XXXX vascular smooth muscle cells produce an intracellular form of @entity1192 receptor antagonist.

@entity1 @entity1356 @entity1359 @entity1193 @entity1192 @entity9302
@entity1192 ( @entity1192 ) is a proinflammatory monocyte- and macrophage-derived cytokine that has potent vasorelaxant effects on vascular smooth muscle cells (VSMC). VSMC themselves also express both @entity1192 - and beta-genes, suggesting that @entity1192 may be an autocrine regulator of VSMC function. The present study demonstrates that @entity1 saphenous vein VSMC (HSVSMC) produce @entity1193 ( @entity1193 ), a specific inhibitor of @entity1192 action. @entity1193 was produced constitutively in most experiments, and its production was upregulated by @entity1359 and by @entity1356 . @entity1193 produced by HSVSMC remained predominately cell associated and was not detectable extracellularly. Furthermore, reverse transcription-polymerase chain reaction analysis and cDNA sequencing indicated that HSVSMC express the alternatively spliced form of @entity1193 which lacks the signal peptide present in secreted @entity1193 . HSVSMC also produced @entity1192 and the precursor form but not the mature form of @entity1356 . These results suggest that HSVSMC lack active @entity9302 . Like @entity1193 , @entity1356 precursor and @entity1192 remained cell associated, predominately in the cytosolic fraction. @entity1356 induced production of both @entity1193 and @entity1192 at each time point and concentration tested. In contrast, platelet-derived growth factor and transforming growth factor-beta augmented production of @entity1193 , but not that of @entity1192 . These results are suggestive of an autocrine role for cell-associated @entity1193 , as well as for @entity1192 and @entity1356 , in the regulation of VSMC function.
