We examined the interaction of a membrane-associated protein, MARCKS-like Protein-1 (MLP-1), and an ion channel, Epithelial Sodium Channel (ENaC), with the anionic lipid, phosphatidylinositol 4, 5-phosphate (PIP). We found that PIP strongly activates ENaC in excised, inside-out patches with a half-activating concentration of 21 ± 1.17 µM.
View Article and Find Full Text PDFHypertension is characterized by increased sodium (Na) reabsorption along the aldosterone-sensitive distal nephron (ASDN) as well as chronic systemic inflammation. Interleukin-6 (IL-6) is thought to be a mediator of this inflammatory process. Interestingly, increased Na reabsorption within the ASDN does not always correlate with increases in aldosterone (Aldo), the primary hormone that modulates Na reabsorption via the mineralocorticoid receptor (MR).
View Article and Find Full Text PDFThe epithelial sodium channel (ENaC) regulates blood pressure by fine-tuning distal nephron sodium reabsorption. Our previous work has shown that ENaC gating is regulated by anionic phospholipid phosphates, including phosphatidylinositol 4,5-bisphosphate (PIP). The PIP-dependent regulation of ENaC is mediated by the myristoylated alanine-rich protein kinase C substrate-like protein-1 (MLP-1).
View Article and Find Full Text PDFIgG4-related disease (IgG-RD) describes a group of fibroinflammatory diseases that affect a variety of tissues resulting in tumor-like effect and/or organ dysfunction. Clinical presentation varies according to the tissue(s) involved, and diagnosis relies on tissue findings of dense infiltration of IgG4-positive plasma cells and a characteristic storiform fibrosis. Treatment is mainly with glucocorticoids, while multiple immunosuppressive medications can be used as adjuvant agents.
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