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Article

Monocyte/Macrophage-Specific Loss of ARNTL Suppresses Chronic Kidney Disease-Associated Cardiac Impairment

by
Yuya Yoshida
1,*,
Naoki Nishikawa
1,
Kohei Fukuoka
1,
Akito Tsuruta
2,
Kaita Otsuki
1,
Taiki Fukuda
1,
Yuma Terada
1,
Tomohito Tanihara
1,
Taisei Kumamoto
1,
Ryotaro Tsukamoto
1,
Takumi Nishi
1,
Kosuke Oyama
3,
Kengo Hamamura
1,
Kouta Mayanagi
4,
Satoru Koyanagi
2,
Shigehiro Ohdo
1 and
Naoya Matsunaga
1,*
1
Department of Clinical Pharmacokinetics, Faculty of Pharmaceutical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan
2
Department of Pharmaceutics, Faculty of Pharmaceutical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan
3
Department of Biological Science and Technology, Faculty of Advanced Engineering, Tokyo University of Science, 1-3 Kagurazaka, Shinjuku-ku, Tokyo 162-8601, Japan
4
Department of Drug Discovery Structural Biology, Faculty of Pharmaceutical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan
*
Authors to whom correspondence should be addressed.
Int. J. Mol. Sci. 2024, 25(23), 13009; https://doi.org/10.3390/ijms252313009
Submission received: 5 November 2024 / Revised: 27 November 2024 / Accepted: 2 December 2024 / Published: 3 December 2024
(This article belongs to the Topic Molecular and Cellular Mechanisms of Heart Disease)
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Abstract

Defects in Aryl hydrocarbon receptor nuclear translocator-like 1 (ARNTL), a central component of the circadian clock mechanism, may promote or inhibit the induction of inflammation by monocytes/macrophages, with varying effects on different diseases. However, ARNTL’s role in monocytes/macrophages under chronic kidney disease (CKD), which presents with systemic inflammation, is unclear. Here, we report that the expression of Arntl in monocytes promoted CKD-induced cardiac damage. The expression of G-protein-coupled receptor 68 (GPR68), which exacerbates CKD-induced cardiac disease, was regulated by ARNTL. Under CKD conditions, GPR68 expression was elevated via ARNTL, particularly in the presence of PU.1, a transcription factor specific to monocytes and macrophages. In CKD mouse models lacking monocyte-specific ARNTL, GPR68 expression in monocytes was reduced, leading to decreased cardiac damage and fibrosis despite no improvement in renal excretory capacity or renal fibrosis and increased angiotensin II production. The loss of ARNTL did not affect the expression of marker molecules, indicating the origin or differentiation of cardiac macrophages, but affected GPR68 expression only in cardiac macrophages derived from mature monocytes, highlighting the significance of the interplay between GPR68 and ARNTL in monocytes/macrophages and its influence on cardiac pathology. Understanding this complex relationship between circadian clock mechanisms and disease could help uncover novel therapeutic strategies.
Keywords: ARNTL; chronic kidney disease; cardiac pathology GPR68; circadian clock mechanism ARNTL; chronic kidney disease; cardiac pathology GPR68; circadian clock mechanism

Share and Cite

MDPI and ACS Style

Yoshida, Y.; Nishikawa, N.; Fukuoka, K.; Tsuruta, A.; Otsuki, K.; Fukuda, T.; Terada, Y.; Tanihara, T.; Kumamoto, T.; Tsukamoto, R.; et al. Monocyte/Macrophage-Specific Loss of ARNTL Suppresses Chronic Kidney Disease-Associated Cardiac Impairment. Int. J. Mol. Sci. 2024, 25, 13009. https://doi.org/10.3390/ijms252313009

AMA Style

Yoshida Y, Nishikawa N, Fukuoka K, Tsuruta A, Otsuki K, Fukuda T, Terada Y, Tanihara T, Kumamoto T, Tsukamoto R, et al. Monocyte/Macrophage-Specific Loss of ARNTL Suppresses Chronic Kidney Disease-Associated Cardiac Impairment. International Journal of Molecular Sciences. 2024; 25(23):13009. https://doi.org/10.3390/ijms252313009

Chicago/Turabian Style

Yoshida, Yuya, Naoki Nishikawa, Kohei Fukuoka, Akito Tsuruta, Kaita Otsuki, Taiki Fukuda, Yuma Terada, Tomohito Tanihara, Taisei Kumamoto, Ryotaro Tsukamoto, and et al. 2024. "Monocyte/Macrophage-Specific Loss of ARNTL Suppresses Chronic Kidney Disease-Associated Cardiac Impairment" International Journal of Molecular Sciences 25, no. 23: 13009. https://doi.org/10.3390/ijms252313009

APA Style

Yoshida, Y., Nishikawa, N., Fukuoka, K., Tsuruta, A., Otsuki, K., Fukuda, T., Terada, Y., Tanihara, T., Kumamoto, T., Tsukamoto, R., Nishi, T., Oyama, K., Hamamura, K., Mayanagi, K., Koyanagi, S., Ohdo, S., & Matsunaga, N. (2024). Monocyte/Macrophage-Specific Loss of ARNTL Suppresses Chronic Kidney Disease-Associated Cardiac Impairment. International Journal of Molecular Sciences, 25(23), 13009. https://doi.org/10.3390/ijms252313009

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