrology. 2007;12:S1 1S14.
Israel KG. NF-κB in life/death decisions: an introduction. Cell Death and Differentiation. 2006;13:685-686.
Perkins. Integrating cell-signalling pathways with NF-κB and IKK function. Molecular Cell Biology 2007;8:49-62.
Sahali.T ranscriptional and Post-T ranscriptional Alterations of IκBα in Active Minimal-Change Nephrotic Syndrome. J Am Soc Nephrol.2001;12:164858.
Hernandez, Guerrero GC, Egido J. In situ non-radioactive detection of nuclear factors in paraffin sections by Southwestern hi stochemi st ry. Kidney Int. 1999;55:209-214.
Mezzano S, Barria M, Droguett MA, et al. Tubular NF-κB and AP-1 activation in human proteinuric renal disease. Kidney International. 2001;60:136677.
Schachter. Increased Nuclear Factor-κB and Angiotensinogen Gene Expression in Posttransplant Recurrent Focal Segmental Glomerulosclerosi s. Transplantation. 2000;70(7):1107-10.
Aviles, Vehaskari VM, Manning J, Ochoe AC, Zea AH. Decreased expression of T-cell NF-κB p65 subunit in steroid-resistant nephrotic12. Hong Y, Ruo P, Jun H, Jun H. Relations of NF-KB Activity in the Kidney of Children with Primary Nephrotic Syndrome to Clinical Manifestations, Pathological T ypes, and Urinary Protein T ypes. China Med J. 2005;118(10):854-6.
Hodson EM, Willis NS, Craig JC. Corticosteroid therapy for nephrotic syndrome in children. Cochrane Database of Systematic Reviews. 2007;4:1-61.
Walker KB, Potter JM, House AK.Interleukin 2 synthesis in the presence of steroids:a model of steroid resistance. Clin. exp. Immunol. 1987;68:162-167.
Kam JC, Szefler SJ, Surs W, Sher ER, Leung DY. Combination IL-2 and IL-4 reduces glucocorticoid receptor-binding affinity and T cell response to glucocorticoids. The Journal of Immunology.1993;151(7):3460-3466.
Araya, Diaz, Wasserfall, et al. T regulatory cell function in idiopathic minimal lesion nephrotic syndrome. Pediatr Nephrol. 2009;24:16918.
Wong HK, Kammer GM, Dennis G, T sokos GC. Abnormal NF-{kappa}B Activity in T Lymphocytes from Patients with Systemic Lupus Erythematosus Is Associated with Decreased p65-RelA Protein Expression. J. Immunol. 1999;163:1682-1689.
Ray A, Prefontaine KE. Physical association and functional antagonism between the p65 subunit of transcription factor NF-κB and the glucocorticoid receptor.Proc.Natl.Acad.Sci.USA. 1994;91:752-56.
McKay , Cidlowski JA. Cross-Talk between nuclear factor-κB and the steroid hormone receptors; mechanism of mutual antagonism. Mol Endo.1998;12:4556
Cao, Lu S, Zhao CDR. Abnormal DNA-binding of transcription factors in minimal change nephrotic syndrome. Pediatr Nephro. 2001;16:7905.
Ito K, Chung KF, Adcock IA. Update on glucocorticoid action and resistance. J Allergy Clin Immunol. 2006;117(3):522-43.
McKay, Cidlowski JA. Molecular Control of Immune/Inflammatory Responses: Interactions Between Nuclear Factor-κB and SteroidReceptor-Signaling Pathways. Endocrine Reviews. 1999; 20(4): 43559.
Jain J, Loh C, Rao A. Transcriptional regulation of the IL-2 gene. Curr. Opin. Immunol.1995;7:333.
Downloads
Published
Issue
Section
License
Authors who publish with this journal agree to the following terms:- Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution License that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.
- Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.
- Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (See The Effect of Open Access).
