scholarly journals Aerobic exercise improves cardiac function in rats with chronic heart failure through inhibition of the long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1)

2021 ◽  
Vol 9 (4) ◽  
pp. 340-340
Author(s):  
Ling Hu ◽  
Ya-Nan Xu ◽  
Qian Wang ◽  
Mei-Jie Liu ◽  
Ping Zhang ◽  
...  
2018 ◽  
Vol 1 (2) ◽  
Author(s):  
Lingjie Li ◽  
Jing Zhang ◽  
Xuefei Chen

Objective To investigate the effects of vascular endothelial growth factor B in aerobic exercise mediated chronic heart failure rats cardiac function improvement and skeletal muscle remodeling. Methods We employed transverse abdominal aortic constriction (TAC) inducing CHF in Sprague Dawley rats. Controls were sham-operated animals. At 4 weeks after surgery, rats were randomized to 4 weeks of aerobic exercise (CHF+E) or to untrained groups (CHF). After 8 weeks, all rats went echocardiography test. After which, rats were sacrificed and samples were collected. Muscular cytokine VEGFB and its receptor NRP1 expression were analyzed. Expression of apoptosis and muscle atrophy markers were assessed in cardiac muscle、gastrocnemius. Results TAC rats developed CHF (preserved LV ejection fraction, hypertrophy of myocardial cells, decreased FS, increased LVAW d and LVID s). Exercise ameliorate CHF rat cardiac function. TAC rat skeletal muscle developed irregular muscle fiber distribution.The two atrophy-related ubiquitin ligases atrogin-1 and MuRF1, as well as genes involved in apoptosis and autophagy were upregulated in muscles in CHF rats. Exercise inhibited muscle atrophy and skeletal muscle apoptosis.VEGFB and its receptor NRPI decreased significantly in CHF muscle. Exercise promoted VEGFB and NRP1 expression in cardiac tissue, gastrocnemius. Conclusions Exercise ameliorates CHF rat cardiac function. VEGFB inhibits cardiac muscle and gastrocnemius apoptosis in CHF rats.


2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Shuang Qu ◽  
Zichen Jiao ◽  
Geng Lu ◽  
Bing Yao ◽  
Ting Wang ◽  
...  

Abstract Background Although using a blockade of programmed death-ligand 1 (PD-L1) to enhance T cell immune responses shows great promise in tumor immunotherapy, the immune-checkpoint inhibition strategy is limited for patients with solid tumors. The mechanism and efficacy of such immune-checkpoint inhibition strategies in solid tumors remains unclear. Results Employing qRT-PCR, Sanger sequencing, and RNA BaseScope analysis, we show that human lung adenocarcinoma (LUAD) all produce a long non-coding RNA isoform of PD-L1 (PD-L1-lnc) by alternative splicing, regardless if the tumor is positive or negative for the protein PD-L1. Similar to PD-L1 mRNA, PD-L1-lnc in various lung adenocarcinoma cells is significantly upregulated by IFNγ. Both in vitro and in vivo studies demonstrate that PD-L1-lnc increases proliferation and invasion but decreases apoptosis of lung adenocarcinoma cells. Mechanistically, PD-L1-lnc promotes lung adenocarcinoma progression through directly binding to c-Myc and enhancing c-Myc transcriptional activity. Conclusions In summary, the PD-L1 gene can generate a long non-coding RNA through alternative splicing to promote lung adenocarcinoma progression by enhancing c-Myc activity. Our results argue in favor of investigating PD-L1-lnc depletion in combination with PD-L1 blockade in lung cancer therapy.


iScience ◽  
2021 ◽  
pp. 102537
Author(s):  
Aowen Zhuang ◽  
Anna C. Calkin ◽  
Shannen Lau ◽  
Helen Kiriazis ◽  
Daniel G. Donner ◽  
...  

2021 ◽  
Vol 40 (4) ◽  
pp. S255
Author(s):  
I. Silacheva ◽  
G. Bondar ◽  
T. Nakade ◽  
T. Grogan ◽  
D. Elashoff ◽  
...  

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