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[H. Cell signaling-4]
p32 conditional knock out of endothelium was increased
vascular function via activation of CaMKll/AMPK/p38
MAPK/Akt/eNOS axis
Byeong Jun Yoon¹, Sung Woo Ryoo¹˙*
¹BIT Medical Convergence, Kangwon National University, Chun-cheon 24341, Korea
Ca²+ is a major secondary messenger and can induce various cellular responses. Cytosolic Ca²+ can activate CaMKll,
which can regulate the eNOS activity. eNOS produces NO using L-arginine and NO plays important role in vascular
homeostasis. p32 is mainly located in the mitochondria and has a donut-shaped homotrimer structure with a pore
in the center. Recent studies show that p32 can regulate cytosolic Ca²+, suggesting that p32 will act as a Ca²+
channel. The cytosolic Ca²+ can regulate the activity of eNOS, so p32 may be related to the activity of eNOS.
Therefore, we investigated whether p32 can modulate eNOS activity in a Ca²+-dependent manner. First, it was
confirmed that p32 was reduced in p32f/f Cre+ mice. Reduced expression of p32 increased the activity of eNOS in
a Ca²+-dependent manner, which increased NO production. In the aorta of p32f/f Cre+ mice, the acetylcholine
response was increased, and the phenylephrine response was decreased. Also, Blood pressure tended to decrease,
but there was no significance. In conclusion, p32 can regulate the cytosolic Ca2+, which can induce eNOS activity.
However, further research is needed on the mechanism by which p32 regulates cytosolic Ca²+.
