Interleukin-12p35 knockout promotes macrophage differentiation, aggravates vascular dysfunction, and elevates blood pressure in angiotensin II-infused mice - Ye, Jing; Que, Bin; Huang, Ying; Lin, Yingzhong; Chen, Jiangbin; Liu, Ling; Shi, Ying; Wang, Yuan; Wang, Menglong; Zeng, Tao; Wang, Zhen; Hu, Haiying; et al. (Cardiovascular research, 2019)
Keywords: Adult; Aged; Angiotensin II; Animals; Antihypertensive Agents - administration & dosage; Aorta - metabolism; Aorta - pathology; Aorta - physiopathology; Blood Pressure - drug effects; Case-Control Studies; Cell Differentiation; Cells, Cultured; Disease Models, Animal; Female; Humans; Hypertension - chemically induced; Hypertension - drug therapy; Hypertension - metabolism; Hypertension - physiopathology; Interleukin-12 - administration & dosage; Interleukin-12 Subunit p35 - blood; Interleukin-12 Subunit p35 - deficiency; Interleukin-12 Subunit p35 - genetics; Macrophages - metabolism; Macrophages - pathology; Male; Mice, Inbred C57BL; Mice, Knockout; Middle Aged; Phenotype; Signal Transduction; Vasoconstriction; Vasodilation; Hypertension; Inflammatory response; Interleukin 12; Interleukin-12p35 deficiency; Angiotensin II; Macrophages