Figures & data
Figure 1. Downregulation of CRNDE and TUG1 was observed in sepsis. Plasma samples from sepsis patients (n = 64) and healthy controls (n = 64) were collected and were subjected to RNA preparations and RT-qPCRs to determine the expression of CRNDE (a) and TUG1 (b). Expression levels of CRNDE and TUG1 in plasma samples from both groups were presented, ***,p < 0.001
![Figure 1. Downregulation of CRNDE and TUG1 was observed in sepsis. Plasma samples from sepsis patients (n = 64) and healthy controls (n = 64) were collected and were subjected to RNA preparations and RT-qPCRs to determine the expression of CRNDE (a) and TUG1 (b). Expression levels of CRNDE and TUG1 in plasma samples from both groups were presented, ***,p < 0.001](/cms/asset/fb166b2f-4de9-4aea-8c63-8098d07d8996/kbie_a_2008658_f0001_oc.jpg)
Figure 2. CRNDE and TUG1 were positively correlated. Pearson’s correlation coefficient was calculated to study the correlations between CRNDE and TUG1 across plasma samples from both sepsis patients (a) and healthy controls (b)
![Figure 2. CRNDE and TUG1 were positively correlated. Pearson’s correlation coefficient was calculated to study the correlations between CRNDE and TUG1 across plasma samples from both sepsis patients (a) and healthy controls (b)](/cms/asset/84136e98-e29f-4a7e-a050-7e2ac8ba776c/kbie_a_2008658_f0002_oc.jpg)
Figure 3. Overexpression of CRNDE and TUG1 increased the expression of each other in cardiomyocytes with and without LPS treatment. To test whether CRNDE and TUG1 can interact with each other, cardiomyocytes with and without LPS treatment (10 μg/ml for 48 h) were overexpressed with CRNDE or TUG1 (a). The effects of CRNDE overexpression on TUG1 (b) and the effects of TUG1 overexpression on CRNDE (c) in both types of cardiomyocytes were also explored by RT-qPCR. *,p < 0.05
![Figure 3. Overexpression of CRNDE and TUG1 increased the expression of each other in cardiomyocytes with and without LPS treatment. To test whether CRNDE and TUG1 can interact with each other, cardiomyocytes with and without LPS treatment (10 μg/ml for 48 h) were overexpressed with CRNDE or TUG1 (a). The effects of CRNDE overexpression on TUG1 (b) and the effects of TUG1 overexpression on CRNDE (c) in both types of cardiomyocytes were also explored by RT-qPCR. *,p < 0.05](/cms/asset/1182f8fe-90fe-44b4-925d-dcb1730a0ddf/kbie_a_2008658_f0003_oc.jpg)
Figure 4. CRNDE and TUG1 overexpression decreased the LPS-induced apoptosis of cardiomyocytes. AC16 cells were subjected to LPS (0, 1, 2, 5, and 10 μg/ml, Sigma-Aldrich) treatment for 48 h, and then CRNDE (a) and TUG1 (b) expression was studied with RT-qPCR. The effects of CRNDE and TUG1 overexpression on the apoptosis of cardiomyocytes treated with LPS (10 μg/ml for 48 h) were analyzed by cell apoptosis assay, and untreated cells were also included (c). *,p < 0.05
![Figure 4. CRNDE and TUG1 overexpression decreased the LPS-induced apoptosis of cardiomyocytes. AC16 cells were subjected to LPS (0, 1, 2, 5, and 10 μg/ml, Sigma-Aldrich) treatment for 48 h, and then CRNDE (a) and TUG1 (b) expression was studied with RT-qPCR. The effects of CRNDE and TUG1 overexpression on the apoptosis of cardiomyocytes treated with LPS (10 μg/ml for 48 h) were analyzed by cell apoptosis assay, and untreated cells were also included (c). *,p < 0.05](/cms/asset/4569ddd3-b018-4d2b-b2bf-1994c90daf4e/kbie_a_2008658_f0004_oc.jpg)