PMID- 9595485
OWN - NLM
STAT- MEDLINE
DCOM- 19980717
LR  - 20190724
IS  - 0160-2446 (Print)
IS  - 0160-2446 (Linking)
VI  - 31 Suppl 1
DP  - 1998
TI  - Regulation of endothelin release from human brain microvessel endothelial cells.
PG  - S370-2
AB  - After approval by the Local Ethical Committee, brain microvessel endothelial 
      cells from human cadavers were isolated by enzymatic digestion and gradient 
      centrifugation. Basal levels of endothelin-1 (ET) in the supernatant increased 
      over time (3 h, 18.3 +/- 4.3 pg/ml; 6 h, 31.3 +/- 1.1 pg/ml; 24 h, 88.0 +/- 5.7 
      pg/ml; 48 h, 86.3 +/- 11.2 pg/ml, mean +/- SD). Tumor necrosis factor-alpha 
      (TNF-alpha) (270 U/ml) increased ET concentration dose-dependently: 3 h, 190 +/- 
      70%; 24 h, 217 +/- 39%; 48 h, 207 +/- 5%; TNF-alpha at 210 U/ml: 3 h, 137%; 24 h, 
      170%; 48 h, 212% (values are relative changes from control, run in parallel to 
      the stimulated wells). Interleukin-1 alpha (IL-1 alpha) (38.8 U/ml) also 
      increased ET dose-dependently: (3 h, 129%; 24 h, 161%; 48 h, 212%; IL-1 alpha 1.4 
      U/ml: 3 h, 116%; 24 h, 122%; 48 h, 180%). Lipoprotein (a) (Lp(a)) had a dual 
      effect on ET, increasing ET in the first 3 h but reducing it by the end of the 
      48-h observation period. This effect was not dose-dependent in the concentration 
      range tested: Lp(a) 450 micrograms/ml; 3 h, 188%; 24 h, 91%; 48 h, 85%; Lp(a) 360 
      micrograms/ml: 3 h, 180%; 24 h, 94%; 48 h, 52%). Lp(a) reduced the stimulatory 
      effect of cytokines on ET release. Maximal values at 48 h were TNF-alpha 207%, 
      TNF-alpha + Lp(a) 91%, IL-1 alpha 212%, IL-1 alpha + Lp(a) 64%. In HPLC analysis, 
      the total ET-like immunoreactivity co-eluted with the synthetic human ET 
      standard. A cell culture of human brain microvessel endothelial cells was 
      established. TNF-alpha and IL-1 alpha increased ET secretion, whereas Lp(a) had a 
      dual effect. When given together, Lp(a) reduced the effect of cytokines on ETs.
FAU - Skopal, J
AU  - Skopal J
AD  - National Stroke Center, Semmelweis University, Budapest, Hungary.
FAU - Turbucz, P
AU  - Turbucz P
FAU - Vastag, M
AU  - Vastag M
FAU - Bori, Z
AU  - Bori Z
FAU - Pek, M
AU  - Pek M
FAU - deChatel, R
AU  - deChatel R
FAU - Nagy, Z
AU  - Nagy Z
FAU - Toth, M
AU  - Toth M
FAU - Karadi, I
AU  - Karadi I
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Cardiovasc Pharmacol
JT  - Journal of cardiovascular pharmacology
JID - 7902492
RN  - 0 (Cytokines)
RN  - 0 (Endothelins)
RN  - 0 (Interleukin-1)
RN  - 0 (Lipoprotein(a))
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Brain Chemistry/*physiology
MH  - Capillaries/cytology/metabolism
MH  - Cells, Cultured
MH  - Chromatography, High Pressure Liquid
MH  - Cytokines/pharmacology
MH  - Endothelins/*metabolism
MH  - Endothelium, Vascular/cytology/*metabolism
MH  - Humans
MH  - Interleukin-1/pharmacology
MH  - Lipoprotein(a)/metabolism
MH  - Tumor Necrosis Factor-alpha/pharmacology
EDAT- 1998/05/22 00:00
MHDA- 1998/05/22 00:01
CRDT- 1998/05/22 00:00
PHST- 1998/05/22 00:00 [pubmed]
PHST- 1998/05/22 00:01 [medline]
PHST- 1998/05/22 00:00 [entrez]
AID - 10.1097/00005344-199800001-00104 [doi]
PST - ppublish
SO  - J Cardiovasc Pharmacol. 1998;31 Suppl 1:S370-2. doi: 
      10.1097/00005344-199800001-00104.