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TG binds USP38. 24 / 24
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"Next, we observed that left atrial weight/tibia length was heavily increased in USP38-TG group compared with NTG group after AB surgery (see xref , xref )."
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"Additionally, the enlargement of LAD was observed in USP38-TG group compared with NTG group under AB stimulation (Figure xref )."
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"Conversely, LVEF and LVFS showed further reduction in USP38-TG AB group compared with NTG AB group (see xref , xref xref xref )."
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"The USP38-TG group showed a more evident atrial electrical remodelling after AB surgery compared with the NTG group."
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"Specifically, after AB surgery, the levels of calcium-handling proteins, increased p-RYR2 and p-PLB and decreased SERCA2a, were observed in the USP38-TG group compared with the NTG group (Figure xref )."
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"Conversely, inflammation also was exacerbated after AB in USP38-TG group by increased levels of serum inflammatory cytokines and atrial tissue inflammatory marker proteins and transcription (Figure xref )."
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"USP38-TG mice were intraperitoneally injected with Amlexanox (an inhibitor of TBK1) or DMSO 2 weeks after AB surgery(Figure xref A)."
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"To further explore whether USP38 is involved in AB-induced AF through NF-κB, we administered intra-peritoneal injection of PDTC (Sigma, USA) 2 weeks after AB surgery in USP38-TG mice (Figure xref ), which has been shown to inhibit NF-κB activation."
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"Notably, the detrimental effects in USP38-TG mice were significantly prevented by Amlexanox, as evidenced by reduced HW, HW/BW, HW/TL and LW/BW ratio(Figure xref B), improved cardiac function(Figure xref C), alleviated hypertrophic degree(Figure xref D), ameliorated myocardial fibrosis(Figure xref E), and decreased the protein expression of TBK1/Akt-GSK3β/mTOR signaling pathway(Figure xref F)in Amlexanox treated-USP38-TG mice compared with USP38-TG DMSO mice."
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"Previous studies have demonstrated that atrial structural and electrical remodelling plays a fundamental role in the trigger and perpetuation of AF. xref Atrial structural remodelling is usually manifested atrial enlargement and atrial fibrosis, causing delayed conduction and local heterogeneous conduction, which creates the substrate for AF. xref It is worth noting that chronic pressure overload promotes collagen synthesis, causing excessive deposition of extra-cellular matrix proteins in the atrial tissue. xref Moreover, the atrial diameter increases under pressure overload stimulation, xref and the atrial enlargement in patients is associated with the occurrence of AF. xref In this study, we noticed that pressure overload caused the enlargement of LAD was more obvious in USP38-TG mice compared with USP38-NTG mice."
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"Moreover, the degree of atrial fibrosis was more severe in USP38-TG mice under pressure overload stimulation, suggesting that USP38 overexpression further exacerbates pressure overload-induced atrial structural remodelling."
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"In addition, inhibition of NF-κB decreased the expression of NLRP3 and IL-1β and reduced susceptibility to AF in USP38-TG mice after AB surgery."
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"Finally, the essential role of the USP38-TBK1 axis in pathological cardiac remodeling is demonstrated by “rescue” experiments using rAAV9-Tbk1 (overexpressing TBK1) in USP38 cko mice or Amlexanox (TBK1 inhibitor) in USP38-TG mice."
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"In contrast, TBK1 inhibitor improves the pro-hypertrophic effects in USP38-TG mice after AB surgery."
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"We further evaluated the role of USP38 overexpression in cardiac remodeling by generating cardiac specific USP38 transgenic mouse line (USP38-TG)."
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"USP38 overexpression in heart tissues from USP38-TG mice was detected by western blot( xref )."
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"Four weeks after AB surgery, the QRS duration and QTc of the USP38-TG group and NTG group were prolonged, with the prolongation in the USP38-TG group being more pronounced than that in the NTG group (Fig.  xref A, B)."
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"After 4 weeks of AB surgery, the expression of Kv4.3, Kv4.2 and Kv2.1, Kv1.5 in USP38-TG and NTG groups decreased drastically, but these changes in USP38-TG hearts were considerably greater than those in NTG hearts (Fig.  xref G–K)."
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"We performed AB surgery on USP38-TG and NTG mice, and found the HW, HW/BW, HW/TL and LW/BW ratio of USP38-TG were higher than NTG mice(Figure xref A)."
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"Moreover, the protein expression of ICaL was significantly lower in USP38-TG group than in the NTG group after AB surgery (Fig.  xref G, xref )."
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"Further findings revealed a significant decrease in the protein level of Cx43 in ventricular tissue in USP38-TG mice after AB surgery compared to NTG-AB mice (Fig.  xref D–F)."
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"After 4 weeks of AB surgery, echocardiography revealed that EF and FS were decreased and LVIDs and LVIDd were increased in USP38-TG mice compared with NTG mice(Figure xref B)."
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"Moreover, USP38-TG mice also displayed greater heart size, cardiomyocyte cross-sectional area and myocardial fibrosis than NTG mice under pressure overload stimulation(Figure xref C and xref D)."
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"Consistent to the histological analysis, the mRNA levels of hypertrophic and fibrotic markers were obviously increased in USP38-TG mice(Figure xref E and xref F)."
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