Hypertension onset is independent of inflammation

Hypertension, like atherosclerosis, is often seen to be coincident with chronic inflammation in large blood vessels. However, it is not clear whether these two disorders are causally related and whether hypertension can develop independently of inflammation.

Strikingly, mice deficient in IEX-1 develop hypertension that is not accompanied by vascular hypertrophy or infiltration of inflammatory cells.  IEX-1 deficiency is associated with enhanced ROS production in mitochondria by stabilizing IF1, an intrinsic inhibitor for the mitochondrial F0F1-ATPase, which may inactivate nitric oxide (NO), reducing the bioavailability of this vasodilator. The absence of vascular inflammation in these mice suggests that inflammation is dispensable for the onset of hypertension.  With this unique hypertension model, we are investigating a role for different inflammatory mediators in hypertension progression.

Projects

• Suppression of Th17 differentiation by IEX-1
• IEX-1 can be a potential target for prevention of colitis and colon cancer
• Hypertension onset independent of inflammation
• Laser vaccine adjuvant effects
• A complex interaction between Gαi2 and Gαi3
• A linkage of Gαi2 and TGF-β signaling via a newly discovered Smad phosphatase