Endothelial TRPV4-eNOS coupling as a vital therapy target for treatment of hypertension.

Background And Purpose: Reduced NO levels and activity are signs of endothelial dysfunction, which is important in mediating BP changes. Previously, we demonstrated that transient receptor potential channel V4 (TRPV4) could form a functional complex with other proteins to mediate vasodilation in endothelial cells (ECs). But how TRPV4 interacts with the NO pathway in larger arteries requires further exploration.

Small molecule compound M12 reduces vascular permeability in obese mice via blocking endothelial TRPV4-Nox2 interaction.

Transient receptor potential channel TRPV4 and nicotinamide adenine dinucleotide phosphate oxidase (Nox2) are involved in oxidative stress that increases endothelial permeability. It has been shown that obesity enhances the physical association of TRPV4 and Nox2, but the role of TRPV4-Nox2 association in obesity has not been clarified. In this study we investigated the function of TRPV4-Nox2 complex in reducing oxidative stress and regulating abnormal vascular permeability in obesity.

Morin attenuates oxidized low-density lipoprotein-mediated injury by inducing autophagy via activating AMPK signalling in HUVECs.

Endothelial dysfunction is a precursor of cardiovascular disease, and oxidized low-density lipoprotein (ox-LDL) has been implicated in the development of atherosclerosis by directly targeting endothelial cells. Morin, a natural flavonol, has been shown to protect endothelial cells from dysfunction. The present study was designed to evaluate the effect of morin on ox-LDL-induced injury and to investigate the underlying molecular mechanisms in human umbilical vein endothelial cells (HUVECs).

Morin induces endothelium-dependent relaxation by activating TRPV4 channels in rat mesenteric arteries.

Morin, a natural flavonol, has been reported to have beneficial pharmacological effects. Although its vascular protective effects have been studied, little is known about its effects on the mesenteric artery and the underlying mechanisms. Transient receptor potential vanilloid type 4 (TRPV4) channels are one of the most important Ca-permeable cation channels in vascular endothelial cells and play an important role in regulating rat mesenteric vascular tone.

SPZ1 is critical for chemoresistance and aggressiveness in drug-resistant breast cancer cells.

It is believed that chemotherapeutic agents can enhance the malignancy of treated cancer cells in clinical situations, which is a major problem for chemotherapy. However, the underlying molecular mechanisms are still not fully understood. Here, we demonstrated that chemotherapy up-regulates the levels of spermatogenic bHLH transcription factor zip 1 (SPZ1), and knockdown of SPZ1 in drug resistant breast cancers showed that SPZ1 is critical for regulating the chemoresistance, migration, invasion and epithelial-mesenchymal transition (EMT) in a Twist1-dependent manner.

Overexpression of TrpC5 promotes tumor metastasis via the HIF-1α-Twist signaling pathway in colon cancer.

In cancer cells, intracellular Ca homeostasis is altered, and this is involved in tumor initiation, progression, and metastasis. However, little is known about the underlying mechanisms. Here, we report that transient receptor potential channel 5 (TrpC5), a receptor-activated non-selective Ca channel, is correlated with tumor metastasis in colon cancer patients.