Format

Send to

Choose Destination
Biochem Biophys Res Commun. 2018 Feb 26;497(1):220-225. doi: 10.1016/j.bbrc.2018.02.058. Epub 2018 Feb 8.

Yoda1-induced phosphorylation of Akt and ERK1/2 does not require Piezo1 activation.

Author information

1
La Jolla Bioengineering Institute, 505 Coast Blvd South, Suite 406, La Jolla, CA 92037, USA. Electronic address: ndelapaz@ljbi.org.
2
La Jolla Bioengineering Institute, 505 Coast Blvd South, Suite 406, La Jolla, CA 92037, USA. Electronic address: frangos@ljbi.org.

Abstract

Piezo1 is a mechanosensitive cation channel that is activated by shear stress in endothelial cells (ECs). It has been shown to mediate shear-induced EC responses, including increased calcium influx, and vascular functions, such as vascular tone and blood pressure. Yoda1, a selective Piezo1 activator, has been shown to mimic shear-induced responses in ECs. Since shear-induced calcium influx causes Akt and ERK1/2 activation in ECs, we examined the effects of Yoda1 and the role of Piezo1 on their activation. Here, we show that Yoda1 robustly activates Akt and ERK1/2 in ECs. Additionally, the Piezo1 antagonists, gadolinium and ruthenium red, but not GsMTx4, effectively blocks Yoda1-induced Akt activation. Our results suggest that Yoda1-induced Akt and ERK1/2 activation is not dependent on Piezo1.

KEYWORDS:

Akt; ERK1/2; Endothelial cells; Piezo1; Yoda1

PMID:
29428723
PMCID:
PMC5835220
DOI:
10.1016/j.bbrc.2018.02.058
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center