Key result
Thrombomodulin activity in HUVECs is modulated by independent mechanisms involving cytoplasmic TM mRNA levels and internalization/degradation of TM molecules, potentially via PKA and PKC.
Population
Human umbilical vein endothelial cells (HUVECs) in vitro
Design
Preclinical
Authors
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No immediate clinical implications from HUVEC data; leaves open in vivo relevance of PKA/PKC pathways for thrombomodulin.
Thrombomodulin expression in human endothelial cells is regulated by independent mechanisms involving mRNA levels and protein internalization/degradation, mediated by PKA and PKC pathways.
Hirokawa et al. (1991) studied this question. Various agents (dibutyryl cAMP, PMA, TNF, IL-1 beta) was evaluated on Time course changes in surface TM activity, total TM antigen, and TM mRNA levels. Thrombomodulin activity in HUVECs is modulated by independent mechanisms involving cytoplasmic TM mRNA levels and internalization/degradation of TM molecules, potentially via PKA and PKC.
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