PMID- 23884236
OWN - NLM
STAT- MEDLINE
DCOM- 20140328
LR  - 20211021
IS  - 1420-908X (Electronic)
IS  - 1023-3830 (Linking)
VI  - 62
IP  - 10
DP  - 2013 Oct
TI  - Inhibitory effects of epi-sesamin on endothelial protein C receptor shedding in 
      vitro and in vivo.
PG  - 895-902
LID - 10.1007/s00011-013-0648-6 [doi]
AB  - OBJECTIVE AND DESIGN: Endothelial protein C receptor (EPCR) plays a pivotal role 
      in augmenting Protein C activation by the thrombin-thrombomodulin complex. The 
      activity of EPCR is markedly changed by ectodomain cleavage and release as the 
      soluble protein (sEPCR). The EPCR shedding is mediated by the tumor necrosis 
      factor-alpha converting enzyme (TACE). Epi-sesamin (ESM), from the roots of Asarum 
      siebodlii, is known to exhibit anti-allergic and anti-fungal activities. However, 
      little is known about the effects of ESM on EPCR shedding. METHODS: We 
      investigated this issue by monitoring the effects of ESM on phorbol-12-myristate 
      13-acetate (PMA), tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and cecal 
      ligation and puncture (CLP)-mediated EPCR shedding. RESULTS: Data showed that ESM 
      induced potent inhibition of PMA, TNF-alpha, IL-1beta, and CLP-induced EPCR shedding, 
      likely through suppression of TACE expression. In addition, treatment with ESM 
      resulted in a reduction of PMA-stimulated phosphorylation of p38, extracellular 
      regulated kinases (ERK) 1/2, and c-Jun N-terminal kinase (JNK). CONCLUSIONS: 
      Given these results, ESM should be viewed as a candidate therapeutic agent for 
      treatment of various severe vascular inflammatory diseases via inhibition of EPCR 
      shedding.
FAU - Ku, Sae-Kwang
AU  - Ku SK
AD  - Department of Anatomy and Histology, College of Oriental Medicine, Daegu Haany 
      University, Gyeongsan, 712-715, Republic of Korea.
FAU - Lee, Wonhwa
AU  - Lee W
FAU - Yoo, Hayoung
AU  - Yoo H
FAU - Han, Chang-Kyun
AU  - Han CK
FAU - Bae, Jong-Sup
AU  - Bae JS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130725
PL  - Switzerland
TA  - Inflamm Res
JT  - Inflammation research : official journal of the European Histamine Research 
      Society ... [et al.]
JID - 9508160
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Antigens, CD)
RN  - 0 (Dioxoles)
RN  - 0 (Endothelial Protein C Receptor)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Lignans)
RN  - 0 (PROCR protein, human)
RN  - 0 (Receptors, Cell Surface)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - NI40JAQ945 (Tetradecanoylphorbol Acetate)
RN  - S7946O4P76 (sesamin)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Antigens, CD/*metabolism
MH  - Cells, Cultured
MH  - Dioxoles/*pharmacology
MH  - Endothelial Protein C Receptor
MH  - Human Umbilical Vein Endothelial Cells/drug effects/metabolism
MH  - Humans
MH  - Interleukin-1beta/pharmacology
MH  - Lignans/*pharmacology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mitogen-Activated Protein Kinases/metabolism
MH  - Receptors, Cell Surface/*metabolism
MH  - Sepsis/metabolism
MH  - Tetradecanoylphorbol Acetate/pharmacology
MH  - Tumor Necrosis Factor-alpha/pharmacology
EDAT- 2013/07/26 06:00
MHDA- 2014/03/29 06:00
CRDT- 2013/07/26 06:00
PHST- 2013/04/11 00:00 [received]
PHST- 2013/07/16 00:00 [accepted]
PHST- 2013/07/26 06:00 [entrez]
PHST- 2013/07/26 06:00 [pubmed]
PHST- 2014/03/29 06:00 [medline]
AID - 10.1007/s00011-013-0648-6 [doi]
PST - ppublish
SO  - Inflamm Res. 2013 Oct;62(10):895-902. doi: 10.1007/s00011-013-0648-6. Epub 2013 
      Jul 25.