| First Author | Shah KH | Year | 2015 |
| Journal | Circ Res | Volume | 117 |
| Issue | 10 | Pages | 858-69 |
| PubMed ID | 26294657 | Mgi Jnum | J:252793 |
| Mgi Id | MGI:6098919 | Doi | 10.1161/CIRCRESAHA.115.306539 |
| Citation | Shah KH, et al. (2015) Myeloid Suppressor Cells Accumulate and Regulate Blood Pressure in Hypertension. Circ Res 117(10):858-69 |
| abstractText | RATIONALE: Chronic inflammation is a major contributor to the progressive pathology of hypertension, and T-cell activation is required for the genesis of hypertension. However, the precise role of myeloid cells in this process is unclear. OBJECTIVE: To characterize and understand the role of peripheral myeloid cells in the development of hypertension. METHODS AND RESULTS: We examined myeloid cells in the periphery of hypertensive mice and found that increased numbers of CD11b(+)Gr1(+) myeloid cells in blood and the spleen are a characteristic of 3 murine models of experimental hypertension (angiotensin II, L-NG-nitroarginine methyl ester, and high salt). These cells express surface markers and transcription factors associated with immaturity and immunosuppression. Also, they produce hydrogen peroxide to suppress T-cell activation. These are characteristics of myeloid-derived suppressor cells (MDSCs). Depletion of hypertensive MDSCs increased blood pressure and renal inflammation. In contrast, adoptive transfer of wild-type MDSCs to hypertensive mice reduced blood pressure, whereas the transfer of nicotinamide adenine dinucleotide phosphate oxidase 2-deficient MDSCs did not. CONCLUSION: The accumulation of MDSCs is a characteristic of experimental models of hypertension. MDSCs limit inflammation and the increase of blood pressure through the production of hydrogen peroxide. |
