Effects of Vitamin D&lt;sub&gt;3&lt;/sub&gt; on Keratinocyte Proliferation and Differentiation in vitro: Modulation by Ligands for Retinoic Acid and Retinoid X Receptors

Sørensen, Steen; Sølvsten, Henrik; Politi, Yaei; Kragballe, Knud

doi:10.1159/000211479

Cited by 17 publications

(10 citation statements)

References 22 publications

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“…25 In addition, NB4 cells express PML-RARa, RARa, RXRa and RXRb in basal conditions as well as RARb upon challenge with ATRA. 26 For these reasons, we first compared the effects of 9-cis RA [pan-RAR and pan-RXR agonist], 25 29 as well as CD2409 [anti-AP1 retinoid] to those of ATRA, using two different concentrations (10 76 and 10 78 M) of each retinoid. We did not take into consideration agonists of RARg, since this type of receptor is not expressed in undifferentiated or ATRA-differentiated NB4 cells.…”

Section: Resultsmentioning

confidence: 99%

Retinoid-dependent growth inhibition, differentiation and apoptosis in acute promyelocytic leukemia cells. Expression and activation of caspases

et al. 2000

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In the NB4 model of acute promyelocytic leukemia (APL), ATRA, 9-cis retinoic acid (9-cis RA), the pan-RAR and RARaselective agonists, TTNPB and AM580, induce growth inhibition, granulocytic differentiation and apoptosis. By contrast, two RXR agonists, a RARb agonist and an anti-AP1 retinoid have very limited activity, ATRA-and AM580-dependent effects are completely inhibited by RAR antagonistic blockade, while 9-cis RA-induced cell-growth-inhibition and apoptosis are equally inhibited by RAR and RXR antagonists. ATRA, 9-cis RA and AM580 cause upregulation of the mRNAs coding for pro-caspase-1, -7, -8, and -9, which, however, results in increased synthesis of only pro-caspase-1 and -7 proteins. These phenomena are associated with activation of pro-caspase-6, -7 and -8, cytochrome c release from the mitochondria, inversion of Bcl-2/Bax ratio and degradation of PML-RARa. Caspase activation is fundamental for retinoid-induced apoptosis, which is suppressed by the caspase-inhibitor z-VAD. Cell Death and Differentiation (2000) 7, 447 ± 460.

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Section: Resultsmentioning

confidence: 99%

Retinoid-dependent growth inhibition, differentiation and apoptosis in acute promyelocytic leukemia cells. Expression and activation of caspases

et al. 2000

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“…39 In studies of hamster sebaceous gland cells in vivo, vitamin D increased the accumulation of wax esters in pilosebaceous units while decreasing the amount of triglycerides. In addition, there is positive biological interaction between the metabolic effects of testosterone and vitamin D in other organ systems, although this has not yet been shown in skin.…”

Section: Discussionmentioning

confidence: 99%

Milk consumption and acne in teenaged boys

Adebamowo

Spiegelman

Berkey

et al. 2008

Journal of the American Academy of Dermatology

228

180

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Objective-We sought to examine the association between dietary dairy intake and teenaged acne among boys.Methods-This was a prospective cohort study. We studied 4273 boys, members of a prospective cohort study of youths and of lifestyle factors, who reported dietary intake on up to 3 food frequency questionnaires from 1996 to 1998 and teenaged acne in 1999. We computed multivariate prevalence ratios and 95% confidence intervals for acne.Results-After adjusting for age at baseline, height, and energy intake, the multivariate prevalence ratios (95% confidence interval; P value for test of trend) for acne comparing highest (>2 servings/d) with lowest (<1/wk) intake categories in 1996 were 1.16 (1.01, 1.34; 0.77) for total milk, 1.10 (0.94, 1.28; 0.83) for whole/2% milk, 1.17 (0.99, 1.39; 0.08) for low-fat (1%) milk, and 1.19 (1.01, 1.40; 0.02) for skim milk.Limitations-Not all members of the cohort responded to the questionnaire. Acne assessment was by self-report and boys whose symptoms might have been part of an underlying disorder were not excluded. We did not adjust for steroid use and other lifestyle factors that may affect occurrence of acne.Conclusion-We found a positive association between intake of skim milk and acne. This finding suggests that skim milk contains hormonal constituents, or factors that influence endogenous hormones, in sufficient quantities to have biological effects in consumers. Reprints not available from the authors. HHS Public Access Author Manuscript Author ManuscriptAuthor Manuscript Author ManuscriptAcne remains a substantial cause of morbidity and occasional mortality among adolescents and young adults. 1 It is a common, chronic, and self-limiting skin disease that causes physical and psychologic morbidity in up to 90% of adolescents and young adults. 2 In Western countries, it affects all ages, but its maximum prevalence peaks at 16 to 18 years when 75% to 98% of this age group is affected. 2 Even though acne is more common in girls, overall and below the age of 12 years, after 15 years of age it is slightly more common in boys. 3 Acne results from androgen-stimulated hyperkeratinization and obstruction of the pilosebaceous follicles secondary to failure of normal desquamation of the follicular epithelium; androgen-stimulated sebum production; subsequent colonization of the follicles by Propionibacterium acnes and Malassezia species ; and, variably, inflammation. 4 Previous studies have shown an association between dietary intake of milk and prevalence of teenaged acne. Ecological studies suggest an association between Western diet and acne 5 whereas Robinson 6 reported that among 1925 patients who kept a food diary, the majority implicated milk in acne flares. In a previous study of US female nurses who reported their high-school diet and prevalence of physician-diagnosed severe teenaged acne, we found a positive association with intake of total and skim milk. 7 We also found a positive association between milk consumption and prevalence of acne among a prospective co...

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“…Vitamin A and vitamin D exert their effects on gene transcription after binding to specific nuclear receptors, retinoic acid receptors or retinoid X receptors (RXRs) [9] , and vitamin D receptor (VDR) [10,11] , respectively. Moreover, it has been known that RXR and VDR may form heterodimers [12] , and many genes that are transcriptionally active in keratinocytes, including those controlling keratinization, inflammation, cell cycle and apoptosis, contain regulatory sequences that are targets for RXR, VDR or their heterodimers [13] .…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, it has been known that RXR and VDR may form heterodimers [12] , and many genes that are transcriptionally active in keratinocytes, including those controlling keratinization, inflammation, cell cycle and apoptosis, contain regulatory sequences that are targets for RXR, VDR or their heterodimers [13] . The formation of RXR/VDR heterodimers may lead to different interactions between the 2 pathways, resulting in additive, synergistic or antagonistic effects upon concomitant administration of vitamins A and D [10,14] . The therapeutical potential of vitamins A and D in skin diseases may be limited by the fact that vitamin D in its active form affects calcium homeostasis [15] , while 15-25% of the patients fail to have satisfactory therapeutical responses to retinoids [16] .…”

Section: Introductionmentioning

confidence: 99%

Antiproliferative Effect of Vitamin A and D Analogues on Adult Human Keratinocytes in vitro

Popadić

Ramić²,

Medenica³

et al. 2008

Skin Pharmacol Physiol

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Background: Vitamin A and D analogues play an important role in epidermal homeostasis and are used in the treatment of various skin diseases. The failure of retinoid and vitamin D treatments is sometimes difficult to explain. Methods: We analyzed the effect of all-trans retinoic acid (all-trans RA), 13-cis retinoic acid (13-cis RA), ergocalciferol and cholecalciferol in keratinocyte cultures established from adult donors, on the cell proliferation by means of [³H]thymidine incorporation and apoptosis after fluorescein diacetate/trypan blue staining. Results: All tested agents exerted a dose-dependent inhibition of keratinocyte proliferation in the concentration range of 1.25–5 µM. Based on IC₅₀ values, the antiproliferative efficiency was as follows: cholecalciferol > ergocalciferol = all-trans RA > 13-cis RA. The observed effect of cholecalciferol and ergocalciferol, but not retinoids, involved the induction of apoptotic cell death. Combining vitamins A and D did not further increase the proliferation block and even displayed an antagonistic effect. Conclusion: The susceptibility of keratinocytes to the antiproliferative action of vitamins A and D was markedly different in cell cultures derived from different donors, indicating a possible predictive value of the in vitro testing for the efficiency of the clinical response to these agents.

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Effects of Vitamin D<sub>3</sub> on Keratinocyte Proliferation and Differentiation in vitro: Modulation by Ligands for Retinoic Acid and Retinoid X Receptors

Cited by 17 publications

References 22 publications

Retinoid-dependent growth inhibition, differentiation and apoptosis in acute promyelocytic leukemia cells. Expression and activation of caspases

Retinoid-dependent growth inhibition, differentiation and apoptosis in acute promyelocytic leukemia cells. Expression and activation of caspases

Milk consumption and acne in teenaged boys

Antiproliferative Effect of Vitamin A and D Analogues on Adult Human Keratinocytes in vitro

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