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miR-23b Attenuates LPS-Induced Inflammatory Responses in Acute Lung Injury via Inhibition of HDAC2
Biochemical Genetics ( IF 2.4 ) Pub Date : 2021-01-07 , DOI: 10.1007/s10528-020-10018-7
Zhi-Feng Luo 1, 2 , Xiang-Hui Jiang 2, 3 , Huan Liu 2, 4 , Li-Yuan He 2, 5 , Xiong Luo 2, 6 , Fu-Chun Chen 2, 7 , Yu-Lin Tan 2, 8
Affiliation  

Inflammatory responses play significant role in infectious etiology-induced acute lung injury (ALI). Histone deacetylase 2 is found to be essential and stimulated in lipopolysaccharide (LPS)-induced ALI by regulating proinflammatory cytokines. miR-23b has been demonstrated to be downregulated in LPS-induced inflammatory injury. In this study, we aimed to explore the interaction between miR-23b and HDAC2 and their function in LPS-induced ALI. LPS treatment was induced on murine alveolar macrophage cell line MH-S. Level of miR-23b and HDAC2 were determined by real-time PCR or Western blot. Proinflammatory cytokines expression and secretion were detected by real-time PCR and ELISA assay. The levels of miR-23b and HDAC2 were manipulated by transient transfection of miRNA mimics, shRNA or overexpression vector. The interaction between miR-23b and HDAC2 were tested by Luciferase reporter assay. LPS treatment inhibited miR-23b expression, while increased HDAC2 level in MH-S cells. Proinflammatory cytokines were stimulated by LPS treatment. Knockdown of HDAC2 or overexpression of miR-23b significantly repressed the expression of proinflammatory cytokines induced by LPS. miR-23b could suppress HDAC2 expression by directly targeting to its mRNA. LPS treatment stimulated the inflammatory responses in macrophages through inhibition of miR-23b, enhanced HDAC2 expression and inducing the expression of its downstream targets TNF-α, IL-6, and IL-1β. Overexpression of miR-23b was sufficient to suppress inflammatory responses by targeting HDAC2, making it a promising therapeutic target to ALI treatment.



中文翻译:

miR-23b通过抑制HDAC2减轻LPS诱导的急性肺损伤中的炎症反应。

炎症反应在感染病因引起的急性肺损伤(ALI)中起重要作用。发现组蛋白脱乙酰基酶2是必需的,并通过调节促炎细胞因子在脂多糖(LPS)诱导的ALI中被刺激。已经证明,miR-23b在LPS诱导的炎症性损伤中被下调。在这项研究中,我们旨在探讨miR-23b和HDAC2之间的相互作用以及它们在LPS诱导的ALI中的功能。LPS处理在鼠肺泡巨噬细胞系MH-S上诱导。miR-23b和HDAC2的水平通过实时PCR或Western blot测定。通过实时PCR和ELISA测定来检测促炎细胞因子的表达和分泌。通过miRNA模拟物,shRNA或过表达载体的瞬时转染来控制miR-23b和HDAC2的水平。miR-23b和HDAC2之间的相互作用通过荧光素酶报告基因检测法进行了测试。LPS处理可抑制miR-23b表达,同时增加MH-S细胞中HDAC2的水平。LPS处理可刺激促炎细胞因子。抑制HDAC2或miR-23b的过表达显着抑制了LPS诱导的促炎细胞因子的表达。miR-23b可以通过直接靶向其mRNA来抑制HDAC2的表达。LPS处理通过抑制miR-23b,增强HDAC2表达并诱导其下游靶标TNF-α,IL-6和IL-1β的表达来刺激巨噬细胞的炎症反应。miR-23b的过表达足以通过靶向HDAC2抑制炎症反应,使其成为ALI治疗的有希望的治疗靶标。LPS处理可抑制miR-23b表达,同时增加MH-S细胞中HDAC2的水平。LPS处理可刺激促炎细胞因子。抑制HDAC2或miR-23b的过表达显着抑制了LPS诱导的促炎细胞因子的表达。miR-23b可以通过直接靶向其mRNA来抑制HDAC2的表达。LPS处理通过抑制miR-23b,增强HDAC2表达并诱导其下游靶标TNF-α,IL-6和IL-1β的表达来刺激巨噬细胞的炎症反应。miR-23b的过表达足以通过靶向HDAC2抑制炎症反应,使其成为ALI治疗的有希望的治疗靶标。LPS处理可抑制miR-23b表达,同时增加MH-S细胞中HDAC2的水平。LPS处理可刺激促炎细胞因子。抑制HDAC2或miR-23b的过表达显着抑制了LPS诱导的促炎细胞因子的表达。miR-23b可以通过直接靶向其mRNA来抑制HDAC2的表达。LPS处理通过抑制miR-23b,增强HDAC2表达并诱导其下游靶标TNF-α,IL-6和IL-1β的表达来刺激巨噬细胞的炎症反应。miR-23b的过表达足以通过靶向HDAC2抑制炎症反应,使其成为ALI治疗的有希望的治疗靶标。抑制HDAC2或miR-23b的过表达显着抑制了LPS诱导的促炎细胞因子的表达。miR-23b可以通过直接靶向其mRNA来抑制HDAC2的表达。LPS处理通过抑制miR-23b,增强HDAC2表达并诱导其下游靶标TNF-α,IL-6和IL-1β的表达来刺激巨噬细胞的炎症反应。miR-23b的过表达足以通过靶向HDAC2抑制炎症反应,使其成为ALI治疗的有希望的治疗靶标。抑制HDAC2或miR-23b的过表达显着抑制了LPS诱导的促炎细胞因子的表达。miR-23b可以通过直接靶向其mRNA来抑制HDAC2的表达。LPS处理通过抑制miR-23b,增强HDAC2表达并诱导其下游靶标TNF-α,IL-6和IL-1β的表达来刺激巨噬细胞的炎症反应。miR-23b的过表达足以通过靶向HDAC2抑制炎症反应,使其成为ALI治疗的有希望的治疗靶标。增强HDAC2的表达并诱导其下游靶标TNF-α,IL-6和IL-1β的表达。miR-23b的过表达足以通过靶向HDAC2抑制炎症反应,使其成为ALI治疗的有希望的治疗靶标。增强HDAC2的表达并诱导其下游靶标TNF-α,IL-6和IL-1β的表达。miR-23b的过表达足以通过靶向HDAC2抑制炎症反应,使其成为ALI治疗的有希望的治疗靶标。

更新日期:2021-01-08
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