PMID- 8498530
OWN - NLM
STAT- MEDLINE
DCOM- 19930621
LR  - 20171213
IS  - 0002-9513 (Print)
IS  - 0002-9513 (Linking)
VI  - 264
IP  - 5 Pt 2
DP  - 1993 May
TI  - LPS-induced MCP-1, IL-1 beta, and TNF-alpha mRNA expression in isolated 
      erythrocyte-perfused rat kidney.
PG  - F774-80
AB  - The capacity of the lipopolysaccharide (LPS)-stimulated isolated 
      erythrocyte-perfused rat kidney (IEPK) to produce monocyte chemoattractant 
      protein-1 (MCP-1), interleukin-1 beta (IL-1 beta), and tumor necrosis 
      factor-alpha (TNF-alpha) mRNA was investigated. The IEPK was chosen to exclude 
      the influence of circulating neutrophils and monocytes that can produce both 
      these mediators when exposed to LPS. The control minimal LPS group (LPS < 10 
      pg/ml) showed a small increase in mRNA expression for MCP-1, IL-1 beta, and 
      TNF-alpha in the cortex and medulla after 80 min of perfusion when compared with 
      the unperfused left kidney in which no IL-1 beta or TNF-alpha mRNA and only 
      minimal amounts of MCP-1 mRNA were detected. LPS stimulation (1 microgram/ml for 
      40 or 80 min) increased MCP-1, IL-1 beta, and TNF-alpha mRNA expression, which 
      was found predominately in peritubular capillary endothelial cells by in situ 
      hybridization. The changes were not due to a marked perturbation of LPS on renal 
      hemodynamics. The renal vascular resistance (RVR) remained constant (40 min LPS 
      exposure) or increased only slightly during the last 5-10 min (80 min LPS 
      exposure) compared with a progressive increase in RVR of the minimal LPS group. 
      The hemodynamic effects of LPS on the IEPK appear to counteract the gradual 
      increase in RVR seen in the minimal LPS group.
FAU - Xia, Y
AU  - Xia Y
AD  - Department of Immunology, Scripps Research Institute, La Jolla, California 92037.
FAU - Feng, L
AU  - Feng L
FAU - Yoshimura, T
AU  - Yoshimura T
FAU - Wilson, C B
AU  - Wilson CB
LA  - eng
GR  - DK-40251/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Physiol
JT  - The American journal of physiology
JID - 0370511
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemotactic Factors)
RN  - 0 (Cytokines)
RN  - 0 (Endotoxins)
RN  - 0 (Interleukin-1)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Chemokine CCL2
MH  - Chemotactic Factors/genetics/*metabolism
MH  - Cytokines/metabolism
MH  - Endotoxins/pharmacology
MH  - Erythrocytes
MH  - Escherichia coli
MH  - In Vitro Techniques
MH  - Interleukin-1/genetics/*metabolism
MH  - Kidney/drug effects/*metabolism/physiology
MH  - Lipopolysaccharides/*pharmacology
MH  - Male
MH  - Perfusion/methods
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Inbred Strains
MH  - Tumor Necrosis Factor-alpha/genetics/*metabolism
EDAT- 1993/05/01 00:00
MHDA- 1993/05/01 00:01
CRDT- 1993/05/01 00:00
PHST- 1993/05/01 00:00 [pubmed]
PHST- 1993/05/01 00:01 [medline]
PHST- 1993/05/01 00:00 [entrez]
AID - 10.1152/ajprenal.1993.264.5.F774 [doi]
PST - ppublish
SO  - Am J Physiol. 1993 May;264(5 Pt 2):F774-80. doi: 
      10.1152/ajprenal.1993.264.5.F774.