Article ; Online: Adaptor protein HIP-55 promotes macrophage M1 polarization through promoting AP-1 complex activation.
2024 Volume 117, Page(s) 111124
Abstract: Overwhelming macrophage M1 polarization induced by malfunction of the renin-angiotensin-aldosterone system (RAAS) initiates inflammatory responses, which play a crucial role in various cardiovascular diseases. However, the underlying regulatory mechanism ...
Abstract | Overwhelming macrophage M1 polarization induced by malfunction of the renin-angiotensin-aldosterone system (RAAS) initiates inflammatory responses, which play a crucial role in various cardiovascular diseases. However, the underlying regulatory mechanism remains elusive. Here, we identified adaptor protein HIP-55 as a critical regulator of macrophage M1 polarization. The expression of HIP-55 was upregulated in M1 macrophage induced by Ang II. Overexpression of HIP-55 significantly promoted Ang II-induced macrophage M1 polarization, whereas genetic deletion of HIP-55 inhibited the Ang II-induced macrophage M1 polarization. Mechanistically, HIP-55 facilitated activator protein-1 (AP-1) complex activation induced by Ang II via promoting ERK1/2 and JNK phosphorylation. Moreover, blocking AP-1 complex activation can attenuate the function of HIP-55 in macrophage polarization. Collectively, our results reveal the role of HIP-55 in macrophage polarization and provide potential therapeutic insights for cardiovascular diseases associated with RAAS dysfunction. |
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MeSH term(s) | Humans ; Adaptor Proteins, Signal Transducing/metabolism ; Angiotensin II/pharmacology ; Angiotensin II/metabolism ; Cardiovascular Diseases/metabolism ; Macrophages/metabolism ; Signal Transduction ; Transcription Factor AP-1 ; Animals ; Mice ; Microfilament Proteins/metabolism ; src Homology Domains |
Chemical Substances | Adaptor Proteins, Signal Transducing ; Angiotensin II (11128-99-7) ; Transcription Factor AP-1 ; Microfilament Proteins |
Language | English |
Publishing date | 2024-02-27 |
Publishing country | England |
Document type | Journal Article ; Research Support, Non-U.S. Gov't |
ZDB-ID | 1002702-6 |
ISSN | 1873-3913 ; 0898-6568 |
ISSN (online) | 1873-3913 |
ISSN | 0898-6568 |
DOI | 10.1016/j.cellsig.2024.111124 |
Database | MEDical Literature Analysis and Retrieval System OnLINE |
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