scholarly journals Triptolide inhibits transforming growth factor-β1-induced proliferation and migration of rat airway smooth muscle cells by suppressing nuclear factor-κB but not extracellular signal-regulated kinase 1/2

Immunology ◽  
2014 ◽  
Vol 144 (3) ◽  
pp. 486-494 ◽  
Author(s):  
Ming Chen ◽  
Jian-Ting Shi ◽  
Zhi-Qiang Lv ◽  
Lin-Jie Huang ◽  
Xiao-Ling Lin ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Transforming Growth Factor ◽  
Nuclear Factor Κb ◽  
Transforming Growth Factor Β1 ◽  
Airway Smooth Muscle Cells ◽  
Nuclear Factor ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals MiR-149 attenuates the proliferation and migration of TGF-β1-induced airway smooth muscle cells by targeting TRPM7 and affecting downstream MAPK signal pathway

2020 ◽  
Author(s):  
Zhengyu Zhu ◽  
Liya Zhang ◽  
Ting Jiang ◽  
Yan Qian ◽  
Yun Sun ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Airway Smooth Muscle ◽  
Transforming Growth Factor ◽  
Muscle Cells ◽  
Airway Smooth Muscle Cells ◽  
And Migration ◽  
Tgf Β1 ◽  
Proliferation And Migration

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.

Hyperin Ameliorates Proliferation, Migration, and Extracellular Matrix Formation in Airway Smooth Muscle Cells by Inhibiting Transforming Growth Factor-β1-Induced Nuclear Factor-κB Activation

2020 ◽  
Vol 19 (2) ◽  
pp. 222-227
Author(s):  
Nan Zhang ◽  
Tingting Zhao ◽  
Meirong Bi ◽  
Xuejia He ◽  
Yamin Zhang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Smooth Muscle Cells ◽  
Airway Smooth Muscle ◽  
Nuclear Factor Kappa B ◽  
Transforming Growth Factor ◽  
Muscle Cells ◽  
Transforming Growth Factor Β1 ◽  
Airway Smooth Muscle Cells ◽  
Nuclear Factor

We have explored the role of hyperin remodeling of airway smooth muscle cells during asthma. To this end, airway smooth muscle cells were isolated from tracheae and bronchi of mice, treated with transforming growth factor-β1 and increasing concentrations of hyperin followed by analysis of cell viability, proliferation, and migration. The levels of extracellular matrix formation were evaluated by analysis of fibronectin and type I collagen. Western blot analysis was used to assess the function of the downstream pathway of nuclear factor-kappa B. Transforming growth factor-β1 treatment led to a dose-dependent increase in type I collagen and fibronectin that was reversed by hyperin. Transforming growth factor-β1 promoted activation of nuclear factor-kappa B pathway with reduced IκBα and enhanced phospho (p)-p65 and p-IκBα. However, hyperin treatment upregulated IκBα and downregulated p-p65/p-IκBα to inactivate NF-κB pathway. In conclusion, hyperin ameliorates proliferation, migration, and extracellular matrix formation in airway smooth muscle cells by inhibiting transforming growth factor-β1-induced nuclear factor-kappa B activation suggesting potential prevention of airway remodeling during asthma.

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