Loss of Function of von Hippel-Lindau Trigger Lipocalin 2-Dependent Inflammatory Responses in Cultured and Primary Renal Tubular Cells

Figure 5

VHL loss of function exhibited an inflammatory response in an LCN2-dependent manner. (a) HK-2 cells were transfected with a vector expressing a scrambled shRNA (SC), an shRNA specific for VHL: shVHL1 (V1), or shLCN2 (L1). Cell lysates were analyzed with Western blot using the indicated antibodies. β-Actin was used as a loading control. The status of LCN2 and VHL was confirmed by assaying the levels of LCN2 and VHL proteins, respectively. The VHL knockdown increased the level of p-JNK, but the increase was attenuated in VHL (V3) and LCN2 (L1) double knockdown cells. (b) The level of p-JNK was quantified using ImageJ. (c) HK-2 cells were transfected with a vector expressing the scrambled shRNA (SC), shRNA specific for VHL: shVHL3 (V3), or shLCN2 (L1). The cell lysates were analyzed by Western blot using the indicated antibodies. β-Actin was used as a loading control. The knockdown of LCN2 and VHL was confirmed by assaying the levels of LCN2 and VHL proteins, respectively. VHL knockdown increased the level of p-JNK, but the increase was attenuated in VHL (V1) and LCN2 (L1) double knockdown cells. (d) The level of p-JNK was quantified using ImageJ. All data are presented as the . and .

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