tretinoin and Hyperhomocysteinemia

tretinoin has been researched along with Hyperhomocysteinemia* in 2 studies

Other Studies

2 other study(ies) available for tretinoin and Hyperhomocysteinemia

Article	Year
Sacroiliitis and muscle cramps in a healthy young man: some spearhead on MTHFR mutations. Rheumatology international, 2010, Volume: 30, Issue:7 Topics: Adult; Anti-Inflammatory Agents, Non-Steroidal; Arthritis; Biomarkers; DNA Mutational Analysis; Gene Expression Regulation, Enzymologic; Genetic Predisposition to Disease; Homocysteine; Humans; Hyperhomocysteinemia; Keratolytic Agents; Low Back Pain; Male; Methionine; Methylenetetrahydrofolate Reductase (NADPH2); Muscle Cramp; Muscle, Skeletal; Mutation; Radiography; Sacroiliac Joint; Sulfasalazine; Tretinoin	2010
Homocysteine inhibits retinoic acid synthesis: a mechanism for homocysteine-induced congenital defects. Experimental cell research, 2000, Oct-10, Volume: 260, Issue:1 Hyperhomocysteinemia is frequently associated with congenital defects of the heart and neural tube and is a suspected pathogenic factor in atherosclerosis and neoplasia. Results in the present report show homocysteine treatment disrupts normal development of avian embryos; and this effect is prevented by retinoic acid. Based on this, we hypothesize that homocysteine may exert its teratogenic effects by disrupting retinoic acid signaling during development. A reporter cell line transfected with a retinoic acid response element (RARE) linked to a lacZ reporter gene was used to identify the site of retinoid inhibition. Using this reporter cell line, we show that homocysteine inhibits the oxidation of retinal to retinoic acid with concentrations of homocysteine that are in the pathophysiological range (.05 to 0.5 mM). In contrast, homocysteine concentrations as high as 5 mM are unable to inhibit the induction of lacZ by retinoic acid. We show that cellular uptake of homocysteine is sensitive to the specific L-system transport inhibitor, bicycloheptane, and bicycloheptane blocks the inhibition of retinoic acid synthesis by homocysteine, demonstrating that this inhibition occurs intracellularly. These results suggest that homocysteine-induced congenital defects are due to the specific ability of homocysteine to inhibit conversion of retinal to retinoic acid. Topics: Abnormalities, Drug-Induced; Animals; Biological Transport, Active; Cell Line; Chick Embryo; Genes, Reporter; Homocysteine; Hyperhomocysteinemia; Lac Operon; Receptors, Retinoic Acid; Signal Transduction; Transfection; Tretinoin	2000

Article

Year

Sacroiliitis and muscle cramps in a healthy young man: some spearhead on MTHFR mutations.

Rheumatology international, 2010, Volume: 30, Issue:7

Topics: Adult; Anti-Inflammatory Agents, Non-Steroidal; Arthritis; Biomarkers; DNA Mutational Analysis; Gene Expression Regulation, Enzymologic; Genetic Predisposition to Disease; Homocysteine; Humans; Hyperhomocysteinemia; Keratolytic Agents; Low Back Pain; Male; Methionine; Methylenetetrahydrofolate Reductase (NADPH2); Muscle Cramp; Muscle, Skeletal; Mutation; Radiography; Sacroiliac Joint; Sulfasalazine; Tretinoin

2010

Homocysteine inhibits retinoic acid synthesis: a mechanism for homocysteine-induced congenital defects.

Experimental cell research, 2000, Oct-10, Volume: 260, Issue:1

Hyperhomocysteinemia is frequently associated with congenital defects of the heart and neural tube and is a suspected pathogenic factor in atherosclerosis and neoplasia. Results in the present report show homocysteine treatment disrupts normal development of avian embryos; and this effect is prevented by retinoic acid. Based on this, we hypothesize that homocysteine may exert its teratogenic effects by disrupting retinoic acid signaling during development. A reporter cell line transfected with a retinoic acid response element (RARE) linked to a lacZ reporter gene was used to identify the site of retinoid inhibition. Using this reporter cell line, we show that homocysteine inhibits the oxidation of retinal to retinoic acid with concentrations of homocysteine that are in the pathophysiological range (.05 to 0.5 mM). In contrast, homocysteine concentrations as high as 5 mM are unable to inhibit the induction of lacZ by retinoic acid. We show that cellular uptake of homocysteine is sensitive to the specific L-system transport inhibitor, bicycloheptane, and bicycloheptane blocks the inhibition of retinoic acid synthesis by homocysteine, demonstrating that this inhibition occurs intracellularly. These results suggest that homocysteine-induced congenital defects are due to the specific ability of homocysteine to inhibit conversion of retinal to retinoic acid.

Topics: Abnormalities, Drug-Induced; Animals; Biological Transport, Active; Cell Line; Chick Embryo; Genes, Reporter; Homocysteine; Hyperhomocysteinemia; Lac Operon; Receptors, Retinoic Acid; Signal Transduction; Transfection; Tretinoin

2000