Key result
Dusp5 deletion promotes pulmonary hypertension and RV hypertrophy in angiotensin II-infused mice.
Why the study?
Dual-specificity phosphatases serve critical roles in the regulation of mitogen-activated protein kinases, but their functions in the cardiovascular system remained poorly defined.
Dual-specificity phosphatases (DUSPs) serve critical roles in the regulation of mitogen-activated protein kinases, but their functions in the cardiovascular system remain poorly defined. Here, we provide evidence that DUSP5, which resides in the nucleus and specifically dephosphorylates extracellular signal-regulated kinase (ERK1/2), blocks pulmonary vascular smooth muscle cell proliferation. In response to angiotensin II infusion, mice lacking DUSP5 develop pulmonary hypertension and right ventricular cardiac hypertrophy. These findings illustrate DUSP5-mediated suppression of ERK signaling in the lungs as a protective mechanism.
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Ferguson et al. (2021) studied Pulmonary hypertension and right ventricular hypertrophy. Dusp5 deletion with Angiotensin II infusion vs. Wild-type mice and sham pump controls was evaluated on Pulmonary artery acceleration time (PAAT) (p=<0.05). Dusp5 deletion in mice infused with angiotensin II significantly reduced pulmonary artery acceleration time (p<0.05) and induced pulmonary hypertension and right ventricular hypertrophy.
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