scholarly journals Corrigendum to “Bionic Silk Fibroin Film Promotes Tenogenic Differentiation of Tendon Stem/Progenitor Cells by Activating Focal Adhesion Kinase”

2021 ◽  
Vol 2021 ◽  
pp. 1-3
Author(s):  
Kang Lu ◽  
Xiaodie Chen ◽  
Hong Tang ◽  
Mei Zhou ◽  
Gang He ◽  
...  
Keyword(s):  
Focal Adhesion Kinase ◽  
Progenitor Cells ◽  
Silk Fibroin ◽  
Focal Adhesion ◽  
Tenogenic Differentiation ◽  
Silk Fibroin Film

scholarly journals Bionic Silk Fibroin Film Promotes Tenogenic Differentiation of Tendon Stem/Progenitor Cells by Activating Focal Adhesion Kinase

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Kang Lu ◽  
Xiaodie Chen ◽  
Hong Tang ◽  
Mei Zhou ◽  
Gang He ◽  
...  
Keyword(s):  
Focal Adhesion Kinase ◽  
Progenitor Cells ◽  
Silk Fibroin ◽  
Focal Adhesion ◽  
Cell Morphology ◽  
Biological Activities ◽  
Biological Effects ◽  
Tendon Injuries ◽  
Regeneration Ability ◽  
Gene And Protein Expression

Background. Tendon injuries are common musculoskeletal disorders in clinic. Due to the limited regeneration ability of tendons, tissue engineering technology is often used as an effective approach to treat tendon injuries. Silk fibroin (SF) films have excellent biological activities and physical properties, which is suitable for tendon regeneration. The present study is aimed at preparing a SF film with a bionic microstructure and investigating its biological effects. Methods. A SF film with a smooth surface or bionic microstructure was prepared. After seeding tendon stem/progenitor cells (TSPCs) on the surface, the cell morphology, the expression level of tenogenic genes and proteins, and the focal adhesion kinase (FAK) activation were measured to evaluate the biological effect of SF films. Results. The TSPCs on SF films with a bionic microstructure exhibited a slender cell morphology, promoted the expression of tenogenic genes and proteins, such as SCX, TNC, TNMD, and COLIA1, and activated FAK. FAK inhibitors blocked the enhanced expression of tenogenic genes and proteins. Conclusion. SF films with a bionic microstructure may serve as a scaffold, provide biophysical cues to alter the cellular adherence arrangement and cell morphology, and enhance the tenogenic gene and protein expression in TSPCs. FAK activation plays a key role during this biological response process.

scholarly journals Mammary Epithelial-Specific Ablation of the Focal Adhesion Kinase Suppresses Mammary Tumorigenesis by Affecting Mammary Cancer Stem/Progenitor Cells

2009 ◽  
Vol 69 (2) ◽  
pp. 466-474 ◽  
Author(s):  
Ming Luo ◽  
Huaping Fan ◽  
Tamas Nagy ◽  
Huijun Wei ◽  
Chenran Wang ◽  
...  
Keyword(s):  
Focal Adhesion Kinase ◽  
Progenitor Cells ◽  
Focal Adhesion ◽  
Mammary Cancer ◽  
Mammary Tumorigenesis ◽  
Mammary Epithelial

scholarly journals Bionic Silk Fibroin Film Induces Morphological Changes and Differentiation of Tendon Stem/Progenitor Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Kang Lu ◽  
Xiaodie Chen ◽  
Hong Tang ◽  
Mei Zhou ◽  
Gang He ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Silk Fibroin ◽  
Morphological Changes ◽  
Quantitative Polymerase Chain Reaction ◽  
Tendon Repair ◽  
Differentiation Potential ◽  
Tendon Regeneration ◽  
Surface Marker Expression ◽  
Tenogenic Differentiation ◽  
Film Group

Purpose. Tendon injuries are common musculoskeletal system disorders, but the ability for tendon regeneration is limited. Silk fibroin (SF) film may be suitable for tendon regeneration due to its excellent biocompatibility and physical properties. This study is aimed at evaluating the application value of bionic SF film in tendon regeneration. Methods. Tendon stem/progenitor cells (TSPCs) were isolated from rat Achilles tendon and characterized based on their surface marker expression and multilineage differentiation potential. SF films with smooth or bionic microstructure surfaces (5, 10, 15, 20 μm) were prepared. The morphology and mechanical properties of natural tendons and SF films were characterized. TSPCs were used as the seed cells, and the cell viability and cell adhesion morphology were analyzed. The tendongenesis-related gene expression of TSPCs was also evaluated using quantitative polymerase chain reaction. Results. Compared to the native tendon, only the 10, 15, and 20 μm SF film groups had comparable maximum loading and ultimate stress, with the exception of the breaking elongation rate. The 10 μm SF film group had the highest percentage of oriented cells and the most significant changes in cell morphology. The most significant upregulations in the expression of COL1A1, TNC, TNMD, and SCX were also observed in the 10 μm SF film group. Conclusion. SF film with a bionic microstructure can serve as a tissue engineering scaffold and provide biophysical cues for the use of TSPCs to achieve proper cellular adherence arrangement and morphology as well as promote the tenogenic differentiation of TSPCs, making it a valuable customizable biomaterial for future applications in tendon repair.

Early signalling events of autophagy

2013 ◽  
Vol 55 ◽  
pp. 1-15 ◽  
Author(s):  
Laura E. Gallagher ◽  
Edmond Y.W. Chan
Keyword(s):  
Protein Kinase ◽  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Mammalian Cells ◽  
Mammalian Target Of Rapamycin ◽  
Interacting Protein ◽  
The Core ◽  
Autophagy Gene ◽  
Autophagy Induction ◽  
Cellular Pathways

Autophagy is a conserved cellular degradative process important for cellular homoeostasis and survival. An early committal step during the initiation of autophagy requires the actions of a protein kinase called ATG1 (autophagy gene 1). In mammalian cells, ATG1 is represented by ULK1 (uncoordinated-51-like kinase 1), which relies on its essential regulatory cofactors mATG13, FIP200 (focal adhesion kinase family-interacting protein 200 kDa) and ATG101. Much evidence indicates that mTORC1 [mechanistic (also known as mammalian) target of rapamycin complex 1] signals downstream to the ULK1 complex to negatively regulate autophagy. In this chapter, we discuss our understanding on how the mTORC1–ULK1 signalling axis drives the initial steps of autophagy induction. We conclude with a summary of our growing appreciation of the additional cellular pathways that interconnect with the core mTORC1–ULK1 signalling module.

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