Molecular and Functional Characterization of Kv1.3 Channels in Rat Articular Cartilage and Primary Chondrocytes: Regulation During Culture and Pro-Inflammatory Stimulation

We examined Kv1.3 expression and function in articular cartilage and primary chondrocytes from male Wistar rats using reverse transcription polymerase chain reaction (RT-PCR), Western blotting, immunofluorescence, and whole-cell patch-clamp recordings. Molecular assays supported Kcna3 transcript and Kv1.3 protein expression. PAP-1 and ShK-186 revealed blocker-sensitive outward currents, depolarized freshly isolated chondrocytes, and increased input resistance. During primary culture, total and PAP-1-sensitive conductance densities decreased, without a statistically significant change in the relative PAP-1-sensitive contribution. In unadjusted paired analyses, IL-1α and IL-1β increased PAP-1-sensitive conductance; IL-1β also reduced total conductance and increased the relative contribution. The relative increase with IL-1α was sensitive to the statistical approach. No statistically significant conductance changes were detected after LPS exposure. Blocker effects varied by cytokine and endpoint: PAP-1 reduced propidium iodide (PI) positivity following IL-1α exposure, whereas both blockers attenuated IL-1β-associated changes in metabolic activity, PI positivity, and cell density in paired analyses; the ShK-186 metabolic effect was sensitive to the statistical approach. These findings support a functional contribution of Kv1.3-sensitive conductance to chondrocyte electrical properties and responses to inflammatory stress.