Assistant Professor of Physiology
The long-term goal of my laboratory is to investigate how ion channels and transporters participate in the development of hypertension and cancers. My laboratory has been continuously funded by NIH. My specific research projects are:
1. Translate ROS regulation of ENaC into salt-sensitive hypertension.
We have previously addressed the interaction between the epithelial sodium channel (ENaC) and anionic phospholipids. Our recent studies suggest an even more interesting hypothesis that reactive oxygen species (ROS) may stimulate ENaC by enhancing such an interaction. Since elevated ENaC activity can cause hypertension, as seen in Liddle's disease, our findings indicate that activation of ENaC by ROS contributes to the pathogenesis of salt-sensitive hypertension. Therefore, we are trying to translate the molecular mechanisms of ENaC regulation into salt-sensitive hypertension.
2: Translate cholesterol regulation of ENaC into obesity hypertension.
Our published data have shown that the local cholesterol in the cell membrane acts as a signaling molecule to stimulate ENaC. Recently, we found that cholesterol could stabilize the microvillar structure where ENaC is located. This project has clinical significance because it suggests that high fat diet not only damages cardiovascular system, but also target the kidney to elevate sodium reabsorption to cause hypertension. To further develop this project, we are trying to use the state-of-the-art techniques such as atomic force microscopy and the in vivo imaging to track cholesterol in the renal epithelial cells in response to high cholesterol-containing diet.
3: Determine the role of transporters and ion channels in cell proliferation and apoptosis.
Our previous studies have shown that the voltage-dependent KP+P channel (Kv1.3) does not inactivate completely in B lymphoma cells, probably due to enhanced cholesterol levels in the plasma membrane. Population studies suggest that obesity is a risk factor of lymphomas and other cancers. Therefore, Kv1.3 channels may be the target of cholesterol and participate in lymphoma development. We have also shown that the apoptosis-related outwardly rectifying chloride channel is silent in B lymphoma cells and that, in contract, the proliferation-related CaP2+P-activated potassium channel is abnormally active due to enhanced phosphatidylinositol 3-kinase activity. We are trying to translate these basic studies into lymphoma treatment.
Publications: PubMed search
Department of Physiology