PMID- 25016099
OWN - NLM
STAT- MEDLINE
DCOM- 20150702
LR  - 20211203
IS  - 1879-3649 (Electronic)
IS  - 1537-1891 (Linking)
VI  - 63
IP  - 1
DP  - 2014 Oct
TI  - Sulforaphane inhibits endothelial protein C receptor shedding in vitro and in 
      vivo.
PG  - 13-8
LID - S1537-1891(14)00108-6 [pii]
LID - 10.1016/j.vph.2014.06.002 [doi]
AB  - Sulforaphane (SFN), a natural isothiocyanate present in cruciferous vegetables 
      such as broccoli and cabbage, is effective in preventing carcinogenesis, 
      diabetes, and inflammatory responses. Increasing evidence has demonstrated that 
      beyond its role in the activation of protein C, endothelial cell protein C 
      receptor (EPCR) is also involved in vascular inflammation. EPCR activity is 
      markedly changed by ectodomain cleavage and its release as the soluble EPCR. EPCR 
      can be shed from the cell surface, which is mediated by tumor necrosis factor-alpha 
      converting enzyme (TACE). However, little is known about the effects of SFN on 
      EPCR shedding. Our results demonstrated that SFN induced potent inhibition of 
      phorbol-12-myristate 13-acetate (PMA)-, tumor necrosis factor (TNF)-alpha-, 
      interleukin (IL)-1beta, and cecal ligation and puncture (CLP)-induced EPCR shedding. 
      SFN also inhibited the expression and activity of PMA-induced TACE in endothelial 
      cells. In addition, treatment with SFN resulted in reduced PMA-stimulated 
      phosphorylation of p38, extracellular regulated kinases (ERK) 1/2, and c-Jun 
      N-terminal kinase (JNK). These results demonstrate the potential of SFN as an 
      anti-sEPCR shedding reagent against PMA and CLP-mediated EPCR shedding.
CI  - Copyright (c) 2014 Elsevier Inc. All rights reserved.
FAU - Ku, Sae-Kwang
AU  - Ku SK
AD  - Department of Anatomy and Histology, College of Korean Medicine, Daegu Haany 
      University, Gyeongsan 712-715, Republic of Korea.
FAU - Han, Min-Su
AU  - Han MS
AD  - Laboratory for Arthritis and Bone Biology, Fatima Research Institute, Daegu 
      Fatima Hospital, Daegu 701-724, Republic of Korea.
FAU - Bae, Jong-Sup
AU  - Bae JS
AD  - College of Pharmacy, CMRI, Research Institute of Pharmaceutical Sciences, 
      Kyungpook National University, Daegu 702-701, Republic of Korea. Electronic 
      address: baejs@knu.ac.kr.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140709
PL  - United States
TA  - Vascul Pharmacol
JT  - Vascular pharmacology
JID - 101130615
RN  - 0 (Blood Coagulation Factors)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Isothiocyanates)
RN  - 0 (Receptors, Cell Surface)
RN  - 0 (Sulfoxides)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (activated protein C receptor)
RN  - EC 3.4.24.- (ADAM Proteins)
RN  - EC 3.4.24.86 (ADAM17 Protein)
RN  - EC 3.4.24.86 (ADAM17 protein, human)
RN  - EC 3.4.24.86 (Adam17 protein, mouse)
RN  - GA49J4310U (sulforaphane)
RN  - NI40JAQ945 (Tetradecanoylphorbol Acetate)
SB  - IM
MH  - ADAM Proteins/metabolism
MH  - ADAM17 Protein
MH  - Animals
MH  - Blood Coagulation Factors/*metabolism
MH  - Cecum/injuries
MH  - Disease Models, Animal
MH  - Human Umbilical Vein Endothelial Cells/drug effects
MH  - Humans
MH  - In Vitro Techniques
MH  - Interleukin-1beta/metabolism
MH  - Isothiocyanates/*pharmacology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Receptors, Cell Surface/*metabolism
MH  - Sepsis/*drug therapy/physiopathology
MH  - Sulfoxides
MH  - Tetradecanoylphorbol Acetate/pharmacology
MH  - Tumor Necrosis Factor-alpha
OTO - NOTNLM
OT  - EPCR shedding
OT  - Sulforaphane
OT  - Vascular inflammation
EDAT- 2014/07/13 06:00
MHDA- 2015/07/03 06:00
CRDT- 2014/07/13 06:00
PHST- 2014/02/22 00:00 [received]
PHST- 2014/04/11 00:00 [revised]
PHST- 2014/06/12 00:00 [accepted]
PHST- 2014/07/13 06:00 [entrez]
PHST- 2014/07/13 06:00 [pubmed]
PHST- 2015/07/03 06:00 [medline]
AID - S1537-1891(14)00108-6 [pii]
AID - 10.1016/j.vph.2014.06.002 [doi]
PST - ppublish
SO  - Vascul Pharmacol. 2014 Oct;63(1):13-8. doi: 10.1016/j.vph.2014.06.002. Epub 2014 
      Jul 9.