دورية أكاديمية

Activation of the transcription factor c-Jun in acute cellular and antibody-mediated rejection after kidney transplantation.

التفاصيل البيبلوغرافية
العنوان: Activation of the transcription factor c-Jun in acute cellular and antibody-mediated rejection after kidney transplantation.
المؤلفون: Kobayashi A; Division of Kidney and Hypertension, Department of Internal Medicine, The Jikei, University School of Medicine, Tokyo, Japan. akimitsu@kk.iij4u.or.jp, Takahashi T, Horita S, Yamamoto I, Yamamoto H, Teraoka S, Tanabe K, Hosoya T, Yamaguchi Y
المصدر: Human pathology [Hum Pathol] 2010 Dec; Vol. 41 (12), pp. 1682-93. Date of Electronic Publication: 2010 Aug 04.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: W B Saunders Country of Publication: United States NLM ID: 9421547 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1532-8392 (Electronic) Linking ISSN: 00468177 NLM ISO Abbreviation: Hum Pathol Subsets: MEDLINE
أسماء مطبوعة: Publication: Philadelphia, PA : W B Saunders
Original Publication: Philadelphia, W B. Saunders Co.
مواضيع طبية MeSH: Kidney Transplantation*, Antibodies/*immunology , Graft Rejection/*metabolism , Proto-Oncogene Proteins c-jun/*metabolism, Acute Disease ; Adult ; Biopsy ; Endothelial Cells/metabolism ; Endothelial Cells/pathology ; Female ; Fluorescent Antibody Technique, Indirect ; Graft Rejection/pathology ; Humans ; Kidney/metabolism ; Kidney Diseases/metabolism ; Kidney Diseases/pathology ; MAP Kinase Kinase 4/metabolism ; Male ; Phosphorylation ; T-Lymphocytes/immunology ; T-Lymphocytes/pathology
مستخلص: c-Jun is a transcription factor that belongs to the activator protein-1 family of proteins. In human kidney disease, c-Jun is activated in glomerular and tubular cells and plays a major role in renal pathophysiology. However, the contribution of this pathway to renal allograft rejection has not been determined. We investigated whether c-Jun is activated in acute allograft rejection. c-Jun activation was assessed with immunohistochemistry using phospho-specific c-Jun antibodies in control human renal tissue and renal tissue from patients with acute cellular rejection, acute antibody-mediated rejection, and no rejection in the month after transplantation. In patients with acute cellular rejection, c-Jun activation was observed primarily in infiltrated T cells associated with tubulitis, interstitial cell infiltration, and endarteritis. The number of infiltrated phosphorylated c-Jun-positive cells in the tubules and interstitium was correlated with the Banff classification "t" and "i" scores. In patients with acute antibody-mediated rejection, c-Jun activation was observed in injured endothelial cells as well as in infiltrated cells, including macrophages, in the glomerular and peritubular capillaries. Furthermore, the serum creatinine levels and changes in serum creatinine from the previous year were significantly correlated with the total tubulointerstitial phosphorylated c-Jun-positive score (representing the number of positive nuclei in the tubules, interstitium, and peritubular capillaries). In conclusion, c-Jun was activated in acute antibody-mediated rejection and acute cellular rejection and was associated with reduced graft function. These findings suggest that c-Jun plays a key role in pathological events and may represent a novel therapeutic target in acute renal allograft rejection.
(Copyright © 2010 Elsevier Inc. All rights reserved.)
المشرفين على المادة: 0 (Antibodies)
0 (Proto-Oncogene Proteins c-jun)
EC 2.7.12.2 (MAP Kinase Kinase 4)
تواريخ الأحداث: Date Created: 20100807 Date Completed: 20101214 Latest Revision: 20101116
رمز التحديث: 20240628
DOI: 10.1016/j.humpath.2010.04.016
PMID: 20688351
قاعدة البيانات: MEDLINE
الوصف
تدمد:1532-8392
DOI:10.1016/j.humpath.2010.04.016