PMID- 9211353
OWN - NLM
STAT- MEDLINE
DCOM- 19970930
LR  - 20190725
IS  - 0085-2538 (Print)
IS  - 0085-2538 (Linking)
VI  - 52
IP  - 1
DP  - 1997 Jul
TI  - In situ hybridization studies of matrix metalloproteinase-3, tissue inhibitor of 
      metalloproteinase-1 and type IV collagen in diabetic nephropathy.
PG  - 111-9
AB  - Progressive expansion of the mesangial matrix is one of the most characteristic 
      histological features of diabetic nephropathy (DN). To determine the balance 
      between the turnover and degradation of extracellular matrix (ECM) in renal 
      tissue of patients with DN, we examined the expression of matrix 
      metalloproteinase-3 (MMP-3), tissue inhibitor of metalloproteinase-1 (TIMP-1) and 
      type IV collagen (IV-C) mRNAs using a high-resolution in situ hybridization. 
      Patients were divided into three grades: mild (grade I), moderate (grade II) and 
      severe (grade III) mesangial expansion and tubulointerstitial injury. The 
      relationship between the expression of these mRNAs and degree of glomerular 
      mesangial expansion and interstitial injury was also examined. Cells positive for 
      each mRNA were observed in glomerular resident cells, including glomerular 
      mesangial, epithelial and endothelial cells and cells of Bowman's capsule. A 
      number of tubular epithelial cells and some infiltrating cells in the 
      interstitium also expressed these mRNAs. The expression of MMP-3 mRNA and TIMP-1 
      mRNA was strongest in glomeruli of grade I and inversely correlated with 
      mesangial expansion. In contrast, the expression of all three types of mRNA was 
      correlated with the degree of interstitial injury. Our results indicate that 
      IV-C, MMP-3 and TIMP-1 mRNAs are expressed in glomerular resident cells, tubular 
      epithelial cells and infiltrating cells in renal tissue of DN, and suggest that 
      their expression changes with the degree of mesangial expansion and interstitial 
      injury. Altered expression of MMP-3 and TIMP-1 may be associated with the 
      progression of DN.
FAU - Suzuki, D
AU  - Suzuki D
AD  - Department of Internal Medicine, School of Medicine, Tokai University, Kanagawa, 
      Japan.
FAU - Miyazaki, M
AU  - Miyazaki M
FAU - Jinde, K
AU  - Jinde K
FAU - Koji, T
AU  - Koji T
FAU - Yagame, M
AU  - Yagame M
FAU - Endoh, M
AU  - Endoh M
FAU - Nomoto, Y
AU  - Nomoto Y
FAU - Sakai, H
AU  - Sakai H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Kidney Int
JT  - Kidney international
JID - 0323470
RN  - 0 (Glycoproteins)
RN  - 0 (Protease Inhibitors)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tissue Inhibitor of Metalloproteinases)
RN  - 9007-34-5 (Collagen)
RN  - EC 3.4.24.17 (Matrix Metalloproteinase 3)
SB  - IM
MH  - Adult
MH  - Biopsy
MH  - Collagen/*genetics
MH  - Diabetic Nephropathies/*metabolism
MH  - Glycoproteins/*genetics
MH  - Humans
MH  - In Situ Hybridization
MH  - Kidney/metabolism
MH  - Kidney Glomerulus/metabolism
MH  - Matrix Metalloproteinase 3/*genetics
MH  - Middle Aged
MH  - Protease Inhibitors/*metabolism
MH  - RNA, Messenger/analysis
MH  - Tissue Inhibitor of Metalloproteinases
EDAT- 1997/07/01 00:00
MHDA- 1997/07/01 00:01
CRDT- 1997/07/01 00:00
PHST- 1997/07/01 00:00 [pubmed]
PHST- 1997/07/01 00:01 [medline]
PHST- 1997/07/01 00:00 [entrez]
AID - S0085-2538(15)60150-8 [pii]
AID - 10.1038/ki.1997.310 [doi]
PST - ppublish
SO  - Kidney Int. 1997 Jul;52(1):111-9. doi: 10.1038/ki.1997.310.