Selected Publication:
GRAIER, WF; SCHMIDT, K; KUKOVETZ, WR. 
ACTIVATION OF G-PROTEIN EVOKES CA2+ INFLUX IN ENDOTHELIAL-CELLS WITHOUT CORRELATION TO INOSITOL PHOSPHATES
J CARDIOVASC PHARMACOL. 1991; 17:  S71-S78. 
 Doi: 10.1097/00005344-199117003-00013
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- Leading authors Med Uni Graz
 
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Graier Wolfgang
 
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- Abstract:
 
- The production of big endothelin-1 (big ET-1) and its processing to endothelin (ET-1) were examined in cocultures of bovine pulmonary artery endothelial cells (BPECs) and human bronchiolar smooth muscle cells (HBSMCs). The BPECs produced immunologically reactive ET-1 (ir-ET-1) and big ET-1 (ir-big ET-1) that increased linearly in the cell culture media over a 72 h time course when confluent monolayers were incubated at 37 degrees C in serum-free media. HBSMCs maintained in serum-free media over a 72-h period did not produce any detectable ir-big ET-1 or ir-ET-1. After coculture of these two cell types for 24 h (the monolayers were physically separated), the culture medium contained no detectable ir-big ET-1 or ir-ET-1. When medium conditioned for 24 h with the HBSMCs was transferred to the BPEC monolayers, the accumulation rates of ET-1 and big ET-1 were attenuated 70 and 10%, respectively. When medium conditioned for 24 h with the BPECs was transferred to the HBSM cell monolayers, the amount of ir-ET-1 and ir-big ET-1 in the medium decreased greater than 90% over the next 24 h. Cellular binding and uptake could not account for this decrease as ascertained by quantitation of cellular levels of ET-1 and big ET-1. When conditioned medium from the HBSMCs was added to conditioned medium from the BPECs in a 1:1, 2:1, 3:1, 1:2, or 1:3 ratio (v/v) in the absence of cells, the amount of ET-1 or big ET-1 present in the EC medium did not decrease significantly over the following 24 h. These data imply that HBSMCs contain a factor that is responsible for decreasing the accumulation of ir-big ET-1 and ir-ET-1 in the cell culture media of BPECs. The data also suggest that the most likely mechanism for this effect is a factor that degrades BET-1 and ET-1 at different rates.
 
- Find related publications in this database (using NLM MeSH Indexing)
 
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Animals -  
 
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Bronchi - metabolism 
 
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Cattle -  
 
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Cells, Cultured -  
 
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Culture Media -  
 
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Endothelin-1 -  
 
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Endothelins - metabolism 
 
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Endothelium, Vascular - metabolism 
 
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Humans -  
 
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Muscle, Smooth - metabolism 
 
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Protein Precursors - metabolism 
 
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Pulmonary Artery - metabolism 
 
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Radioimmunoassay - 
 
- Find related publications in this database (Keywords)
 
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ENDOTHELIAL CELL
 
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G-PROTEIN
 
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ENDOTHELIUM-DERIVED RELAXING FACTOR (EDRF)
 
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CA2+ INFLUX
 
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SODIUM FLUORIDE
 
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IP3
 
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IP4