Molecular and Functional Characterization of Kv1.3 Channels in Rat Articular Cartilage and Primary Chondrocytes: Regulation During Culture and Pro-Inflammatory Stimulation
- 1Department of Physiology, Biophysics and Neurosciences, Centro de Investigacion y Estudios Avanzados del IPN, Ciudad de México 07360, Mexico
Abstract
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.
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BibTeX
@article{ponce2026molecular,
title = {{Molecular and Functional Characterization of Kv1.3 Channels in Rat Articular Cartilage and Primary Chondrocytes: Regulation During Culture and Pro-Inflammatory Stimulation}},
author = {Arturo Ponce and Lorena Hinojosa and Maria Luisa Roldán and Liora Shoshani},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = oct,
doi = {10.3390/ijms27219790},
url = {https://www.mdpi.com/1422-0067/27/21/9790},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Molecular and Functional Characterization of Kv1.3 Channels in Rat Articular Cartilage and Primary Chondrocytes: Regulation During Culture and Pro-Inflammatory Stimulation
AU - Arturo Ponce
AU - Lorena Hinojosa
AU - Maria Luisa Roldán
AU - Liora Shoshani
PY - 2026
DA - 2026/10/31
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms27219790
UR - https://www.mdpi.com/1422-0067/27/21/9790
AB - 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.
SN - 1422-0067
ER -