| 초록 |
Hypertension is a complex condition contributing to world-wide premature death. Approximately 95% of hypertension cases are classified as essential hypertension, of which cause is unknown. Hypertension is closely associated with inflammation; however, whether the inflammation is a cause or effect of hypertension is not well understood. Extracellular vesicle secretion correlates with inflammasome activity. The purpose of this study is to investigate the effect of exocyst Sec10-defficiency in bone marrow-derived myeloid cells in development of hypertension through renal inflammation and angiotensin II expression. Sec10 is known to be a central component of the exocyst complex essential for exocytosis, which plays a critical role in biological processes such as cell growth, cell-cell communication, and cell migration. Twenty-one to twenty-nine week-old female myeloid-specific sec10-deficient (Lyz-Sec10 KO) mice and their wild type littermates were used for animal experiments. Body weights and blood pressures (BP) were measured. Expression of pro-inflammatory cytokines, angiotensinogen adhesion molecules, and sodium transporters in the kidney were determined by QPCR or western blot analysis. Ruffle formation and migration of bone marrow-derived macrophages (BMM) were determined. Lyz-Sec10 KO mice showed higher BP, greater renal inflammation than wild type mice. Lyz-Sec10 KO mice accelerated BMM ruffle formation and migration. Lyz-Sec10 KO mice increased serum Ang II concentration and renal sodium transporter expression. Conclusively, deficiency of exocyst Sec10 in myeloid cells induces hypertension through increased renal inflammation and serum Ang II by enhanced migration of BMM. |