miR-150 was found to target the 3′-untranslated regions of AKT3, and the AKT pathway was affected by SR protein kinase 1 (SRPK1). However, the expression and significance of miR-150, AKT3 and SRPK1 in acute lung injury (ALI) were not clear. Here, we found that the expression of miR-150 was significantly reduced, while the expression of AKT3 and SRPK1 were markedly increased in LPS-treated A549, THP-1 and RAW 264.7 cells. miR-150 significantly decreased levels of pro-inflammatory cytokines IL-1β, IL-6 and TNF-α, reduced the expression of AKT3, but had no impact on SRPK1 expression compared with the control group in LPS-treated A549, THP-1 and RAW 264.7 cells. AKT3 silencing only reduced the production of pro-inflammatory cytokines and showed no effect on miR-150 and SRPK1 expression. Finally, we observed that miR-150 mimics and/or silencing of SRPK1 decreased the expression of AKT3 mRNA. Besides, over-expression of miR-150 or silencing of SRPK1 also reduced the expression of AKT3 protein, which exhibited the lowest level in the miR-150 mimics plus si-SRPK1 group. However, si-SRPK1 had no effect on miR-150 level. In conclusion, miR-150 and SRPK1 separately and cooperatively participate into inflammatory responses in ALI through regulating AKT3 pathway. Increased miR-150 and silenced SRPK1 may be a novel potential factor for preventing and treating more inflammatory lung diseases.

发现 miR-150 靶向 AKT3 的 3'-非翻译区，并且 AKT 通路受 SR 蛋白激酶 1 (SRPK1) 的影响。然而，miR-150、AKT3和SRPK1在急性肺损伤（ALI）中的表达和意义尚不清楚。在这里，我们发现 miR-150 的表达显着降低，而 AKT3 和 SRPK1 的表达在 LPS 处理的 A549、THP-1 和 RAW 264.7 细胞中显着增加。在 LPS 处理的 A549、THP-1 中，与对照组相比，miR-150 显着降低促炎细胞因子 IL-1β、IL-6 和 TNF-α 的水平，降低 AKT3 的表达，但对 SRPK1 的表达没有影响和 RAW 264.7 单元格。AKT3 沉默仅减少促炎细胞因子的产生，对 miR-150 和 SRPK1 表达没有影响。最后，我们观察到 miR-150 模拟和/或 SRPK1 沉默降低了 AKT3 mRNA 的表达。此外，miR-150 的过表达或 SRPK1 的沉默也降低了 AKT3 蛋白的表达，其在 miR-150 模拟物加 si-SRPK1 组中表现出最低水平。然而，si-SRPK1 对 miR-150 水平没有影响。总之，miR-150和SRPK1通过调节AKT3通路分别和协同参与ALI的炎症反应。增加的 miR-150 和沉默的 SRPK1 可能是预防和治疗更多炎症性肺病的新的潜在因素。si-SRPK1 对 miR-150 水平没有影响。总之，miR-150和SRPK1通过调节AKT3通路分别和协同参与ALI的炎症反应。增加的 miR-150 和沉默的 SRPK1 可能是预防和治疗更多炎症性肺病的新的潜在因素。si-SRPK1 对 miR-150 水平没有影响。总之，miR-150和SRPK1通过调节AKT3通路分别和协同参与ALI的炎症反应。增加的 miR-150 和沉默的 SRPK1 可能是预防和治疗更多炎症性肺病的新的潜在因素。