Polo-like Kinase 1 Activation Regulates Angiotensin II-Induced Contraction in Pudendal and Small Mesenteric Arteries from Mice.

Polo-like kinase 1 (PLK1) is a serine/threonine protein kinase expressed in smooth muscle cells (SMCs), with emerging roles in regulating contraction. We hypothesize that PLK1 contributes to smooth muscle contractility in pudendal arteries (PA), small mesenteric arteries (SMA), and the corpus cavernosum (CC). Using male C57BL/6J mice, we assessed mRNA and protein expression of PLK1 in these tissues. In addition, the arteries and CC were mounted in myographs for isometric force measurement. We then investigated whether PLK1 regulates SMC contractility induced by phenylephrine (PE), U46619, and angiotensin II (Ang II) in arteries, and by PE, serotonin (5-HT), and electrical field stimulation (EFS; 1-16 Hz) in the CC, both in the presence and absence of the PLK1 inhibitor volasertib. PLK1 expression was confirmed in the SMA, PA, and CC by RT-qPCR or Western blotting. Notably, PLK1 inhibition significantly reduced Ang II-induced contraction in the PA and SMA and attenuated EFS-induced contraction at 2 and 4 Hz in the CC. In contrast, responses to PE, U46619, and 5-HT were unaffected by PLK1 inhibition. These results suggest that PLK1 selectively mediates contraction in response to Ang II and neurogenic stimuli. PLK1 may therefore represent a novel, stimulus-specific regulator of vascular and erectile smooth muscle contractility.