As a second messenger, Ca
2+ plays important roles in cellular functions such as migration, tube formation, and proliferation [
1]. To date, > 30 transient receptor potential (TRP) channels have been studied. They are divided into seven subfamilies: TRPA (ankyrin), TRPC (canonical), TRPV (vanilloid), TRPM (melastatin), TRPML (mucolipin), TRPP (polycystin), and TRPN (NOMPC-like) [
1,
2]. They are Ca
2+-permeable, nonselective cation channels, which are widely expressed in endothelial cells (ECs) [
3,
4]. They can be activated by a wide variety of stimuli (osmotic, mechanical, and chemical). Now, increasing research has shown that TRPV4 is important in regulating Ca
2+ influx and plays vital roles in endothelial function. For example, flow-induced TRPV4 activation in lung ECs leads to lung permeability edema [
5]; TRPV4 activated by H
2S in mouse aortic ECs regulates vasodilation [
6]; TRPV4 plays a minor role in controlling endothelial progenitor cell proliferation [
7]; and H
2O
2 induces Ca
2+ entry via TRPV4 in lung microvascular ECs [
8].
Recently, several studies have focused on the function of TRPV4 in the retinal microvascular endothelium of rats and mice [
9]. However, human-derived ECs have not been studied. During retinal development, the activation and migration of ECs are important in forming tubular structures. However, retinal neovascularization is also a characteristic pathological consequence of many retinal diseases, including retinopathy of prematurity [
10], diabetic retinopathy [
11], and retinal vein occlusion [
12].
In previous studies, we showed that TRPV4 regulates flow-induced endothelial Ca
2+ entry [
13] and vascular function [
14]. Besides, the TRPV4-KCa2.3 signaling pathway plays an important role in smooth muscle hyperpolarization and relaxation and may be involved in endothelium-derived hyperpolarizing factor dysfunction in diabetic rats [
15]. Here, we show that TRPV4 is expressed in human retinal capillary ECs (HRCECs) and is essential for their migration and tube formation.