Fibroblast Angiotensin II Type 1a Receptors Contribute to Angiotensin II–Induced Medial Hyperplasia in the Ascending Aorta

Aruna Poduri, Debra L. Rateri, Deborah A. Howatt, Anju Balakrishnan, Jessica J. Moorleghen,

Lisa A. Cassis, Alan Daugherty

Angiotensin II promotes SMC proliferation in the media of the aorta. The receptor responsible for this effect is the angiotensin II type 1a (AT1a) receptor in rodents. Surprisingly, deletion of the AT1a receptor in smooth muscle cells had no effect on angiotensin II–mediated cellular proliferation. Deletion of AT1a receptors in endothelial cells also had no effect. Unexpectedly, deletion of AT1a receptors in neuronal cells using the Eno2 promoter significantly attenuated angiotensin II–induced medial proliferation in the ascending aorta. Lineage tracking detected Eno2 positive cells in the adventitia of the ascending aorta that colocalized with fibroblasts. Deletion of the AT1a receptor in fibroblasts also significantly attenuated angiotensin II–mediated cellular proliferation in the ascending aorta. (Read full text here.)

 

 

Figure 4 from Daugherty lab ATVB article_1.png