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30805933
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A20 overexpression exerts protective effects on podocyte injury in lupus nephritis by downregulating UCH-L1.
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30805933
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The study aims to explore the effect of A20 on LN in relation to the nuclear factor-kappa B (NF-κB) signaling pathway.
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30805933
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Next, A20, UCH-L1, and NF-κB expression in LN patients and MRL/lpr mice was determined.
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30805933
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A20 was downregulated, whereas UCH-L1 was upregulated in LN.
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30805933
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Overexpressed A20 declined NF-κB, UCH-L1 expression, and the extent of p65 phosphorylation.
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30805933
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A20 overexpression or UCH-L1 inhibition increased expression of synaptoporin and nephrin but decreased desmin expression and ubiquitin accumulation level in podocytes.
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30805933
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Moreover, A20 overexpression or UCH-L1 inhibition increased the podocyte number but decreased protein level of cleaved caspase-3, podocyte lesion improvement, decreased foot process width, glomerulus basement membrane, and foot process fusion rate.
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30805933
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In addition, urine protein, blood urea nitrogen, serum creatinine, and ds-DNA antibody levels decreased with elevated A20 or depleted UCH-L1.
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30805933
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Collectively, it could be concluded that A20 protects against podocyte injury in LN via UCH-L1 by inactivating the NF-κB signaling pathway.
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