| First Author | Zhao H | Year | 2018 |
| Journal | Biochim Biophys Acta | Volume | 1864 |
| Issue | 1 | Pages | 189-196 |
| PubMed ID | 28988887 | Mgi Jnum | J:254184 |
| Mgi Id | MGI:6104270 | Doi | 10.1016/j.bbadis.2017.10.011 |
| Citation | Zhao H, et al. (2018) IgE induces hypotension in asthma mice by down-regulating vascular NCX1 expression through activating MiR-212-5p. Biochim Biophys Acta 1864(1):189-196 |
| abstractText | Immunoglobulin E (IgE) has been suggested as a risk factor for allergy-induced low blood pressure, which has not been well explained in molecular details. Our current study shows a novel mechanism involving IgE, FcvarepsilonR1, miRNA-212-5p (miR-212-5p), and sodium/calcium exchanger protein 1(NCX1) for asthma to induce hypotension. In arterial smooth muscle cells, IgE up-regulated miR212-5p via its receptor FcvarepsilonR1, which resulted in down-regulation of NCX1 that is a regulating factor for blood pressure. In mice, asthma induced hypotension by interfering vasoconstrictive function; knockout of FcvarepsilonR1 kept the asthmatic mice from developing hypotension; knock-down of miR-212-5p in asthmatic mice resulted in a significant restoration of blood pressure. In human, asthma and IgE were positively correlated with hypotension in cohort study on NIH epidemiological data. This study suggests a novel therapeutic target (miR-212-5p) for treatment of asthma-induced hypotension. |
