Biased three-dimensional cell migration and collagen matrix modification

2011 ◽  
Vol 231 (2) ◽  
pp. 105-119 ◽  
Author(s):  
A. Groh ◽  
M. Wagner
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yingyue Lou ◽  
Yuhan Jiang ◽  
Zhen Liang ◽  
Bingzhang Liu ◽  
Tian Li ◽  
...  

AbstractMigration is one of the five major behaviors of cells. Although RhoC—a classic member of the Rho gene family—was first identified in 1985, functional RhoC data have only been widely reported in recent years. Cell migration involves highly complex signaling mechanisms, in which RhoC plays an essential role. Cell migration regulated by RhoC—of which the most well-known function is its role in cancer metastasis—has been widely reported in breast, gastric, colon, bladder, prostate, lung, pancreatic, liver, and other cancers. Our review describes the role of RhoC in various types of cell migration. The classic two-dimensional cell migration cycle constitutes cell polarization, adhesion regulation, cell contraction and tail retraction, most of which are modulated by RhoC. In the three-dimensional cell migration model, amoeboid migration is the most classic and well-studied model. Here, RhoC modulates the formation of membrane vesicles by regulating myosin II, thereby affecting the rate and persistence of amoeba-like migration. To the best of our knowledge, this review is the first to describe the role of RhoC in all cell migration processes. We believe that understanding the detail of RhoC-regulated migration processes will help us better comprehend the mechanism of cancer metastasis. This will contribute to the study of anti-metastatic treatment approaches, aiding in the identification of new intervention targets for therapeutic or genetic transformational purposes.


2014 ◽  
Vol 111 (11) ◽  
pp. 3949-3954 ◽  
Author(s):  
P.-H. Wu ◽  
A. Giri ◽  
S. X. Sun ◽  
D. Wirtz

2020 ◽  
Vol 318 (2) ◽  
pp. L276-L286 ◽  
Author(s):  
Marisa Tisler ◽  
Samuel Alkmin ◽  
Hsin-Yu Chang ◽  
Jon Leet ◽  
Ksenija Bernau ◽  
...  

Idiopathic pulmonary fibrosis (IPF) is characterized by a profound remodeling of the collagen in the extracellular matrix (ECM), where the fibers become both denser and more highly aligned. However, it is unknown how this reconfiguration of the collagen matrix affects disease progression. Here, we investigate the role of specific alterations in collagen fiber organization on cell migration dynamics by using biomimetic image-based collagen scaffolds representing normal and fibrotic lung, where the designs are derived directly from high-resolution second harmonic generation microscopy images. The scaffolds are fabricated by multiphoton-excited (MPE) polymerization, where the process is akin to three-dimensional printing, except that it is performed at much greater resolution (∼0.5 microns) and with collagen and collagen analogs. These scaffolds were seeded with early passaged primary human normal and IPF fibroblasts to enable the decoupling of the effect of cell-intrinsic characteristics (normal vs. IPF) versus ECM structure (normal vs. IPF) on migration dynamics. We found that the highly aligned IPF collagen structure promoted enhanced cell elongation and F-actin alignment along with increased cell migration speed and straightness relative to the normal tissues. Collectively, the data are consistent with an enhanced contact guidance mechanism on the aligned IPF matrix. Although cell intrinsic effects were observed, the aligned collagen matrix morphology had a larger effect on these metrics. Importantly, these biomimetic models of the lung cannot be synthesized by conventional fabrication methods. We suggest that the MPE image-based fabrication method will enable additional hypothesis-based testing studies of cell-matrix interactions in the context of tissue fibrosis.


2008 ◽  
Vol 95 (11) ◽  
pp. 5374-5384 ◽  
Author(s):  
Paolo P. Provenzano ◽  
David R. Inman ◽  
Kevin W. Eliceiri ◽  
Steven M. Trier ◽  
Patricia J. Keely

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