A synthetic analogue of vitamin D3, 22-oxa-1,25-dihydroxy-vitamin D3, stimulates the production of prostacyclin by vascular tissues

Inoue, Masaharu; Wakasugi, Masakiyo; Wakao, Rie; Gan, Naoya; Tawata, Masato; Nishii, Y.; Onaya, Toshimasa

doi:10.1016/0024-3205(92)90511-m

Cited by 10 publications

(8 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This VDR-dependent action is referred to as the "genomic action" of the hormone. On the other hand, other recent studies (27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37) have suggested that the hormone is also able to induce several biological activities via protein kinase C, ceramide signaling pathways, and via an increase in the intracellular calcium concentration, which are called "nongenomic action. "…”

Section: Tgf-␤1mentioning

confidence: 99%

“…Cells-Several recent studies (27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37) have suggested the presence of VDR-dependent (genomic) and -independent (non-genomic) pathways in 1␣-25-(OH) 2 D 3 signal transduction. Therefore, it was of interest to determine whether the synergistic action of 1␣-25-(OH) 2 D 3 toward AP-1 transcriptional activity in TGF-␤1-treated cells was VDR-dependent or -independent.…”

Section: Effect Of 1␣-25-(oh) 2 D 3 Analogs On Tgf-␤1-induced Ap-1 Trmentioning

confidence: 99%

“…Therefore, it was of interest to determine whether the synergistic action of 1␣-25-(OH) 2 D 3 toward AP-1 transcriptional activity in TGF-␤1-treated cells was VDR-dependent or -independent. In this regard, some studies (34,49) have shown that OCT, a 1␣-25-(OH) 2 D 3 derivative, has a high affinity for VDR and that its biological activity is generated via the VDR-dependent (genomic) pathway. In contrast, 24,25-(OH) 2 D 3 is an analog that has very low affinity for VDR (29,49).…”

Section: Effect Of 1␣-25-(oh) 2 D 3 Analogs On Tgf-␤1-induced Ap-1 Trmentioning

confidence: 99%

“…In this regard, it is of interest to investigate whether 1␣-25-(OH) 2 D 3 negatively or positively regulates TGF-␤1-induced AP-1 transcriptional activity in mouse MC3T3-E1 cells. And our interest also was to define whether the 1␣-25-(OH) 2 D 3 action on the AP-1 activity would be genomic or nongenomic (27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37). Of these two mechanisms, the present study demonstrates that the synergistic action of 1␣-25-(OH) 2 D 3 toward TGF-␤1-induced AP-1 transcriptional activity in the cells occurs via the genomic activity (the receptor-dependent mechanism).…”

Section: ␣-25-(oh) 2 D 3 Stimulates At the Transcriptional Level Thementioning

confidence: 99%

“…On the other hand, recent studies (27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37) have demonstrated that 1␣-25-(OH) 2 D 3 expresses several biological actions via ceramide and protein kinase C signaling pathways and also via intracellular calcium signals. Thus, it was of interest to demonstrate whether 1␣-25-(OH) 2 D 3 synergy in the stimulation of AP-1 transcriptional activity of TGF-␤1-treated MC3T3-E1 cells is genomic action-dependent or -independent.…”

Section: ␣-25-(oh) 2 D 3 Stimulates At the Transcriptional Level Thementioning

confidence: 99%

See 4 more Smart Citations

1α,25-Dehydroxyvitamin D3 Synergism toward Transforming Growth Factor-β1-induced AP-1 Transcriptional Activity in Mouse Osteoblastic Cells via Its Nuclear Receptor

Takeshita¹,

Imai²,

Kato³

et al. 1998

Journal of Biological Chemistry

View full text Add to dashboard Cite

TGF-␤11 is locally produced by osteoblasts and accumulates abundantly in bone matrix tissue (1-3). This local cytokine plays an important role as a "coupling factor" in bone remodeling (4 -7). We (8, 9) previously demonstrated that TGF-␤1 is a potent activator of AP-1, a transcriptional factor that is a heterodimer of FOS and JUN proteins, in mouse osteoblastic MC3T3-E1 cells. AP-1 activates the transcription of target genes by binding to specific promoter elements called TRE. In fact, several studies (10 -16) have suggested that AP-1 is a regulatory factor in bone metabolism. Therefore, it is of interest to investigate the mechanism by which AP-1 regulates the metabolism of TGF-␤1-treated bone cells, which regulation may occur in an autocrine and/or paracrine fashion.1␣-25-(OH) 2 D 3 also is an important systemic hormone in bone metabolism and regulates transcriptionally the expression of several genes involved in the differentiation of osteoblastic cells (17)(18)(19)(20)(21)(22)(23). Many studies (20 -26) have shown that the hormone binds to its receptor, VDR, in the cell nucleus and acts via binding of this complex to the VDR response element. This VDR-dependent action is referred to as the "genomic action" of the hormone. On the other hand, other recent studies (27-37) have suggested that the hormone is also able to induce several biological activities via protein kinase C, ceramide signaling pathways, and via an increase in the intracellular calcium concentration, which are called "nongenomic action."Several investigators (21-24) have demonstrated negative regulation between AP-1 and VDR of the transcriptional activity of osteocalcin and collagen genes, both of which are involved in bone formation. However, positive regulation by 1␣-25-(OH) 2 D 3 of AP-1 transcriptional activity in osteoblastic cells has not been demonstrated in detail. Therefore, it is of interest to explore the possibility of 1␣-25-(OH) 2 D 3 positive regulation of AP-1 transcriptional activity via "genomic" or "nongenomic" action.In this regard, we investigated in the present study the regulation by 1␣-25-(OH) 2 D 3 of TGF-␤1-induced AP-1 transcriptional activity in osteoblastic MC3T3-E1 cells. As a result, we demonstrated the presence of 1␣-25-(OH) 2 D 3 synergism toward TGF-␤1-induced AP-1 transcriptional activity via genomic action. This demonstration suggests the presence of a novel positive regulation by 1␣-25-(OH) 2 D 3 of AP-1 transcriptional activity in osteoblastic cells via the VDR-dependent pathway (genomic action). MATERIALS AND METHODSReagents-Human recombinant TGF-␤1 was purified to homogeneity (Ͼ98.9%, determined by SDS-polyacrylamide gel electrophoresis analysis: King Brewer, Kakogawa, Japan). 1␣-25-(OH) 2 D 3 , 24,25-(OH) 2 D 3 , and 22-oxa-1,25-dihydroxyvitamin D 3 (OCT) were kindly provided by Chugai Pharmaceutical Co., Ltd. (Tokyo, Japan). ␣-MEM was obtained from Flow Laboratories (McLean, VA). FCS was from HyClone (Logan, UT). 5Ј-[␣-32 P]dCTP megaprime DNA labeling system and [␥-32 P]ATP were purchased from Amersham...

show abstract

Section: Tgf-␤1mentioning

confidence: 99%

Section: Effect Of 1␣-25-(oh) 2 D 3 Analogs On Tgf-␤1-induced Ap-1 Trmentioning

confidence: 99%

Section: Effect Of 1␣-25-(oh) 2 D 3 Analogs On Tgf-␤1-induced Ap-1 Trmentioning

confidence: 99%

Section: ␣-25-(oh) 2 D 3 Stimulates At the Transcriptional Level Thementioning

confidence: 99%

Section: ␣-25-(oh) 2 D 3 Stimulates At the Transcriptional Level Thementioning

confidence: 99%

See 3 more Smart Citations

1α,25-Dehydroxyvitamin D3 Synergism toward Transforming Growth Factor-β1-induced AP-1 Transcriptional Activity in Mouse Osteoblastic Cells via Its Nuclear Receptor

Takeshita¹,

Imai²,

Kato³

et al. 1998

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

Vitamin D and the Vessel Wall

Bukoski¹

1996

Endocrinology of the Vasculature

View full text Add to dashboard Cite

Vitamin D and Cardiovascular Disease

Sourij

Dobnig

2011

Vitamin D

View full text Add to dashboard Cite

A synthetic analogue of vitamin D3, 22-oxa-1,25-dihydroxy-vitamin D3, stimulates the production of prostacyclin by vascular tissues

Cited by 10 publications

References 22 publications

1α,25-Dehydroxyvitamin D3 Synergism toward Transforming Growth Factor-β1-induced AP-1 Transcriptional Activity in Mouse Osteoblastic Cells via Its Nuclear Receptor

1α,25-Dehydroxyvitamin D3 Synergism toward Transforming Growth Factor-β1-induced AP-1 Transcriptional Activity in Mouse Osteoblastic Cells via Its Nuclear Receptor

Vitamin D and the Vessel Wall

Vitamin D and Cardiovascular Disease

Contact Info

Product

Resources

About