scholarly journals Upregulation of LncRNA Malat1 Induced Proliferation and Migration of Airway Smooth Muscle Cells via miR-150-eIF4E/Akt Signaling

2019 ◽  
Vol 10 ◽  
Author(s):  
Li Lin ◽  
Qinghai Li ◽  
Wanming Hao ◽  
Yu Zhang ◽  
Long Zhao ◽  
...  
2005 ◽  
Vol 19 (11) ◽  
pp. 1507-1509 ◽  
Author(s):  
Nadia A. Hasaneen ◽  
Stanley Zucker ◽  
Jian Cao ◽  
Christian Chiarelli ◽  
Reynold A. Panettieri ◽  
...  

Pharmacology ◽  
2020 ◽  
Vol 105 (7-8) ◽  
pp. 424-433
Author(s):  
Yibu Kong ◽  
Lizhong Ding ◽  
Yan Xu ◽  
Zhongtian Wang ◽  
Liping Sun

Author(s):  
Zhengyu Zhu ◽  
Liya Zhang ◽  
Ting Jiang ◽  
Yan Qian ◽  
Yun Sun ◽  
...  

Asthma is considered as a general term for various chronic inflammatory diseases of the respiratory tract. Growing evidences have supported that microRNAs were involved in mediating cell proliferation, migration, and other cellular functions. MiR-149 has been found to take part in the development of various cancers. However, whether miR-149 participated in the proliferation and migration of transforming growth factor beta 1 (TGF-β1)-induced airway smooth muscle cells was still unknown. In this study, the expression level of miR-149 in human airway smooth muscle cells (ASMCs) was decreased after TGF-β1 treatment in vitro. Additionally, the over-expression of miR-149 obviously suppressed proliferation and migration in human ASMCs. Besides, we found that overexpression of miR-149 could inhibit the expression of transient receptor potential melastatin 7 (TRPM7) both in protein and gene levels. Furthermore, we demonstrated that miR-149 could inhibit the cell proliferation and migration in human ASMCs by targeting TRPM7 through modulating mitogen-activated protein kinases (MAPKs) signaling pathway. Taken together, we strongly supported that miR-149 might be a key inhibitor of asthma by targeting TRMP7. Therefore, our finding suggests a promising biomarker for the development of further targeted therapies for asthma.


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