PMID- 15496153
OWN - NLM
STAT- MEDLINE
DCOM- 20050425
LR  - 20220318
IS  - 0085-2538 (Print)
IS  - 0085-2538 (Linking)
VI  - 66
IP  - 5
DP  - 2004 Nov
TI  - Gene expression profiling of anti-GBM glomerulonephritis model: the role of 
      NF-kappaB in immune complex kidney disease.
PG  - 1826-37
AB  - BACKGROUND: Immune complexes may cause an irreversible onset of chronic renal 
      disease. Most patients with chronic renal disease undergo a final common pathway, 
      marked by glomerulosclerosis and interstitial fibrosis. We attempted to draw a 
      molecular map of anti-glomerular basement membrane (GBM) glomerulonephritis in 
      mice using oligonucleotide microarray technology. METHODS: Kidneys were harvested 
      at days 1, 3, 7, 11, and 16 after inducing glomerulonephritis by using anti-GBM 
      antibody. In parallel with examining the biochemical and histologic changes, gene 
      expression profiles were acquired against five pooled control kidneys. Gene 
      expression levels were cross-validated by either reverse transcription-polymerase 
      chain reaction (RT-PCR), real-time PCR, or immunohistochemistry. RESULTS: 
      Pathologic changes in anti-GBM glomerulonephritis were confirmed in both BALB/c 
      and C57BL/6 strains. Among the 13,680 spotted 65mer oligonucleotides, 1112 genes 
      showing significant temporal patterns by permutation analysis of variance (ANOVA) 
      with multiple testing correction [false discovery ratio (FDR) < 0.05] were chosen 
      for cluster analysis. From the expression profile, acute inflammatory reactions 
      characterized by the elevation of various cytokines, including interleukin (IL)-1 
      and IL-6, were identified within 3 days of disease onset. After 7 days, tissue 
      remodeling response was prominent with highly induced extracellular-matrix (ECM) 
      genes. Although cytokines related to lymphocyte activation were not detected, 
      monocyte or mesangial cell proliferation-related genes were increased. Tumor 
      necrosis factor-alpha (TNF-alpha) and nuclear factor-kappaB (NF-kappaB) pathway 
      were consistently activated along the entire disease progression, inducing 
      various target genes like complement 3, IL-1b, IL-6, Traf1, and Saa1. CONCLUSION: 
      We made a large-scale gene expression time table for mouse anti-GBM 
      glomerulonephritis model, providing a comprehensive overview on the mechanism 
      governing the initiation and the progression of inflammatory renal disease.
FAU - Kim, Ju Han
AU  - Kim JH
AD  - Seoul National University Biomedical Informatics (SNUBI), Seoul, Korea.
FAU - Ha, Il Soo
AU  - Ha IS
FAU - Hwang, Chang-Il
AU  - Hwang CI
FAU - Lee, Young-Ju
AU  - Lee YJ
FAU - Kim, Jihoon
AU  - Kim J
FAU - Yang, Seung-Hee
AU  - Yang SH
FAU - Kim, Yon Su
AU  - Kim YS
FAU - Cao, Yun Anna
AU  - Cao YA
FAU - Choi, Sangdun
AU  - Choi S
FAU - Park, Woong-Yang
AU  - Park WY
LA  - eng
SI  - OMIM/GSE954
SI  - OMIM/GSE955
SI  - OMIM/GSE956
SI  - OMIM/GSE957
SI  - OMIM/GSE958
SI  - OMIM/GSE969
SI  - OMIM/GSM15078
SI  - OMIM/GSM15079
SI  - OMIM/GSM15080
SI  - OMIM/GSM15081
SI  - OMIM/GSM15082
SI  - OMIM/GSM15083
SI  - OMIM/GSM15084
SI  - OMIM/GSM15085
SI  - OMIM/GSM15086
SI  - OMIM/GSM15087
SI  - OMIM/GSM15088
SI  - OMIM/GSM15089
SI  - OMIM/GSM15090
SI  - OMIM/GSM15091
SI  - OMIM/GSM15092
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Kidney Int
JT  - Kidney international
JID - 0323470
RN  - 0 (Antigen-Antibody Complex)
RN  - 0 (Cytokines)
RN  - 0 (NF-kappa B)
SB  - IM
MH  - Animals
MH  - Anti-Glomerular Basement Membrane Disease/*genetics/*immunology/metabolism
MH  - Antigen-Antibody Complex/*metabolism
MH  - Cytokines/metabolism
MH  - *Gene Expression Profiling
MH  - Glomerulosclerosis, Focal Segmental/genetics
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - Monocytes/metabolism
MH  - NF-kappa B/*metabolism
MH  - Nephritis, Interstitial/genetics
MH  - Oligonucleotide Array Sequence Analysis
MH  - Rabbits
EDAT- 2004/10/22 09:00
MHDA- 2005/04/26 09:00
CRDT- 2004/10/22 09:00
PHST- 2004/10/22 09:00 [pubmed]
PHST- 2005/04/26 09:00 [medline]
PHST- 2004/10/22 09:00 [entrez]
AID - S0085-2538(15)50272-X [pii]
AID - 10.1111/j.1523-1755.2004.00956.x [doi]
PST - ppublish
SO  - Kidney Int. 2004 Nov;66(5):1826-37. doi: 10.1111/j.1523-1755.2004.00956.x.