Effect of age on duodenal 1,25-dihydroxyvitamin D-3 receptors in Wistar rats

Takamoto, Shoshi; Seino, Yoshiki; Sacktor, Bertram; Liang, Chunyu

doi:10.1016/0304-4165(90)90148-p

Cited by 42 publications

(32 citation statements)

References 29 publications

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“…Previous studies have also indicated an age-related decrease in the number of VDR (Horst et al 1990, Takamoto et al 1990). The number of VDR is a primary determinant of the biological response to 1,25(OH) 2 D 3 , as previously shown in osteoblastic cell lines (Dokoh et al 1984, Liel et al 1992 and in human populations in association with VDR-gene polymorphism (Gross et al 1996, Arai et al 1997, Harris et al 1997.…”

Section: Introductionmentioning

confidence: 86%

Regulation of vitamin D receptor expression via estrogen-induced activation of the ERK 1/2 signaling pathway in colon and breast cancer cells

Gilad

Bresler²,

J³

et al. 2005

Journal of Endocrinology

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We previously demonstrated that 17 -estradiol (E2) regulates the transcription and expression of the vitamin D receptor (VDR) in rat colonocytes and duodenocytes in vivo. The aim of the present study was to assess whether the extracellular signal-regulated kinase (ERK) induced by E2 is involved in regulating VDR expression. We compared E2-associated signaling activity in HT29 colon cancer cells, a non-classical E2-target, with that in MCF-7 breast cancer cells, the natural targets of the hormone. E2 did not affect proliferation of HT29 cells, but enhanced proliferation of MCF-7 cells. Vitamin D inhibited proliferation of both cell lines and the combined treatment induced potentiation of vitamin D activity. E2 upregulated VDR transcription and protein expression concomitantly with ERK 1/2 phosphorylation in both cell lines. PD98059, a specific mitogen-activated protein kinase (MAPK) inhibitor, prevented E2-mediated activation of ERK 1/2, with concomitant inhibition of VDR expression. ICI182780 inhibited VDR expression in HT29 and MCF-7 cell lines. A conjugate of E2 and bovine serum albumin upregulated phosphorylation of ERK 1/2 and concomitantly enhanced VDR expression in a similar fashion as the nonconjugated hormone. Expression of ER and ER was detected in MCF-7 and HT29 cell lines respectively, which localized to the nuclei, cytosol and caveolar membrane rather than non-caveolar membrane. Disruption of lipid rafts/caveolae by depleting cellular cholesterol with the cholesterol-binding reagentmethylcyclodextrin blocked ERK 1/2 phosphorylation concomitantly with VDR upregulation. The tyrosine phosphorylation inhibitor suramin and src kinase inhibitor PP2 inhibited both ERK 1/2 phosphorylation and VDR expression. E2 induced phosphorylation of Raf and Jun in a time-dependent manner. The Ras/Raf dependent inhibitor of transactivation sulindac sulfide also blocked E2 effects. The specific c-Jun phosphorylation inhibitor SP600125 dose dependently inhibited c-Jun phosphorylation and VDR expression. The MAPK/ERK kinase inhibitor PD 98059 downregulated both c-Jun phosphorylation and VDR expression indicating that upstream and downstream events in the signaling cascade are all related to the control of VDR expression. Taken together, our data suggest that E2 binds to receptors compartmentalized to membranal caveolar domains in HT29 and MCF-7 cells, inducing ERK 1/2 activation and transcriptional activity, which finally results in upregulation of expression of the VDR gene.

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Section: Introductionmentioning

confidence: 86%

Regulation of vitamin D receptor expression via estrogen-induced activation of the ERK 1/2 signaling pathway in colon and breast cancer cells

Gilad

Bresler²,

J³

et al. 2005

Journal of Endocrinology

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“…In contrast, the VDR content of kidney does not change with aging, but the affinity of kidney VDR for DNA-cellulose has been shown to decline in aging (144). This decline in VDR affinity for DNA is not seen in duodenum, however (138,144). Two different VDR bands (50K and 52K) were detected by immunoblotting in kidney, but only a single 52K band was detected in duodenum (144).…”

Section: Vitamin Dmentioning

confidence: 89%

“…The VDR also declines with aging in rat bone (142). The apparent affinity of intestinal and bone VDR for 1,25(0H)2D3 remained unchanged (138,142). In contrast, the VDR content of kidney does not change with aging, but the affinity of kidney VDR for DNA-cellulose has been shown to decline in aging (144).…”

Section: Vitamin Dmentioning

confidence: 91%

“…In kidney, VDR mRNA is induced sometime between birth and one wk of age (141). Both the VDR and its mRNA decline in rat intestine with aging after about one mo of age (138,142,143). The VDR also declines with aging in rat bone (142).…”

Section: Vitamin Dmentioning

confidence: 99%

“…Concentrations of l,25(OH)2D3 in plasma have been shown to decline with aging in humans and several animal species (27,137,138,139). The defect seems to be in decreased activity of the kidney la-hydroxylase enzyme (28 than in young adults (137).…”

Section: Vitamin Dmentioning

confidence: 99%

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Age, gender and diet effects on gene expression regulated by 1,25-dihydroxyvitamin D3

Johnson

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This manuscript has been reproduced from the microfilm master. UMI films the text directly from the original or copy submitted. Thus, some thesis and dissertation copies are in typewriter face, while others may be from any type of computer printer.The quality of this reproduction is dependent upon the quality of the copy submitted. Broken or indistinct print, colored or poor quality illustrations and photographs, print bleedthrough, substandard margins, and improper alignment can adversely affect reproduction.In the unlikely event that the author did not send UMI a complete manuscript and there are missing pages, these will be noted. Also, if unauthorized copyright material had to be removed, a note will indicate the deletion.Oversize materials (e.g., maps, drawings, charts) are reproduced by sectioning the original, beginning at the upper left-hand comer and continuing from left to right in equal sections with small overlaps. Each original is also photographed in one exposure and is included in reduced form at the back of the book.

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1,25(OH)2-vitamin D3 affects the subcellular distribution of protein kinase C isoenzymes in rat duodenum: Influence of aging

Balogh

Boland

2000

J. Cell. Biochem.

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We have previously shown that the steroid hormone 1, 25-dihydroxy-vitamin D(3) [1,25(OH)(2)D(3)] stimulates total cell protein kinase C (PKC) activity in rat duodenum, an effect that is severely impaired in old animals. We further examined the role of 1, 25(OH)(2)D(3) on PKC as it relates to aging by measuring hormone-induced changes in subcellular localization of PKC activity and isoenzymes in duodenal mucosae from young (three-month-old) and aged (24-month-old) rats. Short treatment of duodenum with 1, 25(OH)(2)D(3) (0.1 nM, 1 min) increased membrane-associated PKC activity, whereas it decreased the activity in the cytosol of young rats but was without significant effect in aged animals. Furthermore, the ability to translocate was present in young animals after a short treatment with the phorbol ester 12-O-tetradecanoyl phorbol 13-acetate (TPA; 100 nM) or dioctanoyl-glycerol (50 microM), whereas the ability was absent in aged rats, suggesting that PKC function was impaired with aging independent of agonist stimulation. The expression of specific PKC isoenzymes and changes in their subcellular distribution after short exposure of the duodenum to the hormone were determined. Western blot analysis of total homogenates using antibodies to various PKC isoforms allowed detection of PKC alpha, beta, and delta. The expression of the straight theta and the zeta isoforms was in addition demonstrated by reverse transcription-polymerase chain reaction. The pattern of isoenzymes present in the duodenum was unaffected by aging. In young rats, 1, 25(OH)(2)D(3) translocates PKC alpha, beta, and delta to the membrane and nucleus; however, no translocation of PKC isoforms was observed in 24-month-old animals in response to the hormone. In summary, in rat duodenum, 1,25(OH)(2)D(3) modulation of PKC activity and isoenzyme subcellular distribution are impaired with aging and may explain age-induced alterations in the intestinal processes under the control of the hormone.

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Effect of age on duodenal 1,25-dihydroxyvitamin D-3 receptors in Wistar rats

Cited by 42 publications

References 29 publications

Regulation of vitamin D receptor expression via estrogen-induced activation of the ERK 1/2 signaling pathway in colon and breast cancer cells

Regulation of vitamin D receptor expression via estrogen-induced activation of the ERK 1/2 signaling pathway in colon and breast cancer cells

Age, gender and diet effects on gene expression regulated by 1,25-dihydroxyvitamin D3

1,25(OH)2-vitamin D3 affects the subcellular distribution of protein kinase C isoenzymes in rat duodenum: Influence of aging

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