| First Author | Aldi S | Year | 2014 |
| Journal | Am J Pathol | Volume | 184 |
| Issue | 2 | Pages | 376-81 |
| PubMed ID | 24262755 | Mgi Jnum | J:205195 |
| Mgi Id | MGI:5544358 | Doi | 10.1016/j.ajpath.2013.10.016 |
| Citation | Aldi S, et al. (2014) IgE Receptor-Mediated Mast-Cell Renin Release. Am J Pathol 184(2):376-81 |
| abstractText | Renin is a newly discovered constituent of mast cells. Given that mast cells play a major role in IgE-mediated allergic hypersensitivity, we investigated whether activation of the high-affinity IgE receptor FcepsilonRI elicits release of mast-cell renin. Cross-linking of FcepsilonRI on the surface of mature bone marrow-derived mast cells elicited release of enzymatically active renin protein. The angiotensin I-forming activity of the renin protein was completely blocked by the selective renin inhibitor BILA 2157, which excludes formation of angiotensin I by proteases other than renin. FcepsilonRI-mediated mast-cell renin release was inhibited by dexamethasone and potentiated by the proinflammatory mediator PGE2. Furthermore, cross-linking of mast-cell FcepsilonRI in ex vivo murine hearts passively sensitized with monoclonal anti-DNP IgE also resulted in mast-cell degranulation and overflow of renin. Our findings indicate that IgE-mediated allergic hypersensitivity provokes release of renin from both cultured and resident cardiac mast cells, a process likely to be exacerbated in a chronic inflammatory background. Given the widespread distribution of mast cells, and the presence of angiotensinogen and angiotensin-converting enzyme in many tissues, renin release in immediate hypersensitivity reactions could result in local angiotensin II generation and multiorgan dysfunctions. |
