Effect of surfactant protein A on lipopolysaccharide-induced tumor necrosis factor-α expression in human proximal tubular epithelial cells.

Jiao Liu; Zhiyong Liu; Lizhi Feng; Guohua Ding; Dechang Chen; Qingshan Zhou

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Effect of surfactant protein A on lipopolysaccharide-induced tumor necrosis factor-α expression in human proximal tubular epithelial cells.

Author: Jiao LIU ¹ ; Zhiyong LIU ² ; Lizhi FENG ¹ ; Guohua DING ³ ; Dechang CHEN ⁴ ; Qingshan ZHOU ¹
Author Information

1. Department of Critical Care Medicine, Wuhan University Renmin Hospital, Wuhan, Hubei 430060, China.
2. Department of General Surgery, Wuhan University Renmin Hospital, Wuhan, Hubei 430060, China.
3. Department of Nephropathy, Wuhan University Renmin Hospital, Wuhan, Hubei 430060, China.
4. Critical Care and Emergency Department, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai 200003, China.
Publication Type:Journal Article
MeSH: Cell Line; Epithelial Cells; cytology; drug effects; metabolism; Fluorescent Antibody Technique, Indirect; Humans; Kidney Tubules, Proximal; cytology; Lipopolysaccharides; pharmacology; Pulmonary Surfactant-Associated Protein A; metabolism; pharmacology; Tumor Necrosis Factor-alpha; metabolism
From: Chinese Medical Journal 2014;127(2):343-347
CountryChina
Language:English
Abstract:
BACKGROUNDSurfactant protein A (SP-A) contributes to the regulation of sepsis-induced acute lung injury. In a previous study, we demonstrated the expression and localization of SP-A in the kidneys. The present study evaluated the effect of SP-A on lipopolysaccharide (LPS)-induced tumor necrosis factor-a (TNF-α) expression and its underlying mechanisms in the human renal tubular epithelial (HK-2) cells.
METHODSIndirect immunofluorescence assay was used to detect SP-A distribution and expression in HK-2 cells. HK-2 cells were treated with various concentrations of LPS (0, 0.1, 1, 2, 5, and 10 mg/L) for 8 hours and with 5 mg/L LPS for different times (0, 2, 4, 8, 16, and 24 hours) to determine the effects of LPS on SP-A and TNF-α expression. Then, HK-2 cells were transfected with SP-A siRNA to analyze nuclear factor κB (NF-κB) P65 and TNF-α expression of HK-2 cells after LPS-treatment.
RESULTSIndirect immunofluorescence assay revealed that SP-A is localized to the membrane and cytoplasm of HK-2 cells. Interestingly, SP-A1/SP-A2 and TNF-a expression were found to be significantly increased in HK-2 cells upon LPS treatment. Transfection of LPS-treated HK-2 cells with SP-A siRNA resulted in significant increases in the levels of NF-κB P65 protein and TNF-α mRNA and protein compared to those in non-transfected LPS-treated HK-2 cells.
CONCLUSIONSP-A plays an important role in protecting cells against sepsis-induced acute kidney injury by inhibiting NF-κB activity to modulate LPS-induced increase in TNF-α expression.