Therefore, this study was designed to (a) determine the role of CaV channels in TNF-α-induced CCL-2 and IL-6 secretion from human pulmonary endothelial cells, two key inflammatory cytokines involved in the development of ALI [12,13], (b) explore the potential of counteracting Ca2+ influx-dependent inflammatory cytokine secretion via pharmacological Em hyperpolarization, and (c) establish the intracellular signaling mechanisms and PPI networks that confer such protection. This evidence concerns the gene TNF and acute respiratory distress syndrome.