Journal: Journal of Cardiovascular Development and Disease

Article Title: Study on the Role and Mechanism of TOPORS in Regulating Aortic Dissection by Mediating SUMOylation

doi: 10.3390/jcdd13030110

Figure Lengend Snippet: Inhibition of TOPORS mitigated aortic dissection (AD) in mice. ( A ): Ultrasound imaging of the mouse thoracic aorta depicting changes in aortic diameter (scale bar = 1 mm); ( B ): Gross anatomical images of the thoracic aorta demonstrating morphological variations (scale bar = 2 mm); ( C ): Representative transverse sections of aortic tissues from AD mice stained with hematoxylin and eosin (H&E) for structural analysis and elastica van Gieson (EVG) for visualization of elastic fibers; ( D , E ): Expression levels of TOPORS in aorta tissues determined by qRT-PCR for mRNA ( D ) and Western blot ( E ) for protein; F-I: Enzyme-linked immunosorbent assay (ELISA) quantification of pro-inflammatory factors in aortic tissues: ( F ) interferon-α ( IFN- α), ( G ) interleukin-6 ( IL-6 ), ( H ) tumor necrosis factor-α ( TNF-α ), and ( I ) interleukin-1β (IL-1β). Data are presented as mean ± standard deviation (SD) ( n = 10). Significance levels are denoted as * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, where “ns” indicates no significant difference.

Article Snippet: Specifically, the following ELISA kits were employed: Mouse TNF-α Elisa Kit (H052-1-2), Mouse IFN-α Elisa Kit (H023-1-1), Mouse IL-6 Elisa Kit (H007-1-2), and Mouse IL-1β Elisa Kit (H002-1-2), all purchased from Nanjing Jiancheng Bioengineering Institute (Nanjing, China).

Techniques: Inhibition, Dissection, Imaging, Staining, Expressing, Quantitative RT-PCR, Western Blot, Enzyme-linked Immunosorbent Assay, Standard Deviation

Journal: Journal of Cardiovascular Development and Disease

Article Title: Study on the Role and Mechanism of TOPORS in Regulating Aortic Dissection by Mediating SUMOylation

doi: 10.3390/jcdd13030110

Figure Lengend Snippet: Effects of TOPORS on Ang-II-induced vascular smooth muscle cells (VSMCs). ( A ): Ang-II treatment leads to a dose-dependent downregulation of mRNA expression for calponin and SM22α , which are critical markers of the contractile VSMC phenotype; ( B ): The mRNA expression level of TOPORS in VSMC lines with TOPORS knockout (si TOPORS ) or overexpression (oe TOPORS ) was determined by qRT-PCR; ( C ): Regulation of TOPORS knockout or overexpression on the viability of Ang-II-stimulated VSMCs was assessed by CCK-8 assay; ( D , E ): Regulation of TOPORS knockout or overexpression on the apoptosis of Ang-II-stimulated VSMCs was evaluated by flow cytometry analysis ( D ) and TUNEL staining ( E ); ( F – I ): Regulation of TOPORS knockout or overexpression on the secretion of pro-inflammatory cytokines in VSMC lines were determined by ELISA: interleukin-6 ( IL-6 ) ( F ), interferon-α ( IFN- α) ( G ), tumor necrosis factor-α ( TNF-α ) ( H ), and interleukin-1β ( IL-1β ) ( I ). Data are presented as mean ± standard deviation (SD) ( n = 3). Significance levels are denoted as * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, where “ns” represents no significant difference.

Article Snippet: Specifically, the following ELISA kits were employed: Mouse TNF-α Elisa Kit (H052-1-2), Mouse IFN-α Elisa Kit (H023-1-1), Mouse IL-6 Elisa Kit (H007-1-2), and Mouse IL-1β Elisa Kit (H002-1-2), all purchased from Nanjing Jiancheng Bioengineering Institute (Nanjing, China).

Techniques: Expressing, Knock-Out, Over Expression, Quantitative RT-PCR, CCK-8 Assay, Flow Cytometry, TUNEL Assay, Staining, Enzyme-linked Immunosorbent Assay, Standard Deviation

Journal: Journal of Cardiovascular Development and Disease

Article Title: Study on the Role and Mechanism of TOPORS in Regulating Aortic Dissection by Mediating SUMOylation

doi: 10.3390/jcdd13030110

Figure Lengend Snippet: Effects of TOPORS on PI3K/AKT and p53 signaling pathways in VSMC model of aortic dissection ( A ). ( A – C ): the mRNA expression profiles of AKT ( A ), PI3K ( B ), and p53 ( C ) quantified by qRT-PCR. ( D ): Western blot analysis of protein expression, including AKT, p-AKT, PI3K, p-PI3K, and p53 . ( E , F ): The apoptosis of AD model VSMC after PFT-ɑ treatment was evaluated by TUNEL staining ( E ) and flow cytometry analysis ( F ); ( G – J ): ELISA quantification of pro-inflammatory cytokines after PFT-ɑ treatment: tumor necrosis factor-α ( TNF-α ) ( G ), interleukin-6 ( IL-6 ) ( H ), interleukin-1β ( IL-1β ) ( I ), and interferon-α ( IFN- α) ( J ). Data are presented as mean ± standard deviation (SD) ( n = 3). Significance levels are denoted as * p < 0.05, *** p < 0.001, **** p < 0.0001, where “ns” represents no significant difference. ( K ): The SUMOylation level of the p53 gene was detected by co-immunoprecipitation (Co-IP) in the model-si TOPORS group and model-oe TOPORS group.

Article Snippet: Specifically, the following ELISA kits were employed: Mouse TNF-α Elisa Kit (H052-1-2), Mouse IFN-α Elisa Kit (H023-1-1), Mouse IL-6 Elisa Kit (H007-1-2), and Mouse IL-1β Elisa Kit (H002-1-2), all purchased from Nanjing Jiancheng Bioengineering Institute (Nanjing, China).

Techniques: Protein-Protein interactions, Dissection, Expressing, Quantitative RT-PCR, Western Blot, TUNEL Assay, Staining, Flow Cytometry, Enzyme-linked Immunosorbent Assay, Standard Deviation, Immunoprecipitation, Co-Immunoprecipitation Assay