Deisher T A, Haddix T L, Montgomery K F, Pohlman T H, Kaushansky K, Harlan J M
Department of Medicine, University of Washington Health Sciences, Seattle 98195.
FEBS Lett. 1993 Oct 4;331(3):285-90. doi: 10.1016/0014-5793(93)80354-w.
The role of protein kinase C (PKC) in interleukin-1 beta- (II-1 beta)-, tumor necrosis factor-alpha- (TNF-alpha)-, and lipopolysaccharide- (LPS)-induced vascular cell adhesion molecule-1 (VCAM-1) expression on human umbilical vein endothelial cells (HUVEC) was studied. PKC inhibition or downregulation diminished VCAM-1 mRNA accumulation and protein expression. Interleukin-1 beta, TNF-alpha, and LPS induce nuclear factor (NF)-kappa B-like binding activity, which precedes VCAM-1 transcription. PKC inhibition did not prevent NF-kappa B-like binding activity, indicating that this is PKC-independent, and NF-kappa B-like binding activity is insufficient for transcription of VCAM-1.
