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Article: Adipose c-Jun NH2-terminal kinase promotes angiotensin II-induced and deoxycorticosterone acetate salt-induced hypertension and vascular dysfunction by inhibition of adiponectin production and activation of SGK1 in mice
Title | Adipose c-Jun NH2-terminal kinase promotes angiotensin II-induced and deoxycorticosterone acetate salt-induced hypertension and vascular dysfunction by inhibition of adiponectin production and activation of SGK1 in mice |
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Authors | |
Issue Date | 21-Dec-2023 |
Publisher | Lippincott, Williams & Wilkins |
Citation | Journal of Hypertension, 2023 How to Cite? |
Abstract | Background:Adipose c-Jun NH2-terminal kinase 1/2 (JNK1/2) is a central mediator involved in the development of obesity and its complications. However, the roles of adipose JNK1/2 in hypertension remain elusive. Here we explored the role of adipose JNK1/2 in hypertension. Methods and results:The roles of adipose JNK1/2 in hypertension were investigated by evaluating the impact of adipose JNK1/2 inactivation in both angiotensin II (Ang II)-induced and deoxycorticosterone acetate (DOCA) salt-induced hypertensive mice. Specific inactivation of JNK1/2 in adipocytes significantly alleviates Ang II-induced and DOCA salt-induced hypertension and target organ damage in mice. Interestingly, such beneficial effects are also observed in hypertensive mice after oral administration of JNK1/2 inhibitor SP600125. Mechanistically, adipose JNK1/2 acts on adipocytes to reduce the production of adiponectin (APN), then leads to promote serum and glucocorticoid-regulated kinase 1 (SGK1) phosphorylation and increases epithelial Na+ channel α-subunit (ENaCα) expression in both renal cells and adipocytes, respectively, finally exacerbates Na+ retention. In addition, chronic treatment of recombinant mouse APN significantly augments the beneficial effects of adipose JNK1/2 inactivation in DOCA salt-induced hypertension. By contrast, the blood pressure-lowering effects of adipose JNK1/2 inactivation are abrogated by adenovirus-mediated SGK1 overexpression in Ang II -treated adipose JNK1/2 inactivation mice. Conclusion:Adipose JNK1/2 promotes hypertension and targets organ impairment via fine-tuning the multiorgan crosstalk among adipose tissue, kidney, and blood vessels. |
Persistent Identifier | http://hdl.handle.net/10722/339854 |
ISSN | 2023 Impact Factor: 3.3 2023 SCImago Journal Rankings: 1.134 |
DC Field | Value | Language |
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dc.contributor.author | Gan J | - |
dc.contributor.author | Shi Y | - |
dc.contributor.author | Zhao R | - |
dc.contributor.author | Li D | - |
dc.contributor.author | Jin H | - |
dc.contributor.author | Wu M | - |
dc.contributor.author | Liu Z | - |
dc.contributor.author | Li X | - |
dc.contributor.author | Xu A | - |
dc.contributor.author | Li Y | - |
dc.contributor.author | Lin Z | - |
dc.contributor.author | Wu F | - |
dc.date.accessioned | 2024-03-11T10:39:47Z | - |
dc.date.available | 2024-03-11T10:39:47Z | - |
dc.date.issued | 2023-12-21 | - |
dc.identifier.citation | Journal of Hypertension, 2023 | - |
dc.identifier.issn | 0263-6352 | - |
dc.identifier.uri | http://hdl.handle.net/10722/339854 | - |
dc.description.abstract | <h3><span>Background: </span></h3><p>Adipose c-Jun NH2-terminal kinase 1/2 (JNK1/2) is a central mediator involved in the development of obesity and its complications. However, the roles of adipose JNK1/2 in hypertension remain elusive. Here we explored the role of adipose JNK1/2 in hypertension.</p><h3><span>Methods and results: </span></h3><p>The roles of adipose JNK1/2 in hypertension were investigated by evaluating the impact of adipose JNK1/2 inactivation in both angiotensin II (Ang II)-induced and deoxycorticosterone acetate (DOCA) salt-induced hypertensive mice. Specific inactivation of JNK1/2 in adipocytes significantly alleviates Ang II-induced and DOCA salt-induced hypertension and target organ damage in mice. Interestingly, such beneficial effects are also observed in hypertensive mice after oral administration of JNK1/2 inhibitor SP600125. Mechanistically, adipose JNK1/2 acts on adipocytes to reduce the production of adiponectin (APN), then leads to promote serum and glucocorticoid-regulated kinase 1 (SGK1) phosphorylation and increases epithelial Na<sup>+</sup> channel α-subunit (ENaCα) expression in both renal cells and adipocytes, respectively, finally exacerbates Na<sup>+</sup> retention. In addition, chronic treatment of recombinant mouse APN significantly augments the beneficial effects of adipose JNK1/2 inactivation in DOCA salt-induced hypertension. By contrast, the blood pressure-lowering effects of adipose JNK1/2 inactivation are abrogated by adenovirus-mediated SGK1 overexpression in Ang II -treated adipose JNK1/2 inactivation mice.</p><h3><span>Conclusion: </span></h3><p>Adipose JNK1/2 promotes hypertension and targets organ impairment via fine-tuning the multiorgan crosstalk among adipose tissue, kidney, and blood vessels.</p> | - |
dc.language | eng | - |
dc.publisher | Lippincott, Williams & Wilkins | - |
dc.relation.ispartof | Journal of Hypertension | - |
dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. | - |
dc.title | Adipose c-Jun NH2-terminal kinase promotes angiotensin II-induced and deoxycorticosterone acetate salt-induced hypertension and vascular dysfunction by inhibition of adiponectin production and activation of SGK1 in mice | - |
dc.type | Article | - |
dc.identifier.doi | 10.1097/HJH.0000000000003649 | - |
dc.identifier.pmid | 38164960 | - |
dc.identifier.eissn | 1473-5598 | - |
dc.identifier.issnl | 0263-6352 | - |