lncR-GAS5 upregulates the splicing factor SRSF10 to impair endothelial autophagy, leading to atherogenesis / 医学前沿

Long noncoding RNAs (lncRNAs) play a critical role in the regulation of atherosclerosis. Here, we investigated the role of the lncRNA growth arrest-specific 5 (lncR-GAS5) in atherogenesis. We found that the enforced expression of lncR-GAS5 contributed to the development of atherosclerosis, which presented as increased plaque size and reduced collagen content. Moreover, impaired autophagy was observed, as shown by a decreased LC3II/LC3I protein ratio and an elevated P62 level in lncR-GAS5-overexpressing human aortic endothelial cells. By contrast, lncR-GAS5 knockdown promoted autophagy. Moreover, serine/arginine-rich splicing factor 10 (SRSF10) knockdown increased the LC3II/LC3I ratio and decreased the P62 level, thus enhancing the formation of autophagic vacuoles, autolysosomes, and autophagosomes. Mechanistically, lncR-GAS5 regulated the downstream splicing factor SRSF10 to impair autophagy in the endothelium, which was reversed by the knockdown of SRSF10. Further results revealed that overexpression of the lncR-GAS5-targeted gene miR-193-5p promoted autophagy and autophagic vacuole accumulation by repressing its direct target gene, SRSF10. Notably, miR-193-5p overexpression decreased plaque size and increased collagen content. Altogether, these findings demonstrate that lncR-GAS5 partially contributes to atherogenesis and plaque instability by impairing endothelial autophagy. In conclusion, lncR-GAS5 overexpression arrested endothelial autophagy through the miR-193-5p/SRSF10 signaling pathway. Thus, miR-193-5p/SRSF10 may serve as a novel treatment target for atherosclerosis.

Kinesio taping methods for stroke survivors with shoulder-hand syndrome / 中华物理医学与康复杂志

Objective:To observe the effects of different kinesio taping methods on hand swelling, shoulder pain, upper limb motor function and ability in the activities of daily living of stroke survivors with shoulder-hand syndrome.Methods:Sixty stroke survivors with shoulder-hand syndrome were randomly divided into groups A, B, C and a control group, each of 15. In addition to routine rehabilitation training and drug treatment, as well as claw-shaped and I-shaped taping of the hand and wrist, group A received I-shaped kinesio taping, B received Y-shape and C received I-shape plus Y-shaped taping of the shoulder. Before and after 4 weeks, the drainage method was employed to calculate the difference in volume between the two hands. Their temperatures were also measured. The subjects reported shoulder pain using a visual analog scale (VAS). Upper limb motor functioning was quantified using Fugl-Meyer scores, and difficulties in the activities of daily living were evaluated using the modified Barthel index (MBI).Results:Before the treatment there were no significant differences among the four groups in terms of any of the measurements. Afterward the treatment, significant improvement was observed in the volume and temperature differences between hands, as well as in the VAS, FMA and MBI scores. After the treatment, group C′s average FMA score was significantly higher than those of the other groups. There was no significant difference in MBI scores among the four groups.Conclusions:Supplementing rehabilitation training with I-shaped plus Y-shaped kinesio taping can effectively reduce the volume and temperature differences between the hands, relieve shoulder pain, and improve effectiveness in the activities of daily living of persons with shoulder-hand syndrome after a stroke. Hand-claw and wrist-I taping also have some effect.

Pro-inflammatory effect of transforming growth factor β1 in rat peritoneal mesothelial cells / 中华肾脏病杂志

Objective To investigate the pro-inflammatory effect of transforming growth factor β1 (TGF-β1) in rat peritoneal mesothelial cells (RPMCs) and its machanism. Methods TGF-β1-induced RPMCs model in vitro was established, and the expression of MCP-1 in the TGF-β1-induced RPMCs was observed. The intervention of Smad7 on the expression of MCP-1 and p38 signal proteins induced by TGF-β1 in RPMCs was explored as well as the intervention of p38 inhibitor SB203580 on the expression of MCP-1 induced by TGF-β1 in RPMCs. Results TGF-β1 could stimulate MCP-1 expression in RPMCs. Compared with control group, MCP-1 mRNA levels were significantly increased after 3 h treatment with TGF-β1 (P<0.05), peak MCP-1 induction occurred at 6 h (P<0.01), and the stimulatory effect of TGF-β1 persisted through 24 h (P<0.05). MCP-1 protein levels were significantly increased after 6 h treatment with TGF-β1(P<0.05), peak MCP-1 induction occurred at 48 h(P<0.01). Over-expressed Smad7 and p38 inhibitor could reduce the expression of MCP-1 induced by TGF-β1 (P<0.05). TGF-β1 could activate p38 signaling pathway, but over-expressed Smad7 could inhibit this role of TGF-β1. Compared with control group, the expression level of p-p38 was increased in TGF-β1-stimulated group. Compared with TGF-β1-stimulated group, the expression level of p-p38 was reduced in Smad7 gene transfer group. Conclusions TGF-β1-induced MCP-1 expression in rat peritoneal mesothelial cells is p38MAPK dependent.