Targeted inhibition of YAP/TAZ alters the biological behaviors of keloid fibroblasts

2021 ◽  
Author(s):  
Na Gao ◽  
Lulu Lu ◽  
Xiaolei Ma ◽  
Zhengyi Liu ◽  
Shuxia Yang ◽  
...  

2008 ◽  
Vol 39 (5) ◽  
pp. 24
Author(s):  
BRUCE JANCIN
Keyword(s):  




Author(s):  
David Wai Meng Tai ◽  
Thi Bich Uyen Le ◽  
Aldo Prawira ◽  
Rebecca Zhi Wen Ho ◽  
Hung Huynh


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Cheng-Cheng Deng ◽  
Yong-Fei Hu ◽  
Ding-Heng Zhu ◽  
Qing Cheng ◽  
Jing-Jing Gu ◽  
...  

AbstractFibrotic skin disease represents a major global healthcare burden, characterized by fibroblast hyperproliferation and excessive accumulation of extracellular matrix. Fibroblasts are found to be heterogeneous in multiple fibrotic diseases, but fibroblast heterogeneity in fibrotic skin diseases is not well characterized. In this study, we explore fibroblast heterogeneity in keloid, a paradigm of fibrotic skin diseases, by using single-cell RNA-seq. Our results indicate that keloid fibroblasts can be divided into 4 subpopulations: secretory-papillary, secretory-reticular, mesenchymal and pro-inflammatory. Interestingly, the percentage of mesenchymal fibroblast subpopulation is significantly increased in keloid compared to normal scar. Functional studies indicate that mesenchymal fibroblasts are crucial for collagen overexpression in keloid. Increased mesenchymal fibroblast subpopulation is also found in another fibrotic skin disease, scleroderma, suggesting this is a broad mechanism for skin fibrosis. These findings will help us better understand skin fibrotic pathogenesis, and provide potential targets for fibrotic disease therapies.



Biology Open ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. bio053298
Author(s):  
Jingjing Wu ◽  
Youqile Wu ◽  
Xuemei Lian

ABSTRACTThis study investigated the pathophysiological role of GRP78 in the survival of lung cancer cells. Lung cancer patient data from public databases were used to analyze the expression of GRP78 and its influence on prognoses. In vivo, GRP78 protein expression was analyzed in an established urethane-induced lung tumor mouse model. In vitro, the effects of targeted inhibition of GRP78 by HA15 in lung cancer cells were assessed, with cell viability analyzed using a CCK-8 assay, cell proliferation using an EdU assay, apoptosis and cell cycle using flow cytometry, subcellular structure using electron microscopy, and relative mRNA and protein expression using RT-PCR, western blotting or immunofluorescence assays. The results showed that GRP78 was highly expressed in the lung tissue of lung cancer mice model or patients, and was associated with a poor prognosis. After inhibition of GRP78 in lung cancer cells by HA15, cell viability was decreased in a dose- and time-dependent manner, proliferation was suppressed and apoptosis promoted. Unfolded protein response signaling pathway proteins were activated, and the autophagy-related proteins and mRNAs were upregulated. Therefore, targeted inhibition of GRP78 by HA15 promotes apoptosis of lung cancer cells accompanied by ER stress and autophagy.



1988 ◽  
Vol 10 (6) ◽  
pp. 505-508 ◽  
Author(s):  
Lois Y. Matsuoka ◽  
Jouni Uitto ◽  
Jacobo Wortsman ◽  
R. Patrick Abergel ◽  
John Dietrich


2012 ◽  
Vol 129 (6) ◽  
pp. 1259-1271 ◽  
Author(s):  
Dorothy M. Supp ◽  
Jennifer M. Hahn ◽  
Kathryn Glaser ◽  
Kevin L. McFarland ◽  
Steven T. Boyce


2016 ◽  
Vol 29 (6) ◽  
pp. 643-655 ◽  
Author(s):  
Bih‐Rong Wei ◽  
Helen T. Michael ◽  
Charles H.C. Halsey ◽  
Cody J. Peer ◽  
Amit Adhikari ◽  
...  


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