scholarly journals Membrane-type 1 matrix metalloproteinase regulates fibronectin assembly to promote cell motility

FEBS Letters ◽  
2011 ◽  
Vol 585 (21) ◽  
pp. 3378-3384 ◽  
Author(s):  
Takahisa Takino ◽  
Ryota Nagao ◽  
Ri-ichiroh Manabe ◽  
Takahiro Domoto ◽  
Kiyotoshi Sekiguchi ◽  
...  
2014 ◽  
Vol 450 (2) ◽  
pp. 1016-1020 ◽  
Author(s):  
Takahisa Takino ◽  
Taisuke Yoshimoto ◽  
Mitsutoshi Nakada ◽  
Zichen Li ◽  
Takahiro Domoto ◽  
...  

2001 ◽  
Vol 153 (5) ◽  
pp. 893-904 ◽  
Author(s):  
Masahiro Kajita ◽  
Yoshifumi Itoh ◽  
Tadashige Chiba ◽  
Hidetoshi Mori ◽  
Akiko Okada ◽  
...  

Migratory cells including invasive tumor cells frequently express CD44, a major receptor for hyaluronan and membrane-type 1 matrix metalloproteinase (MT1-MMP) that degrades extracellular matrix at the pericellular region. In this study, we demonstrate that MT1-MMP acts as a processing enzyme for CD44H, releasing it into the medium as a soluble 70-kD fragment. Furthermore, this processing event stimulates cell motility; however, expression of either CD44H or MT1-MMP alone did not stimulate cell motility. Coexpression of MT1-MMP and mutant CD44H lacking the MT1-MMP–processing site did not result in shedding and did not promote cell migration, suggesting that the processing of CD44H by MT1-MMP is critical in the migratory stimulation. Moreover, expression of the mutant CD44H inhibited the cell migration promoted by CD44H and MT1-MMP in a dominant-negative manner. The pancreatic tumor cell line, MIA PaCa-2, was found to shed the 70-kD CD44H fragment in a MT1-MMP–dependent manner. Expression of the mutant CD44H in the cells as well as MMP inhibitor treatment effectively inhibited the migration, suggesting that MIA PaCa-2 cells indeed use the CD44H and MT1-MMP as migratory devices. These findings revealed a novel interaction of the two molecules that have each been implicated in tumor cell migration and invasion.


2005 ◽  
Vol 280 (28) ◽  
pp. 26160-26168 ◽  
Author(s):  
Pamela Osenkowski ◽  
Samy O. Meroueh ◽  
Dumitru Pavel ◽  
Shahriar Mobashery ◽  
Rafael Fridman

2002 ◽  
Vol 298 (5) ◽  
pp. 646-650 ◽  
Author(s):  
Toshiya Nakamura ◽  
Takashi Ishikawa ◽  
Naoki Nanashima ◽  
Tomisato Miura ◽  
Hiroyuki Nozaka ◽  
...  

2019 ◽  
Vol 316 (1) ◽  
pp. C92-C103 ◽  
Author(s):  
Hojin Kang ◽  
Zhigang Hong ◽  
Ming Zhong ◽  
Jennifer Klomp ◽  
Kayla J. Bayless ◽  
...  

Angiogenesis is initiated in response to a variety of external cues, including mechanical and biochemical stimuli; however, the underlying signaling mechanisms remain unclear. Here, we investigated the proangiogenic role of the endothelial mechanosensor Piezo1. Genetic deletion and pharmacological inhibition of Piezo1 reduced endothelial sprouting and lumen formation induced by wall shear stress and proangiogenic mediator sphingosine 1-phosphate, whereas Piezo1 activation by selective Piezo1 activator Yoda1 enhanced sprouting angiogenesis. Similarly to wall shear stress, sphingosine 1-phosphate functioned by activating the Ca2+ gating function of Piezo1, which in turn signaled the activation of the matrix metalloproteinase-2 and membrane type 1 matrix metalloproteinase during sprouting angiogenesis. Studies in mice in which Piezo1 was conditionally deleted in endothelial cells demonstrated the requisite role of sphingosine 1-phosphate-dependent activation of Piezo1 in mediating angiogenesis in vivo. These results taken together suggest that both mechanical and biochemical stimuli trigger Piezo1-mediated Ca2+ influx and thereby activate matrix metalloproteinase-2 and membrane type 1 matrix metalloproteinase and synergistically facilitate sprouting angiogenesis.


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