PMID- 26859198
OWN - NLM
STAT- MEDLINE
DCOM- 20170911
LR  - 20170911
IS  - 1533-4023 (Electronic)
IS  - 0160-2446 (Linking)
VI  - 67
IP  - 6
DP  - 2016 Jun
TI  - Rutaecarpine Reverses the Altered Connexin Expression Pattern Induced by Oxidized 
      Low-density Lipoprotein in Monocytes.
PG  - 519-25
LID - 10.1097/FJC.0000000000000372 [doi]
AB  - Adhesion of monocytes to the vascular endothelium is crucial in atherosclerosis 
      development. Connexins (Cxs) which form hemichannels or gap junctions, modulate 
      monocyte-endothelium interaction. We previously found that rutaecarpine, an 
      active ingredient of the Chinese herbal medicine Evodia, reversed the altered Cx 
      expression induced by oxidized low-density lipoprotein (ox-LDL) in human 
      umbilical vein endothelial cells, and consequently decreases the adhesive 
      properties of endothelial cells to monocytes. This study further investigated the 
      effect of rutaecarpine on Cx expression in monocytes exposed to ox-LDL. In 
      cultured human monocytic cell line THP-1, ox-LDL rapidly reduced the level of 
      atheroprotective Cx37 but enhanced that of atherogenic Cx43, thereby inhibiting 
      adenosine triphosphate release through hemichannels. Pretreatment with 
      rutaecarpine recovered the expression of Cx37 but inhibited the upregulation of 
      Cx43 induced by ox-LDL, thereby improving adenosine triphosphate-dependent 
      hemichannel activity and preventing monocyte adhesion. These effects of 
      rutaecarpine were attenuated by capsazepine, an antagonist of transient receptor 
      potential vanilloid subtype 1. The antiadhesive effects of rutaecarpine were also 
      attenuated by hemichannel blocker 18alpha-GA. This study provides additional evidence 
      that rutaecarpine can modulate Cx expression through transient receptor potential 
      vanilloid subtype 1 activation in monocytes, which contributes to the 
      antiadhesive properties of rutaecarpine.
FAU - Liu, Yong
AU  - Liu Y
AD  - *Medical College, Nanchang University, Nanchang, Jiangxi Province, China; 
      daggerGanzhou Cancer Hospital, Ganzhou, Jiangxi Province, China; and double daggerJiangxi Academy 
      of Medical Sciences, Nanchang, Jiangxi Province, China.
FAU - Fu, Yan-Qi
AU  - Fu YQ
FAU - Peng, Wei-Jie
AU  - Peng WJ
FAU - Yu, Yan-Rong
AU  - Yu YR
FAU - Wu, Yu-Si
AU  - Wu YS
FAU - Yan, Hang
AU  - Yan H
FAU - Huang, Qi-Ren
AU  - Huang QR
FAU - He, Ming
AU  - He M
FAU - Luo, Dan
AU  - Luo D
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Cardiovasc Pharmacol
JT  - Journal of cardiovascular pharmacology
JID - 7902492
RN  - 0 (Connexins)
RN  - 0 (Indole Alkaloids)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (Quinazolines)
RN  - 0 (oxidized low density lipoprotein)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
RN  - 8XZV289PRY (rutecarpine)
SB  - IM
MH  - Adenosine Triphosphate/metabolism
MH  - Atherosclerosis/physiopathology
MH  - Cells, Cultured
MH  - Connexins/*drug effects
MH  - Dose-Response Relationship, Drug
MH  - Endothelium, Vascular/*metabolism
MH  - Humans
MH  - Indole Alkaloids/*pharmacology
MH  - Lipoproteins, LDL/*metabolism
MH  - Monocytes/*metabolism
MH  - Quinazolines/*pharmacology
MH  - Time Factors
EDAT- 2016/02/10 06:00
MHDA- 2017/09/12 06:00
CRDT- 2016/02/10 06:00
PHST- 2016/02/10 06:00 [entrez]
PHST- 2016/02/10 06:00 [pubmed]
PHST- 2017/09/12 06:00 [medline]
AID - 10.1097/FJC.0000000000000372 [doi]
PST - ppublish
SO  - J Cardiovasc Pharmacol. 2016 Jun;67(6):519-25. doi: 10.1097/FJC.0000000000000372.