PMID- 19138739
OWN - NLM
STAT- MEDLINE
DCOM- 20090415
LR  - 20191210
IS  - 0960-0760 (Print)
IS  - 0960-0760 (Linking)
VI  - 113
IP  - 1-2
DP  - 2009 Jan
TI  - Anti-inflammatory effect of 1alpha,25-dihydroxyvitamin D(3) in human coronary 
      arterial endothelial cells: Implication for the treatment of Kawasaki disease.
PG  - 134-8
LID - 10.1016/j.jsbmb.2008.12.004 [doi]
AB  - Kawasaki disease (KD) is an acute febrile vasculitis in childhood that is 
      associated with inflammatory cytokines, in which the vascular inflammation 
      results in damage to the coronary arteries. The active form of vitamin D, 
      1alpha,25-dihydroxyvitamin D(3) 1alpha,25-(OH)(2)D(3) exhibits 
      anti-inflammatory activities. In this study, we determined the mRNA and protein 
      expression of the vitamin D receptor in human coronary arterial endothelial cells 
      (HCAEC) by RT-PCR and Western blotting, respectively. We examined whether or not 
      1alpha,25-(OH)(2)D(3) inhibits the tumor necrosis factor-alpha 
      (TNF-alpha)-induced activation of nuclear transcription factor-kappaB 
      (NF-kappaB), which is essential for the expression of proinflammatory cytokines 
      in HCAEC, by ELISA. In addition, we determined the inhibitory effect of 
      1alpha,25-(OH)(2)D(3) on E-selectin expression induced by TNF-alpha in HCAEC by 
      flow cytometry. RT-PCR revealed mRNA for the vitamin D receptor in HCAEC. Western 
      blotting demonstrated vitamin D receptor protein in HCAEC. ELISA showed that 
      pretreatment with 1alpha,25-(OH)(2)D(3) significantly inhibited the 
      TNF-alpha-induced NF-kappaB activation in HCAEC. Moreover, flow cytometry 
      revealed that pretreatment with 1alpha,25-(OH)(2)D(3) significantly inhibited the 
      TNF-alpha-induced expression of E-selectin on HCAEC. Our results suggest that 
      adjunctive 1alpha,25-(OH)(2)D(3) may modulate the inflammatory response during KD 
      vasculitis.
FAU - Suzuki, Yasuo
AU  - Suzuki Y
AD  - Department of Pediatrics, Yamaguchi University Graduate School of Medicine, 1-1-1 
      Minami-kogushi, Ube, Yamaguchi 755-8505, Japan.
FAU - Ichiyama, Takashi
AU  - Ichiyama T
FAU - Ohsaki, Ayami
AU  - Ohsaki A
FAU - Hasegawa, Shunji
AU  - Hasegawa S
FAU - Shiraishi, Masahiro
AU  - Shiraishi M
FAU - Furukawa, Susumu
AU  - Furukawa S
LA  - eng
PT  - Journal Article
DEP - 20081224
PL  - England
TA  - J Steroid Biochem Mol Biol
JT  - The Journal of steroid biochemistry and molecular biology
JID - 9015483
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (E-Selectin)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Calcitriol)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (dihydroxy-vitamin D3)
RN  - 1406-16-2 (Vitamin D)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents/pharmacology/*therapeutic use
MH  - Blotting, Western
MH  - COS Cells
MH  - Chlorocebus aethiops
MH  - Coronary Vessels/*cytology
MH  - E-Selectin/metabolism
MH  - Endothelial Cells/drug effects/*metabolism
MH  - Gene Expression Regulation/drug effects
MH  - Humans
MH  - Jurkat Cells
MH  - Mucocutaneous Lymph Node Syndrome/*drug therapy
MH  - NF-kappa B/metabolism
MH  - RNA, Messenger/genetics/metabolism
MH  - Receptors, Calcitriol/genetics/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Tumor Necrosis Factor-alpha/pharmacology
MH  - Vitamin D/*analogs & derivatives/pharmacology/therapeutic use
EDAT- 2009/01/14 09:00
MHDA- 2009/04/16 09:00
CRDT- 2009/01/14 09:00
PHST- 2008/07/17 00:00 [received]
PHST- 2008/11/17 00:00 [revised]
PHST- 2008/12/15 00:00 [accepted]
PHST- 2009/01/14 09:00 [entrez]
PHST- 2009/01/14 09:00 [pubmed]
PHST- 2009/04/16 09:00 [medline]
AID - S0960-0760(08)00287-2 [pii]
AID - 10.1016/j.jsbmb.2008.12.004 [doi]
PST - ppublish
SO  - J Steroid Biochem Mol Biol. 2009 Jan;113(1-2):134-8. doi: 
      10.1016/j.jsbmb.2008.12.004. Epub 2008 Dec 24.