Abstract：
UNASSIGNED: The effect of the functionally unknown gene C6orf120 on autoimmune hepatitis was investigated on C6orf120 knockout rats ( C6orf120 -/- ) and THP-1 cells.
UNASSIGNED: Six-eight-week-old C6orf120 -/- and wild-type (WT) SD rats were injected with Con A (16 mg/kg), and euthanized after 24 h. The sera, livers, and spleens were collected. THP-1 cells and the recombinant protein (rC6ORF120) were used to explore the mechanism in vitro. The frequency of M1 and M2 macrophages was analyzed using flow cytometry. Western blotting and PCR were used to detect macrophage polarization-associated factors.
UNASSIGNED: C6orf120 knockout attenuated Con A-induced autoimmune hepatitis. Flow cytometry indicated that the proportion of CD68 +CD86 +M1 macrophages from the liver and spleen in the C6orf120 -/- rats decreased. C6orf120 knockout induced downregulation of CD86 protein and the mRNA levels of related inflammatory factors TNF-α, IL-1β, and IL-6 in the liver. C6orf120 knockout did not affect the polarization of THP-1 cells. However, rC6ORF120 promoted the THP-1 cells toward CD68 +CD80 +M1 macrophages and inhibited the CD68 +CD206 +M2 phenotype.
UNASSIGNED: C6orf120 knockout alleviates Con A-induced autoimmune hepatitis by inhibiting macrophage polarization toward M1 macrophages and reducing the expression of related inflammatory factors in C6orf120 -/- rats.
UNASSIGNED: Six-eight-week-old C6orf120 -/- and wild-type (WT) SD rats were injected with Con A (16 mg/kg), and euthanized after 24 h. The sera, livers, and spleens were collected. THP-1 cells and the recombinant protein (rC6ORF120) were used to explore the mechanism in vitro. The frequency of M1 and M2 macrophages was analyzed using flow cytometry. Western blotting and PCR were used to detect macrophage polarization-associated factors.
UNASSIGNED: C6orf120 knockout attenuated Con A-induced autoimmune hepatitis. Flow cytometry indicated that the proportion of CD68 +CD86 +M1 macrophages from the liver and spleen in the C6orf120 -/- rats decreased. C6orf120 knockout induced downregulation of CD86 protein and the mRNA levels of related inflammatory factors TNF-α, IL-1β, and IL-6 in the liver. C6orf120 knockout did not affect the polarization of THP-1 cells. However, rC6ORF120 promoted the THP-1 cells toward CD68 +CD80 +M1 macrophages and inhibited the CD68 +CD206 +M2 phenotype.
UNASSIGNED: C6orf120 knockout alleviates Con A-induced autoimmune hepatitis by inhibiting macrophage polarization toward M1 macrophages and reducing the expression of related inflammatory factors in C6orf120 -/- rats.
摘要：
■在C6orf120敲除大鼠（C6orf120-/-）和THP-1细胞上研究了功能未知基因C6orf120对自身免疫性肝炎的影响。
■对6-8周龄的C6orf120-/-和野生型（WT）SD大鼠注射ConA（16mg/kg），并在24小时后实施安乐死。血清，肝脏,收集脾脏。用THP-1细胞和重组蛋白(rC6ORF120)体外研究其作用机制。使用流式细胞术分析M1和M2巨噬细胞的频率。采用Westernblotting和PCR检测巨噬细胞极化相关因子。
■C6orf120基因敲除减毒ConA诱导的自身免疫性肝炎。流式细胞术显示C6orf120-/-大鼠肝脏和脾脏中CD68+CD86+M1巨噬细胞的比例降低。C6orf120基因敲除诱导CD86蛋白及相关炎症因子TNF-αmRNA水平下调,IL-1β,和肝脏中的IL-6。C6orf120敲除不影响THP-1细胞的极化。然而,rC6ORF120促进THP-1细胞向CD68+CD80+M1巨噬细胞转移,抑制CD68+CD206+M2表型。
■C6orf120基因敲除通过抑制C6orf120-/-大鼠巨噬细胞向M1巨噬细胞的极化和减少相关炎症因子的表达来缓解ConA诱导的自身免疫性肝炎。
■对6-8周龄的C6orf120-/-和野生型（WT）SD大鼠注射ConA（16mg/kg），并在24小时后实施安乐死。血清，肝脏,收集脾脏。用THP-1细胞和重组蛋白(rC6ORF120)体外研究其作用机制。使用流式细胞术分析M1和M2巨噬细胞的频率。采用Westernblotting和PCR检测巨噬细胞极化相关因子。
■C6orf120基因敲除减毒ConA诱导的自身免疫性肝炎。流式细胞术显示C6orf120-/-大鼠肝脏和脾脏中CD68+CD86+M1巨噬细胞的比例降低。C6orf120基因敲除诱导CD86蛋白及相关炎症因子TNF-αmRNA水平下调,IL-1β,和肝脏中的IL-6。C6orf120敲除不影响THP-1细胞的极化。然而,rC6ORF120促进THP-1细胞向CD68+CD80+M1巨噬细胞转移,抑制CD68+CD206+M2表型。
■C6orf120基因敲除通过抑制C6orf120-/-大鼠巨噬细胞向M1巨噬细胞的极化和减少相关炎症因子的表达来缓解ConA诱导的自身免疫性肝炎。
