Retinoid Concentrations in the Mouse during Postnatal Development and after Maternal Vitamin A Supplementation

García, Ada L.; Rühl, Ralph; Schweigert, Florian J.

doi:10.1159/000087697

Cited by 8 publications

(12 citation statements)

References 61 publications

(61 reference statements)

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“…Immunoprecipitated PI3K was incubated with 10 mg PI, retinol vehicle (ethanol) or increasing concentrations of retinol (0, 10, 20, 50, and 100 mg; corresponding to 0, 0.6, 1.2, 2.9, and 5.8 mM retinol, respectively) for 10 min at room temperature prior to the addition of 10 mCi of [g- 32 P] ATP and 20 mM MgCl 2 for 20 min at room temperature. In addition, immunoprecipitated PI3K was incubated with 10 mg retinol and increasing concentrations of PI (10,20, and 50 mg). The total volume of ethanol vehicle was the same in all samples, regardless of retinol concentration.…”

Section: Pi3k Substrate Competition Assaymentioning

confidence: 99%

Retinol decreases phosphatidylinositol 3‐kinase activity in colon cancer cells

Park

Wilder

Chipuk

et al. 2007

Molecular Carcinogenesis

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Previously, we showed that retinol inhibited all-trans-retinoic acid (ATRA)-resistant human colon cancer cell invasion via a retinoic acid receptor-independent mechanism. Because phosphatidylinositol 3-kinase (PI3K) regulates cell invasion, the objective of the current study was to determine if retinol affected PI3K activity. Following 24 h of serum starvation, the ATRA resistant human colon cancer cell lines HCT-116 and SW620 were treated with 0, 1, or 10 microM retinol. Thirty minutes of retinol treatment resulted in a significant decrease in PI3K activity in both cell lines. To determine the mechanism by which retinol reduces PI3K activity, the levels and heterodimerization of the regulatory subunit, p85, and the catalytic subunit, p110, of PI3K were examined. Retinol treatment did not alter p85 or p110 protein levels or the heterodimerization of these subunits at any time point examined. To determine if retinol affected the ability of PI3K to phosphorylate the substrate, phosphatidylinositol (PI), PI3K was immunoprecipitated from control cells and incubated with 10 microg PI and increasing concentrations of retinol or 10 microg retinol and increasing concentrations of PI. Retinol decreased PI3K activity in a dose-responsive manner and increased PI suppressed the inhibitory effect of retinol on PI3K activity. Finally, the PI3K inhibitor, LY294002, mimicked the ability of retinol to decrease cell invasion. Computational modeling revealed that retinol may inhibit PI3K activity in a manner similar to that of wortmannin. Thus, a decrease in PI3K activity due to retinol treatment may confer the ability of retinol to inhibit ATRA-resistant colon cancer cell invasion.

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Section: Pi3k Substrate Competition Assaymentioning

confidence: 99%

Retinol decreases phosphatidylinositol 3‐kinase activity in colon cancer cells

Park

Wilder

Chipuk

et al. 2007

Molecular Carcinogenesis

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“…Lactation is another physiological process where retinoids and carotenoids are not homeostatically regulated in breast milk [6,11,12,13,14]. Low or high dietary intake of retinoids and carotenoids results in low or increased concentrations of retinoids and carotenoids in breast milk [15,16].…”

Section: Introductionmentioning

confidence: 99%

“…Various factors are involved in allergic sensitization and a clear statement cannot be drawn based on current knowledge [95,96]. The concentration of carotenoids and retinoids in breast milk seems not to be homeostatically regulated like the retinol levels in human serum [12,13,97]. Various reports clearly display that an increased maternal consumption of vitamin A results in an increased amount of vitamin A in breast milk [14,98,99,100].…”

Section: Introductionmentioning

confidence: 99%

Non-Pro-Vitamin A and Pro-Vitamin A Carotenoids in Atopy Development

Rühl

2013

Int Arch Allergy Immunol

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Carotenoids are important derivatives of the human diet and occur in high concentrations in the human organism. Various carotenoids are also present in human breast milk and are transferred to breast-fed children. The alternative to breastfeeding is supplementation with an infant milk formula, but these formulas contain only a limited variety of carotenoids. Our question is: ‘What is the function of various carotenoids in human nutrition with a special emphasis on child development and the development of atopy?’ In this review, the mechanisms of action of the most important non-pro-vitamin A and pro-vitamin A carotenoids: α-carotene, β-carotene, β-cryptoxanthin, lutein, zeaxanthin, lycopene and retinoids are discussed. In summary, the combination of carotenoids, especially lycopene, seems to be of great importance, and exclusive usage of β-carotene in infant formula may yield in an increased atopy prevalence mediated in various target organs like the skin, lungs and immune competent cells. We conclude that the determination of novel bioactive metabolites of various carotenoids, at various stages in different organs during atopy development, might be the key to understanding the potential importance of carotenoids on atopy development.

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“…In addition, loss of the ability to convert retinol to ATRA along with the loss of RAR is a common event in cancer progression (1,47). Colonocytes, primary colon tumors, and hepatic metastases are all exposed to elevated levels of retinol following dietary vitamin A supplementation (3)(4)(5). Using a nude mouse xenograft model, we showed previously that dietary vitamin A supplementation with retinyl palmitate for 1 mo prior to and 5 wk following (the same timecourse used herein) intrasplenic injection of HCT-116 colorectal tumor cells decreased the multiplicity of hepatic metastatic tumors (3).…”

Section: Discussionmentioning

confidence: 99%

“…In addition, vitamin A is stored in the liver as retinyl esters. Elevated intestinal lumen and hepatic concentrations of retinol have been attained by dietary vitamin A supplementation (3)(4)(5).…”

Section: Introductionmentioning

confidence: 99%

Phosphatidylinositol 3-Kinase Mediates the Ability of Retinol to Decrease Colorectal Cancer Cell Invasion

Lengyel

Park

Brunson

et al. 2014

Nutrition and Cancer

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Previously, we showed that retinol (vitamin A) decreased both colorectal cancer cell invasion and phosphatidylinositol 3-kinase (PI3K) activity through a retinoic acid receptor-independent mechanism. Here, we determined if these phenomena were related by using parental HCT-116 cells that harbor 1 allele of wild-type PI3K and 1 allele of constitutively active (ca) PI3K and 2 mutant HCT-116 cell lines homozygous for caPI3K. In vitro, treatment of parental HCT-116 cells with 10 μM retinol reduced cell invasion whereas treatment of mutant HCT-116 cell lines with retinol did not. Treatment with 10 μM retinol also decreased the activity of matrixmetalloproteinase-9 and increased tissue inhibitor of matrixmetalloproteinase-I levels in parental, but not mutant, HCT-116 cells. Finally, parental or mutant cells were intrasplenically injected into athymic mice consuming diets with or without supplemental vitamin A. As expected, vitamin A supplementation tended (P = 0.18) to reduce the incidence of metastases in mice injected with the parental cell line and consuming the supplemented diet. In contrast, metastatic incidence was not affected (P = 1.00) by vitamin A supplementation in mice injected with mutant cells. These data indicate that the capacity of retinol to inhibit PI3K activity confers its ability to decrease colorectal cancer metastasis.

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Retinoid Concentrations in the Mouse during Postnatal Development and after Maternal Vitamin A Supplementation

Cited by 8 publications

References 61 publications

Retinol decreases phosphatidylinositol 3‐kinase activity in colon cancer cells

Retinol decreases phosphatidylinositol 3‐kinase activity in colon cancer cells

Non-Pro-Vitamin A and Pro-Vitamin A Carotenoids in Atopy Development

Phosphatidylinositol 3-Kinase Mediates the Ability of Retinol to Decrease Colorectal Cancer Cell Invasion

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