Thromboxane A2 Modulates de novo Synthesis of Adrenal Corticosterone in Mice via p38/14‐3‐3γ/StAR Signaling
Prostanoids are endogenous lipid bioactive mediators that play essential roles in physiological processes such as glucocorticoid secretion. Here, it is found that the thromboxane (Tx)A2 receptor (TP) is highly expressed in the adrenal cortex of mice. Both global and adrenocortical‐specific deletion...
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Published in | Advanced science Vol. 11; no. 18; pp. e2307926 - n/a |
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Main Authors | , , , , |
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Language | English |
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John Wiley & Sons, Inc
01.05.2024
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Abstract | Prostanoids are endogenous lipid bioactive mediators that play essential roles in physiological processes such as glucocorticoid secretion. Here, it is found that the thromboxane (Tx)A2 receptor (TP) is highly expressed in the adrenal cortex of mice. Both global and adrenocortical‐specific deletion of the TP receptor lead to increased adiposity in mice by elevating corticosterone synthesis. Mechanistically, the TP receptor deletion increases the phosphorylation of steroidogenic acute regulatory protein (StAR) and corticosterone synthesis in adrenal cortical cells by suppressing p‐p38‐mediated phosphorylation of 14‐3‐3γ adapter protein at S71. The activation of the p38 in the adrenal cortical cells by forced expression of the MKK6EE gene attenuates hypercortisolism in TP‐deficient mice. These observations suggest that the TxA2/TP signaling regulates adrenal corticosterone homeostasis independent of the hypothalamic–pituitary–adrenal axis and the TP receptor may serve as a promising therapeutic target for hypercortisolism.
Glucocorticoids are essential steroid hormones produced from the cortex of adrenal glands and play a pivotal role in various physiological processes. This study reveals that the TP receptor‐a regulator of platelet activation, modulates endogenous corticosterone biosynthesis via p‐p38/14‐3‐3γ/p‐StAR signaling in the adrenal glands. Therefore, the TP‐mediated pathway may be an attractive therapeutic target for the treatment of hypercortisolism. |
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AbstractList | Prostanoids are endogenous lipid bioactive mediators that play essential roles in physiological processes such as glucocorticoid secretion. Here, it is found that the thromboxane (Tx)A2 receptor (TP) is highly expressed in the adrenal cortex of mice. Both global and adrenocortical-specific deletion of the TP receptor lead to increased adiposity in mice by elevating corticosterone synthesis. Mechanistically, the TP receptor deletion increases the phosphorylation of steroidogenic acute regulatory protein (StAR) and corticosterone synthesis in adrenal cortical cells by suppressing p-p38-mediated phosphorylation of 14-3-3γ adapter protein at S71. The activation of the p38 in the adrenal cortical cells by forced expression of the MKK6EE gene attenuates hypercortisolism in TP-deficient mice. These observations suggest that the TxA2/TP signaling regulates adrenal corticosterone homeostasis independent of the hypothalamic-pituitary-adrenal axis and the TP receptor may serve as a promising therapeutic target for hypercortisolism.Prostanoids are endogenous lipid bioactive mediators that play essential roles in physiological processes such as glucocorticoid secretion. Here, it is found that the thromboxane (Tx)A2 receptor (TP) is highly expressed in the adrenal cortex of mice. Both global and adrenocortical-specific deletion of the TP receptor lead to increased adiposity in mice by elevating corticosterone synthesis. Mechanistically, the TP receptor deletion increases the phosphorylation of steroidogenic acute regulatory protein (StAR) and corticosterone synthesis in adrenal cortical cells by suppressing p-p38-mediated phosphorylation of 14-3-3γ adapter protein at S71. The activation of the p38 in the adrenal cortical cells by forced expression of the MKK6EE gene attenuates hypercortisolism in TP-deficient mice. These observations suggest that the TxA2/TP signaling regulates adrenal corticosterone homeostasis independent of the hypothalamic-pituitary-adrenal axis and the TP receptor may serve as a promising therapeutic target for hypercortisolism. Prostanoids are endogenous lipid bioactive mediators that play essential roles in physiological processes such as glucocorticoid secretion. Here, it is found that the thromboxane (Tx)A2 receptor (TP) is highly expressed in the adrenal cortex of mice. Both global and adrenocortical‐specific deletion of the TP receptor lead to increased adiposity in mice by elevating corticosterone synthesis. Mechanistically, the TP receptor deletion increases the phosphorylation of steroidogenic acute regulatory protein (StAR) and corticosterone synthesis in adrenal cortical cells by suppressing p‐p38‐mediated phosphorylation of 14‐3‐3γ adapter protein at S71. The activation of the p38 in the adrenal cortical cells by forced expression of the MKK6EE gene attenuates hypercortisolism in TP‐deficient mice. These observations suggest that the TxA2/TP signaling regulates adrenal corticosterone homeostasis independent of the hypothalamic–pituitary–adrenal axis and the TP receptor may serve as a promising therapeutic target for hypercortisolism. Glucocorticoids are essential steroid hormones produced from the cortex of adrenal glands and play a pivotal role in various physiological processes. This study reveals that the TP receptor‐a regulator of platelet activation, modulates endogenous corticosterone biosynthesis via p‐p38/14‐3‐3γ/p‐StAR signaling in the adrenal glands. Therefore, the TP‐mediated pathway may be an attractive therapeutic target for the treatment of hypercortisolism. Prostanoids are endogenous lipid bioactive mediators that play essential roles in physiological processes such as glucocorticoid secretion. Here, it is found that the thromboxane (Tx)A 2 receptor (TP) is highly expressed in the adrenal cortex of mice. Both global and adrenocortical‐specific deletion of the TP receptor lead to increased adiposity in mice by elevating corticosterone synthesis. Mechanistically, the TP receptor deletion increases the phosphorylation of steroidogenic acute regulatory protein (StAR) and corticosterone synthesis in adrenal cortical cells by suppressing p‐p38‐mediated phosphorylation of 14‐3‐3γ adapter protein at S71. The activation of the p38 in the adrenal cortical cells by forced expression of the MKK6EE gene attenuates hypercortisolism in TP‐deficient mice. These observations suggest that the TxA 2 /TP signaling regulates adrenal corticosterone homeostasis independent of the hypothalamic–pituitary–adrenal axis and the TP receptor may serve as a promising therapeutic target for hypercortisolism. Glucocorticoids are essential steroid hormones produced from the cortex of adrenal glands and play a pivotal role in various physiological processes. This study reveals that the TP receptor‐a regulator of platelet activation, modulates endogenous corticosterone biosynthesis via p‐p38/14‐3‐3γ/p‐StAR signaling in the adrenal glands. Therefore, the TP‐mediated pathway may be an attractive therapeutic target for the treatment of hypercortisolism. Abstract Prostanoids are endogenous lipid bioactive mediators that play essential roles in physiological processes such as glucocorticoid secretion. Here, it is found that the thromboxane (Tx)A2 receptor (TP) is highly expressed in the adrenal cortex of mice. Both global and adrenocortical‐specific deletion of the TP receptor lead to increased adiposity in mice by elevating corticosterone synthesis. Mechanistically, the TP receptor deletion increases the phosphorylation of steroidogenic acute regulatory protein (StAR) and corticosterone synthesis in adrenal cortical cells by suppressing p‐p38‐mediated phosphorylation of 14‐3‐3γ adapter protein at S71. The activation of the p38 in the adrenal cortical cells by forced expression of the MKK6EE gene attenuates hypercortisolism in TP‐deficient mice. These observations suggest that the TxA2/TP signaling regulates adrenal corticosterone homeostasis independent of the hypothalamic–pituitary–adrenal axis and the TP receptor may serve as a promising therapeutic target for hypercortisolism. Prostanoids are endogenous lipid bioactive mediators that play essential roles in physiological processes such as glucocorticoid secretion. Here, it is found that the thromboxane (Tx)A2 receptor (TP) is highly expressed in the adrenal cortex of mice. Both global and adrenocortical‐specific deletion of the TP receptor lead to increased adiposity in mice by elevating corticosterone synthesis. Mechanistically, the TP receptor deletion increases the phosphorylation of steroidogenic acute regulatory protein (StAR) and corticosterone synthesis in adrenal cortical cells by suppressing p‐p38‐mediated phosphorylation of 14‐3‐3γ adapter protein at S71. The activation of the p38 in the adrenal cortical cells by forced expression of the MKK6EE gene attenuates hypercortisolism in TP‐deficient mice. These observations suggest that the TxA2/TP signaling regulates adrenal corticosterone homeostasis independent of the hypothalamic–pituitary–adrenal axis and the TP receptor may serve as a promising therapeutic target for hypercortisolism. |
Author | Wang, Bei Wang, Yuanyang Yan, Shuai Yu, Ying Zuo, Shengkai |
AuthorAffiliation | 3 Department of Biopharmaceutics Tianjin Key Laboratory of Technologies Enabling Development of Clinical Therapeutics and Diagnostics School of Pharmacy Tianjin Medical University Tianjin 300070 P. R. China 1 Department of Pharmacology Tianjin Key Laboratory of Inflammatory Biology State Key Laboratory of Experimental Hematology Key Laboratory of Immune Microenvironment and Disease (Ministry of Education) The Province and Ministry Co‐sponsored Collaborative Innovation Center for Medical Epigenetics School of Basic Medical Sciences Tianjin Medical University Tianjin 300070 P. R. China 2 Division of Endocrinology, Diabetes, and Metabolism Beth Israel Deaconess Medical Center Harvard Medical School 330 Brookline Avenue Boston Massachusetts 02115 USA |
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Snippet | Prostanoids are endogenous lipid bioactive mediators that play essential roles in physiological processes such as glucocorticoid secretion. Here, it is found... Abstract Prostanoids are endogenous lipid bioactive mediators that play essential roles in physiological processes such as glucocorticoid secretion. Here, it... |
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SubjectTerms | 14‐3‐3γ Ablation Adipocytes adrenal corticosterone Adrenal glands Biosynthesis Body composition Body fat Cushing syndrome Enzymes Hormones Hyperplasia Kinases Metabolism Morphology p38 Pituitary gland Plasma Proteins Regulation Statistical significance steroidogenic acute regulatory protein Steroids Student's t-test thromboxane receptor |
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Title | Thromboxane A2 Modulates de novo Synthesis of Adrenal Corticosterone in Mice via p38/14‐3‐3γ/StAR Signaling |
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