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All-trans retinoic acid

PloS one, 2022-11, Vol.17 (11), p.e0276541 [Peer Reviewed Journal]

COPYRIGHT 2022 Public Library of Science ;ISSN: 1932-6203 ;EISSN: 1932-6203 ;DOI: 10.1371/journal.pone.0276541

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  • Title:
    All-trans retinoic acid
  • Author: Hasbullah, Jafar S ; Scott, Erika N ; Bhavsar, Amit P ; Gunaretnam, Erandika P ; Miao, Fudan ; Soliman, Hesham ; Carleton, Bruce C ; Ross, Colin J. D
  • Subjects: Analysis ; Anthracyclines ; Cancer ; Chemotherapy ; Composition ; Gene expression ; Health aspects ; Patient outcomes ; Toxicity testing ; Tretinoin
  • Is Part Of: PloS one, 2022-11, Vol.17 (11), p.e0276541
  • Description: The effectiveness of anthracycline chemotherapeutics (e.g., doxorubicin) is limited by anthracycline-induced cardiotoxicity (ACT). A nonsynonymous variant (S427L) in the retinoic acid receptor-[gamma] (RARG) gene has been associated with ACT. This variant causes reduced RARG activity, which is hypothesized to lead to increased susceptibility to ACT through reduced activation of the retinoic acid pathway. This study explored the effects of activating the retinoic acid pathway using a RAR-agonist, all-trans retinoic acid (ATRA), in human cardiomyocytes and mice treated with doxorubicin. In human cardiomyocytes, ATRA induced the gene expression of RARs (RARG, RARB) and repressed the expression of topoisomerase II enzyme genes (TOP2A, TOP2B), which encode for the molecular targets of anthracyclines and repressed downstream ACT response genes. Importantly, ATRA enhanced cell survival of human cardiomyocytes exposed to doxorubicin. The protective effect of ATRA was also observed in a mouse model (B6C3F1/J) of ACT, in which ATRA treatment improved heart function compared to doxorubicin-only treated mice. Histological analyses of the heart also indicated that ATRA treatment reduced the pathology associated with ACT. These findings provide additional evidence for the retinoic acid pathway's role in ACT and suggest that the RAR activator ATRA can modulate this pathway to reduce ACT.
  • Publisher: Public Library of Science
  • Language: English
  • Identifier: ISSN: 1932-6203
    EISSN: 1932-6203
    DOI: 10.1371/journal.pone.0276541
  • Source: PubMed Central (Open access)
    Geneva Foundation Free Medical Journals at publisher websites
    AUTh Library subscriptions: ProQuest Central
    Directory of Open Access Journals
    Public Library of Science
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