Disease relevance of Retin-A

• In the trachea, hyperplasia of basal epithelial cells was observed by Day 4 (T4) following the withdrawal of retinoic acid from retinoate-cycled, stringently deficient rats [1].
• The cytotoxicity was determined using an MTT assay with HCT116 colon cancer cells, and the IC(50) of N-acylated retinamide derivative 4A and O-acylated retinoate derivative 5B was 1.67 microM and 0.65 microM, respectively, which are about five and 13-fold better than that of 4-HPR (8.21 microM), a prototype N-acylated derivative [2].

High impact information on Retin-A

• In wild-type cells, fatty acids induced a thermogenic response similar to norepinephrine, but fatty acids (and retinoate) were practically without effect in Ucp1(-/-) cells [3].
• Methyl retinoate is the major product of hydrolysis with CH3OH:KOH [4].
• Ethyl (E)-9-(2-norbornenyl)-3,7-dimethylnona-2,4,6,8-tetraenoate (9), (E)-3,7-dimethyl-9-(2-ethyl-6,6-dimethyl-1-cyclohexen-1-yl)nona-2,4,6,8-tetraenoic acid (25), and 2-(2'-methoxyethoxy)ethyl retinoate (26) displayed good activity in the inhibition of tumor promoter-induced mouse epidermal ornithine decarboxylase assay [5].
• The effect of vitamin A deficiency on the functional integrity of the reticuloendothelial system and the phagocytic capacity of circulating polymorphonuclear leukocytes was evaluated in retinoate-cycled vitamin A-deficient rats under conditions such that secondary dietary imbalances were eliminated [6].
• ADAMTS-5 was expressed constitutively in synovium with little or no transcriptional regulation by recombinant human interleukin-1 alpha or all-trans-retinoate, factors previously shown to upregulate aggrecanase activity in cartilage [7].

Biological context of Retin-A

• 10-9359-TMMP ethyl retinoate on plating efficiency, sister-chromatid exchange (SCE) and on mitomycin-C (MMC)-induced SCE were studied in Chinese hamster V79 cells [8].
• Preclinical studies pertaining to the pharmacology and toxicology of BMY 30123 (4-acetamidophenyl retinoate) are reported [9].
• After methylation this compound eluted as 13-cis-methyl retinoate and as all-trans-methyl retinoate [10].

Anatomical context of Retin-A

• Biological activities of ethyl retinoate on HL-60 cells were also very weak [11].
• Both phorbol retinoate acetate and mezerein stimulated growth in lung normal cell lines (human fibroblastic PEH cells and rat epithelial TP9 cells) while inhibiting growth in lung tumor cell lines (human small-cell cancer-derived cell line IRSC-10M and adenocarcinoma-derived cell line A549) [12].

Associations of Retin-A with other chemical compounds

• Modulation of secreted plasminogen activator activity of human renal carcinoma cells by dimethylsulfoxide, butyrate and retinoate [13].

Gene context of Retin-A

• In contrast, the O-acylated retinoate derivatives (1B-5B) activated all three RAR isotypes without specificity to an extent similar to ATRA [2].

Analytical, diagnostic and therapeutic context of Retin-A

• Radioimmunoassay revealed that the amount (pmol of epitope/mg of total glycosaminoglycan) of (342)FFGVG epitope released from cartilage remained constant over a 5-day culture period and was not increased by IL-1alpha or retinoate [14].

References