BACKGROUND: Among various cardiovascular disease risk factors, hypertension represents a major factor and continues to be a significant health challenge. Prohypertensive factors, such as angiotensin II (AngII), can induce inflammation that triggers or aggravates hypertension. Depletion of monocytes or deficiency in the macrophage colony stimulating factor prevents AngII‐induced hypertension and vascular remodeling. However, the underlying mechanisms are still unknown. Previously, we identified several blood pressure (BP) -related genes (CRIP1, MYADM, TIPARP, TSC22D3, CEBPA, F12, LMNA, and TPPP3) in human monocytes as being most strongly associated with blood pressure. In this study we aimed to assess the role of monocytes for BP-related gene expression in AngII-induced hypertensive mouse models.

METHODS: C57BL/6 mice were short-term (7 days) and long-term (28 days) treated with AngII (1mg/kg/d) and expression of BP-related genes was assessed in PBMC, aorta, kidney and spleen using qPCR. Additionally, by using mice with Cre-inducible expression of the diphtheria toxin receptor in lysozyme M+ cells (LysM^iDTR mice), myelomonocytic cells were depleted in parallel to AngII (1 mg/kg/d) administration for 7 days. Subsequently, the expression of 8 BP-related genes in kidney and aortic tissue was analyzed via qPCR.

RESULTS: CRIP1, LMNA, MYADM and TIPARP were differentially expressed in PBMC and aorta, while no differences were observed in kidney tissue of short-term AngII-treated mice compared to the control mice. The differential expression of CRIP1, LMNA, MYADM and TIPARP in the aorta was not dependent on the presence of monocytes. Long-term AngII-treatment induced significantly increased CRIP1 mRNA expression in the spleen.

CONCLUSION: Differential expression of BP-related genes in immune cells and aorta of hypertensive mice demonstrate an important role of CRIP1, LMNA, MYADM and TIPARP in the pathophysiology of hypertension affecting vascular and immune system.