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2′–5′ oligoadenylate synthetase‑like 1 (OASL1) protects against atherosclerosis by maintaining endothelial nitric oxide synthase mRNA stability

Author

Listed:
  • Tae Kyeong Kim

    (Ewha Womans University)

  • Sejin Jeon

    (Ewha Womans University
    Andong National University)

  • Seonjun Park

    (Ulsan National Institute of Science & Technology (UNIST))

  • Seong-Keun Sonn

    (Ewha Womans University)

  • Seungwoon Seo

    (Ewha Womans University)

  • Joowon Suh

    (Ewha Womans University)

  • Jing Jin

    (Ewha Womans University)

  • Hyae Yon Kweon

    (Ewha Womans University)

  • Sinai Kim

    (Ewha Womans University)

  • Shin Hye Moon

    (Ewha Womans University)

  • Okhee Kweon

    (Ewha Womans University)

  • Bon-Hyeock Koo

    (Kangwon National University
    University of Pennsylvania)

  • Nayoung Kim

    (The Catholic University of Korea
    The Catholic University of Korea)

  • Hae-Ock Lee

    (The Catholic University of Korea
    The Catholic University of Korea)

  • Young-Myeong Kim

    (Kangwon National University)

  • Young-Joon Kim

    (Yonsei University)

  • Sung Ho Park

    (Ulsan National Institute of Science & Technology (UNIST))

  • Goo Taeg Oh

    (Ewha Womans University)

Abstract

Endothelial nitric oxide synthase (eNOS) decreases following inflammatory stimulation. As a master regulator of endothelial homeostasis, maintaining optimal eNOS levels is important during cardiovascular events. However, little is known regarding the mechanism of eNOS protection. In this study, we demonstrate a regulatory role for endothelial expression of 2′–5′ oligoadenylate synthetase-like 1 (OASL1) in maintaining eNOS mRNA stability during athero-prone conditions and consider its clinical implications. A lack of endothelial Oasl1 accelerated plaque progression, which was preceded by endothelial dysfunction, elevated vascular inflammation, and decreased NO bioavailability following impaired eNOS expression. Mechanistically, knockdown of PI3K/Akt signaling-dependent OASL expression increased Erk1/2 and NF-κB activation and decreased NOS3 (gene name for eNOS) mRNA expression through upregulation of the negative regulatory, miR-584, whereas a miR-584 inhibitor rescued the effects of OASL knockdown. These results suggest that OASL1/OASL regulates endothelial biology by protecting NOS3 mRNA and targeting miR-584 represents a rational therapeutic strategy for eNOS maintenance in vascular disease.

Suggested Citation

  • Tae Kyeong Kim & Sejin Jeon & Seonjun Park & Seong-Keun Sonn & Seungwoon Seo & Joowon Suh & Jing Jin & Hyae Yon Kweon & Sinai Kim & Shin Hye Moon & Okhee Kweon & Bon-Hyeock Koo & Nayoung Kim & Hae-Ock, 2022. "2′–5′ oligoadenylate synthetase‑like 1 (OASL1) protects against atherosclerosis by maintaining endothelial nitric oxide synthase mRNA stability," Nature Communications, Nature, vol. 13(1), pages 1-19, December.
    • Handle: RePEc:nat:natcom:v:13:y:2022:i:1:d:10.1038_s41467-022-34433-z
    DOI: 10.1038/s41467-022-34433-z
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    References listed on IDEAS

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    1. Peter Libby & Paul M Ridker & Göran K. Hansson, 2011. "Progress and challenges in translating the biology of atherosclerosis," Nature, Nature, vol. 473(7347), pages 317-325, May.
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