KLFII is an Epigenetic Mediator of DRD2/Dopaminergic Signaling in Endometriosis
This study investigated how transcription factor KLF11 regulates DRD2 expression in endometriosis, finding KLF11 binding activates the DRD2 promoter and gene expression, with its loss associated with fibrosis and decreased DRD2 in a mouse model.
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The study investigated how the transcription factor KLFII regulates dopamine receptor 2 (DRD2) by examining KLFII binding/activation of the DRD2 promoter in eutopic and ectopic endometrial cell lines and in a surgically induced murine model of endometriosis. KLFII-driven promoter activation of DRD2 was conserved across species and corresponded to increased DRD2 expression in an endometrial cell line and in primary endometriotic cells, while Klf11 knockout animals showed progressive fibrosis with decreased Drd2 expression. The authors note a mechanistic limitation: activation of DRD2 by KLFII could not be fully explained by loss of epigenetic corepressor binding and likely involves selective coactivator recruitment, which was not identified in this work. This paper is centrally about endometriosis — it defines KLFII as an epigenetic regulator of DRD2/dopaminergic signaling in endometriotic lesions and models.
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Cited by (9)
- Potential link between the nerve injury-induced protein (Ninjurin) and the pathogenesis of endometriosis 2022
- Additional file 1 of Possible involvement of neuropeptide and neurotransmitter receptors in Adenomyosis 2021
- Possible involvement of neuropeptide and neurotransmitter receptors in Adenomyosis 2021
- Cellular Components Contributing to Fibrosis in Endometriosis: A Literature Review 2019
- Novel TRERF1 mutations in Chinese patients with ovarian endometriosis 2018
- Evaluation of PAI-1 in endometriosis using a homologous immunocompetent mouse model† 2018
- Epigenetics of Endometriosis 2018
- From Endometriosis to Cancer: Spotlight on Intracellular Signaling Cascades and MicroRNAs 2018
- p38 Mitogen-Activated Protein Kinase is Involved in the Pathogenesis of Endometriosis by Modulating Inflammation, but not Cell Survival 2017
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