PMID- 10549855
OWN - NLM
STAT- MEDLINE
DCOM- 19991217
LR  - 20190719
IS  - 0918-6158 (Print)
IS  - 0918-6158 (Linking)
VI  - 22
IP  - 10
DP  - 1999 Oct
TI  - Rapid control of transmembrane calcium influx by 1alpha,25-dihydroxyvitamin D3 
      and its analogues in rat osteoblast-like cells.
PG  - 1058-63
AB  - 1alpha,25-Dihydroxyvitamin D3 [1alpha,25(OH)2D3] has been shown to exert both its 
      nuclear vitamin D receptor (nVDR)-mediated genomic actions and membrane vitamin D 
      receptor (mVDR)-mediated nongenomic actions. In this study, the effects of 
      1alpha,25(OH)2D3 and its analogues on transmembrane Ca2+ influx were examined in 
      the growth phase of rat osteosarcoma ROS17/2.8 cells. Like BAYK8644 (2 x 
      10(-5)M), a well-known L-type Ca2+ channel agonist, 1alpha,25(OH)2D3 (10(-8)M) 
      increased transmembrane influx of Ca2+ through voltage-dependent Ca2+ channels 
      and increased intracellular Ca2+ concentration within 2 min of addition to the 
      medium. The 1alpha,25(OH)2D3-induced Ca2+ influx was completely blocked by 
      pre-treatment with nifedipine (2 x 10(-5)M), an L-type Ca2+ channel antagonist. 
      Two vitamin D analogues, 22-oxa-1alpha,25(OH)2D3 (OCT, 10(-8) M) and 
      20-epi-22-oxa-24a, 26a,27a-trihomo-1alpha,25(OH)2D3 (KH1060, 10(-8)M), which were 
      3.8 and 3600-fold more active than 1alpha,25(OH)2D3 in stimulating 
      differentiation on human promyelocytic leukemic HL-60 cells, respectively, also 
      increased intracellular Ca2+ concentration, while their Ca2+ channeling 
      activities were similar to or significantly weaker than that of 1alpha,25(OH)2D3. 
      Furthermore, the enhanced transmembrane Ca2+ influx induced by 1alpha,25(OH)2D3 
      (10(-8)M) or OCT (10(-8)M) was completely blocked by pre-treatment with the 
      respective 1beta epimer [1beta,25(OH)2D3 and 1beta-OCT] at equal concentration. 
      These findings suggest that 1alpha,25(OH)2D3 and its analogues modulate 
      transmembrane Ca2+ influx in osteoblast-like cells by opening L-type Ca2+ 
      channels which can recognize 1alpha-hydroxy analogues as agonists and 
      1beta-hydroxy analogues as antagonists.
FAU - Nakagawa, K
AU  - Nakagawa K
AD  - Department of Hygienic Sciences, Kobe Pharmaceutical University, Japan.
FAU - Tsugawa, N
AU  - Tsugawa N
FAU - Okamoto, T
AU  - Okamoto T
FAU - Kishi, T
AU  - Kishi T
FAU - Ono, T
AU  - Ono T
FAU - Kubodera, N
AU  - Kubodera N
FAU - Okano, T
AU  - Okano T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Japan
TA  - Biol Pharm Bull
JT  - Biological & pharmaceutical bulletin
JID - 9311984
RN  - 0 (Antineoplastic Agents)
RN  - 0 (Calcium Channel Blockers)
RN  - 0 (Calcium Channels, L-Type)
RN  - 131875-08-6 (KH 1060)
RN  - B7IN85G1HY (Dinoprost)
RN  - FXC9231JVH (Calcitriol)
RN  - I9ZF7L6G2L (Nifedipine)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Antineoplastic Agents/pharmacology
MH  - Calcitriol/analogs & derivatives/*pharmacology
MH  - Calcium/*metabolism
MH  - Calcium Channel Blockers/pharmacology
MH  - Calcium Channels, L-Type/drug effects/metabolism
MH  - Cell Differentiation/drug effects
MH  - Dinoprost/pharmacology
MH  - HL-60 Cells
MH  - Humans
MH  - Nifedipine/pharmacology
MH  - Osteoblasts/*drug effects/metabolism
MH  - Rats
MH  - Tumor Cells, Cultured
EDAT- 1999/11/05 00:00
MHDA- 1999/11/05 00:01
CRDT- 1999/11/05 00:00
PHST- 1999/11/05 00:00 [pubmed]
PHST- 1999/11/05 00:01 [medline]
PHST- 1999/11/05 00:00 [entrez]
AID - 10.1248/bpb.22.1058 [doi]
PST - ppublish
SO  - Biol Pharm Bull. 1999 Oct;22(10):1058-63. doi: 10.1248/bpb.22.1058.