AMOTL2 restrains transforming growth factor‐β1‐induced proliferation and extracellular matrix deposition of airway smooth muscle cells via the down‐regulation of YAP1 activation

2021 ◽  
Author(s):  
Ping Fang ◽  
Wen‐jing Deng ◽  
Na Fan ◽  
Jie Shi ◽  
Hong‐yang Shi ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Smooth Muscle Cells ◽  
Airway Smooth Muscle ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Airway Smooth Muscle Cells ◽  
Matrix Deposition ◽  
Extracellular Matrix Deposition

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.

Carvacrol Ameliorates Transforming Growth Factor-β1-Induced Extracellular Matrix Deposition and Reduces Epithelial-Mesenchymal Transition by Regulating The Phosphatidylinositol 3-Kinase/Protein Kinase B Pathway In Hk-2 Cells

2021 ◽  
Vol 19 (4) ◽  
pp. 501-507
Author(s):  
Yunhe Gu ◽  
Peiyao Guo ◽  
Guangbiao Xu
Keyword(s):  
Extracellular Matrix ◽  
Growth Factor ◽  
Renal Fibrosis ◽  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Transforming Growth Factor Β1 ◽  
Mesenchymal Transition ◽  
Matrix Deposition ◽  
Extracellular Matrix Deposition ◽  
Dose Dependent

Transforming growth factor-β1 promotes excessive extracellular matrix deposition and epithelial-mesenchymal transition of tubular epithelial cells, thus stimulating the progression of renal fibrosis. Carvacrol has been shown to alleviate cardiac and liver fibrosis and attenuate renal injury. However, the role of carvacrol on renal fibrosis has not been examined. First, measurements using Cell Counting Kit-8 showed that carvacrol reduced cell viability of tubular epithelial cell line HK-2 in a dose-dependent fashion. Second, transforming growth factor-β1 induced excessive extracellular matrix deposition in HK-2 cells with enhanced collagen I, collagen IV, and fibronectin expression. However, carvacrol decreased the expression of collagen I, collagen IV in a dose-dependent manner and fibronectin to attenuate the extracellular matrix deposition in HK-2. Third, carvacrol attenuated TGF-β1-induced decrease of E-cadherin and increase of snail, vimentin, and alpha-smooth muscle actin in HK-2 cells. Transforming growth factor-β1-induced increase in PI3K and AKT phosphorylation in HK-2 were also reversed by carvacrol. Collectively, carvacrol ameliorates renal fibrosis through inhibition of transforming growth factor-β1-induced extracellular matrix deposition and epithelial-mesenchymal transition of HK-2 cells, providing potential therapy for the treatment of renal fibrosis.

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