PMID- 7564102
OWN - NLM
STAT- MEDLINE
DCOM- 19951114
LR  - 20190725
IS  - 0085-2538 (Print)
IS  - 0085-2538 (Linking)
VI  - 48
IP  - 2
DP  - 1995 Aug
TI  - Regulation of manganese superoxide dismutase in glomerular epithelial cells: 
      mechanisms for interleukin 1 induction.
PG  - 354-62
AB  - Reactive oxygen species have been implicated as mediators of tissue injury in 
      glomerular inflammation. The expression of the antioxidant enzyme, manganese 
      superoxide dismutase (MnSOD), was examined in primary cultures of rat glomerular 
      epithelial cells (GEC) in response to inflammatory mediators. The results 
      demonstrate that GEC respond to interleukin-1 (IL-1) and bacterial 
      lipopolysaccharride (LPS) with an increase in MnSOD steady-state mRNA levels. The 
      IL-1 alpha-mediated induction of MnSOD mRNA levels was both time- and 
      dose-dependent. Maximal levels approximately 40-fold above controls, were 
      observed at 12 hours with 2 ng/ml of IL-1 alpha. MnSOD protein levels were also 
      markedly elevated by IL-1 alpha. The induction of MnSOD mRNA by IL-1 alpha 
      required de novo transcription as well as some degree of protein synthesis. To 
      elucidate the potential intracellular signal that mediates IL-1 alpha-dependent 
      MnSOD expression, three classical signaling pathways were examined. We found no 
      evidence that MnSOD induction by IL-1 alpha is mediated by either the 
      cyclooxygenase or lipoxygenase pathway or via activation of protein kinase C. 
      Based on the presence of IL-1 alpha in several forms of glomerular inflammation, 
      the observed increase in MnSOD expression by this immunoregulatory cytokine must 
      have an important role in the antioxidant defense of glomerular epithelial cells.
FAU - Gwinner, W
AU  - Gwinner W
AD  - Department of Biochemistry and Molecular Biology, College of Medicine, University 
      of Florida, Gainesville, USA.
FAU - Tisher, C C
AU  - Tisher CC
FAU - Nick, H S
AU  - Nick HS
LA  - eng
GR  - DK-28330/DK/NIDDK NIH HHS/United States
GR  - HL-39593/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Kidney Int
JT  - Kidney international
JID - 0323470
RN  - 0 (Cytokines)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Interleukin-1)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (RNA, Messenger)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Cytokines/pharmacology
MH  - Epithelial Cells
MH  - Epithelium/drug effects/enzymology
MH  - Inflammation Mediators/pharmacology
MH  - Interleukin-1/*physiology
MH  - Kidney Glomerulus/cytology/drug effects/*enzymology
MH  - Lipopolysaccharides/pharmacology
MH  - Male
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Superoxide Dismutase/genetics/*metabolism
EDAT- 1995/08/01 00:00
MHDA- 1995/08/01 00:01
CRDT- 1995/08/01 00:00
PHST- 1995/08/01 00:00 [pubmed]
PHST- 1995/08/01 00:01 [medline]
PHST- 1995/08/01 00:00 [entrez]
AID - S0085-2538(15)59075-3 [pii]
AID - 10.1038/ki.1995.303 [doi]
PST - ppublish
SO  - Kidney Int. 1995 Aug;48(2):354-62. doi: 10.1038/ki.1995.303.