Abstract：
UNASSIGNED: Proliferative vitreoretinopathy (PVR) can cause blindness and the pathogenesis is unclear. Transforming growth factor (TGF)-β-induced epithelial-mesenchymal transition (EMT) of RPE cells is vital. P53 protein 2 (ASPP2) was previously reported to inhibit EMT in PVR rats, but the specific mechanism is unveiled.
UNASSIGNED: TGF-β was used to induce EMT in ARPE-19 cells, and evaluated by immunofluorescence and western blot. ARPE-19 cells were transfected with scrambled/ASPP2-lentivirus, followed by TGF-β treatment. After that, alterations of EMT and autophagy were measured by western blot and transmission electron microscopy. Moreover, TGF-β and ARPE-19 cells treated with scrambled/ASPP2-lentivirus were employed to establish the PVR model via intravitreal injection to SD rats, and retinal changes as well as EMT and autophagy activity were evaluated accordingly.
UNASSIGNED: ASPP2 expression was decreased during TGF-β-induced EMT in ARPE-19 cells. In vitro, EMT and autophagy was activated by TGF-β, which could be partly reversed by ASPP2 upregulation. In vivo, ASPP2 upregulation protected against structural and functional changes in PVR retinas. Additionally, expressions of EMT and autophagy markers in retinas were inhibited by ASPP2 upregulation.
UNASSIGNED: ASPP2 upregulation inhibited the EMT and autophagy process caused by TGF-β in ARPE-19 cells. Correspondingly, upregulation of ASPP2 alleviated intraocular fibrosis and protected visual function in PVR rats.
UNASSIGNED: TGF-β was used to induce EMT in ARPE-19 cells, and evaluated by immunofluorescence and western blot. ARPE-19 cells were transfected with scrambled/ASPP2-lentivirus, followed by TGF-β treatment. After that, alterations of EMT and autophagy were measured by western blot and transmission electron microscopy. Moreover, TGF-β and ARPE-19 cells treated with scrambled/ASPP2-lentivirus were employed to establish the PVR model via intravitreal injection to SD rats, and retinal changes as well as EMT and autophagy activity were evaluated accordingly.
UNASSIGNED: ASPP2 expression was decreased during TGF-β-induced EMT in ARPE-19 cells. In vitro, EMT and autophagy was activated by TGF-β, which could be partly reversed by ASPP2 upregulation. In vivo, ASPP2 upregulation protected against structural and functional changes in PVR retinas. Additionally, expressions of EMT and autophagy markers in retinas were inhibited by ASPP2 upregulation.
UNASSIGNED: ASPP2 upregulation inhibited the EMT and autophagy process caused by TGF-β in ARPE-19 cells. Correspondingly, upregulation of ASPP2 alleviated intraocular fibrosis and protected visual function in PVR rats.
摘要：
■增生性玻璃体视网膜病变（PVR）可导致失明，其发病机制尚不清楚。转化生长因子（TGF）-β诱导的RPE细胞上皮间质转化（EMT）至关重要。P53蛋白2（ASPP2）先前报道抑制PVR大鼠的EMT，但具体机制已经揭晓。
■TGF-β用于诱导ARPE-19细胞的EMT，并通过免疫荧光和免疫印迹进行评价。用乱序/ASPP2-慢病毒转染ARPE-19细胞，随后是TGF-β治疗。之后,通过蛋白质印迹和透射电子显微镜测量EMT和自噬的改变。此外，采用TGF-β和ARPE-19细胞经玻璃体腔注射给SD大鼠建立PVR模型,和视网膜变化以及EMT和自噬活性进行相应评估。
■在TGF-β诱导的ARPE-19细胞EMT过程中，ASPP2表达降低。体外，EMT和自噬被TGF-β激活，可以通过ASPP2上调部分逆转。在体内,ASPP2上调可防止PVR视网膜的结构和功能变化。此外,ASPP2上调抑制视网膜EMT和自噬标志物的表达。
■ASPP2上调抑制了TGF-β引起的ARPE-19细胞EMT和自噬过程。相应地,ASPP2上调减轻PVR大鼠眼内纤维化和保护视功能。
■TGF-β用于诱导ARPE-19细胞的EMT，并通过免疫荧光和免疫印迹进行评价。用乱序/ASPP2-慢病毒转染ARPE-19细胞，随后是TGF-β治疗。之后,通过蛋白质印迹和透射电子显微镜测量EMT和自噬的改变。此外，采用TGF-β和ARPE-19细胞经玻璃体腔注射给SD大鼠建立PVR模型,和视网膜变化以及EMT和自噬活性进行相应评估。
■在TGF-β诱导的ARPE-19细胞EMT过程中，ASPP2表达降低。体外，EMT和自噬被TGF-β激活，可以通过ASPP2上调部分逆转。在体内,ASPP2上调可防止PVR视网膜的结构和功能变化。此外,ASPP2上调抑制视网膜EMT和自噬标志物的表达。
■ASPP2上调抑制了TGF-β引起的ARPE-19细胞EMT和自噬过程。相应地,ASPP2上调减轻PVR大鼠眼内纤维化和保护视功能。
