Exogenous C-type natriuretic peptide therapy for impaired skeletal growth in a murine model of glucocorticoid treatment

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  • 植田, 洋平
    Department of Diabetes, Endocrinology and Nutrition, Kyoto University Graduate School of Medicine
  • 廣田, 圭昭
    Department of Diabetes, Endocrinology and Nutrition, Kyoto University Graduate School of Medicine･Clinical Research Center, National Hospital Organization Kyoto Medical Center
  • 山内, 一郎
    Department of Diabetes, Endocrinology and Nutrition, Kyoto University Graduate School of Medicine
  • 坂根, 依利子
    Department of Diabetes, Endocrinology and Nutrition, Kyoto University Graduate School of Medicine
  • 藤井, 寿人
    Department of Diabetes, Endocrinology and Nutrition, Kyoto University Graduate School of Medicine
  • 稲垣, 暢也
    Department of Diabetes and Endocrinology, Osaka Red Cross Hospital
  • Sakane, Yoriko
    Preemptive Medicine and Lifestyle Related Disease Research Center, Kyoto University Hospital
  • Fujii, Toshihito
    Department of Diabetes, Endocrinology and Nutrition, Kyoto University Graduate School of Medicine
  • Inagaki, Nobuya
    Department of Diabetes, Endocrinology and Nutrition, Kyoto University Graduate School of Medicine

説明

Growth retardation is an important side effect of glucocorticoid (GC)-based drugs, which are widely used in various preparations to treat many pediatric diseases. We investigated the therapeutic effect of exogenous CNP-53, a stable molecular form of intrinsic CNP, on a mouse model of GC-induced growth retardation. We found that CNP-53 successfully restored GC-induced growth retardation when both dexamethasone (DEX) and CNP-53 were injected from 4 to 8 weeks old. Notably, CNP-53 was not effective during the first week. From 4 to 5 weeks old, neither CNP-53 in advance of DEX, nor high-dose CNP-53 improved the effect of CNP. Conversely, when CNP-53 was started at 5 weeks old, final body length at 8 weeks old was comparable to that when CNP-53 was started at 4 weeks old. As for the mechanism of resistance to the CNP effect, DEX did not impair the production of cGMP induced by CNP. CNP reduced Erk phosphorylation even under treatment with DEX, while CNP did not changed that of p38 or GSK3β. Collectively, the effect of CNP-53 on GC-induced growth retardation is dependent on age in a mouse model, suggesting adequate and deliberate use of CNP would be effective for GC-induced growth retardation in clinical settings.

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