The Strain Response of Lung Myofibroblasts Cultured on Electrospun Polycaprolactone Nanofibers

2013 ◽  
Author(s):  
Timothy J. Fee ◽  
Yong Zhou ◽  
Lauren E. Marshall ◽  
Joel L. Berry
Keyword(s):  
Smooth Muscle ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Smooth Muscle Actin ◽  
Strain Response ◽  
Muscle Actin ◽  
Alpha Smooth Muscle Actin

Idiopathic Pulmonary Fibrosis is a devastating condition characterized by excessive localized production of collagen in the lungs. Over 131,000 people are living with IPF in America (1, 2). There is currently no known treatment or cure for the disease. It has recently been shown that IPF myofibroblasts are sensitive to the stiffness of their substrate. Specifically, alpha Smooth Muscle Actin (alpha-SMA), a known indicator of IPF activity, was differentially produced on soft vs. stiff substrates (3). This suggests a mechanotransduction pathway within the IPF myofibroblasts.

scholarly journals Akt1 regulates pulmonary fibrosis via modulating IL-13 expression in macrophages

2019 ◽  
Vol 25 (7) ◽  
pp. 451-461 ◽  
Author(s):  
Yunjuan Nie ◽  
Yudong Hu ◽  
Kaikai Yu ◽  
Dan Zhang ◽  
Yinze Shi ◽  
...  
Keyword(s):  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Smooth Muscle Actin ◽  
In Vivo Studies ◽  
Muscle Actin ◽  
Alpha Smooth Muscle Actin ◽  
Fibrosis Progression ◽  
Matrix Components ◽  
Deficient Mice

Idiopathic pulmonary fibrosis is a progressive interstitial pneumonia characterised by fibroblast accumulation, collagen deposition and extracellular matrix (ECM) remodelling. It was reported that Akt1 mediated idiopathic pulmonary fibrosis progression through regulating the apoptosis of alveolar macrophage, while its effect on macrophage-produced cytokines remains largely unknown. In the present study, we first examined the phosphorylation of Akt1 in lung sections from idiopathic pulmonary fibrosis patients by immunohistochemistry before applying a bleomycin-induced idiopathic pulmonary fibrosis model using Akt1−/− mice and Akt1+/+ littermates. The results showed that Akt1 was remarkably up-regulated in idiopathic pulmonary fibrosis patients, while in vivo studies revealed that Akt1-deficient mice had well-preserved alveolar structure and fewer collagens, secreted fewer matrix components, including alpha smooth-muscle actin and fibronectin and survived significantly longer than Akt1+/+ littermates. Additionally, the pro-fibrogenic cytokine IL-13 was down-regulated at least twofold in Akt1−/−mice compared to the Akt1+/+group on d 3 and 7 after bleomycin treatment. Furthermore, it was found that Akt1–/– macrophages displayed down-regulation of IL-13 compared to Akt1+/+ macrophages in which Akt1 was phosphorylated in response to IL-33 stimulation. These findings indicate that Akt1 modulates pulmonary fibrosis through inducing IL-13 production by macrophages, suggesting that targeting Akt1 may simultaneously block the fibrogenic processes of idiopathic pulmonary fibrosis.

scholarly journals Increased fibroblast telomerase expression precedes myofibroblast α-smooth muscle actin expression in idiopathic pulmonary fibrosis

Clinics ◽  
2012 ◽  
Vol 67 (9) ◽  
pp. 1039-1046 ◽  
Author(s):  
DR Waisberg ◽  
ER Parra ◽  
JV Barbas-Filho ◽  
S Fernezlian ◽  
VL Capelozzi
Keyword(s):  
Smooth Muscle ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Smooth Muscle Actin ◽  
Muscle Actin ◽  
Actin Expression

Expression of alpha-smooth muscle actin, TGF-β1 and TGF-β type II receptor during connective tissue contraction

1997 ◽  
Vol 33 (8) ◽  
pp. 622-627 ◽  
Author(s):  
M. Reza Ghassemifar ◽  
Roy W. Tarnuzzer ◽  
Nasser Chegini ◽  
Erkki Tarpila ◽  
Gregory S. Schultz ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Connective Tissue ◽  
Smooth Muscle Actin ◽  
Type Ii ◽  
Muscle Actin ◽  
Alpha Smooth Muscle Actin ◽  
Tissue Contraction ◽  
Tgf Β1
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