Key result
Interleukin-1β acutely suppressed inwardly rectifying K+ channel activity in cultured human renal proximal tubule cells to 33.5% of control levels via a PKC-dependent pathway.
IL-1β suppresses inwardly rectifying K+ channel activity in human renal proximal tubule cells via a PKC-dependent pathway, independent of intracellular Ca2+ increases.
Answers are grounded in this paper and cite their sources.
May alter renal tubular ion handling in inflammation; leaves open relevance to cardiorenal disease.
We investigated the effect of interleukin-1β (IL-1β) on activity of an inwardly rectifying K+ channel in cultured human proximal tubule cells (RPTECs), using the patch-clamp technique and Fura-2 Ca2+ imaging. IL-1β (15 pg/ml) acutely reduced K+ channel activity in cell-attached patches. This effect was blocked by the IL-1 receptor antagonist (20 ng/ml), an inhibitor of phospholipase C, neomycin (300 μM), and an inhibitor of protein kinase C (PKC), GF109203X (500 nM). The Fura-2 Ca2+ imaging revealed that IL-1β increased intracellular Ca2+ concentration even after removal of extracellular Ca2+, which was blocked by an inhibitor of inositol 1,4,5-trisphosphate receptors, 2-aminoethoxydiphenyl borate (2-APB, 1 μM). Moreover, IL-1β suppressed channel activity in the presence of 2-APB without extracellular Ca2+. These results suggest that IL-1β suppresses K+ channel activity in RPTECs through binding to its specific receptor and activation of the PKC pathway even though intracellular Ca2+ does not increase.
No takes yet. Share an insight, caveat, or question.
Nakamura et al. (2013) studied In vitro study of renal proximal tubule cells. Interleukin-1β (IL-1β) vs. Control conditions was evaluated on Normalized K+ channel activity (NPo) (p=<0.01). Interleukin-1β acutely suppressed inwardly rectifying K+ channel activity in cultured human renal proximal tubule cells to 33.5% of control levels via a PKC-dependent pathway.
Synapse has enriched 10 related papers. Consider them for comparative context: