Neoplastic modulation of extracellular matrix: Stimulation of chondroitin sulfate proteoglycan and hyaluronic acid synthesis in co-cultures of human colon carcinoma and smooth muscle cells

1989 ◽  
Vol 39 (4) ◽  
pp. 355-378 ◽  
Author(s):  
Renato V. Iozzo ◽  
Phyllis M. Sampson ◽  
Gail K. Schmitt
Keyword(s):  
Extracellular Matrix ◽  
Smooth Muscle ◽  
Hyaluronic Acid ◽  
Smooth Muscle Cells ◽  
Human Colon ◽  
Acid Synthesis ◽  
Chondroitin Sulfate Proteoglycan ◽  
Sulfate Proteoglycan ◽  
Human Colon Carcinoma ◽  
Stimulation Of

scholarly journals Activation of the GTPase ARF6 regulates Invasion of Human Vascular Smooth Muscle Cells by Stimulating MMP14 Activity

2021 ◽  
Author(s):  
Emilie Fiola-Masson ◽  
Julie Artigalas ◽  
Shirley Campbell ◽  
Audrey Claing
Keyword(s):  
Extracellular Matrix ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Molecular Mechanisms ◽  
Muscle Cells ◽  
Human Model ◽  
Ang Ii ◽  
Stimulation Of

Abstract Hormones and growth factors stimulate vascular smooth muscle cells (VSMC) invasive capacities during the progression of atherosclerosis. The GTPase ARF6 is an important regulator of migration and proliferation of various cell types, but whether this small G protein can be activated by a variety of stimuli to promote invasion of VSMC remains unknown. Here, we aimed to define whether Platelet-derived growth factor (PDGF), a mitogenic stimulant of vascular tissues, and Angiotensin II (Ang II), a potent vasoactive peptide, can result in the activation of ARF6 in a human model of aortic SMC (HASMC). We report that these two stimuli can promote loading of GTP on this ARF isoform. Knockdown of ARF6 reduced the ability of both PDGF and Ang II to promote invasion suggesting that this GTPase regulates key molecular mechanisms mediating degradation of the extracellular matrix and migration. We report that PDGF-BB-mediated stimulation of ARF6 results in the activation of the MAPK/ERK1/2, PI3K/AKT and PAK pathways essential for invasion of HASMC. However, Ang II-mediated stimulation of ARF6 only promotes activation of the MAPK/ERK1/2 and PAK pathways. These ARF6-mediated signaling cascades leads to activation of MMP14, which in turns controls the activity of MMP2 to degrade the extracellular matrix. Altogether, our findings demonstrate that the GTPase ARF6 acts as a molecular switch to regulate specific signaling pathways that coordinate the process of invasion.

scholarly journals Arterial chondroitin sulfate proteoglycan: localization with a monoclonal antibody.

1988 ◽  
Vol 36 (10) ◽  
pp. 1211-1221 ◽  
Author(s):  
M W Lark ◽  
T K Yeo ◽  
H Mar ◽  
S Lara ◽  
I Hellström ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Extracellular Matrix ◽  
Smooth Muscle ◽  
Chondroitin Sulfate ◽  
Chondroitin Sulfate Proteoglycan ◽  
Elastic Fibers ◽  
Immunogold Electron Microscopy ◽  
Sulfate Proteoglycan ◽  
Arterial Smooth Muscle ◽  
Matrix Components

We generated a monoclonal antibody (Mab) against a large chondroitin sulfate proteoglycan (CSPG) isolated from bovine aorta. This Mab (941) immunoprecipitates a CSPG synthesized by cultured monkey arterial smooth muscle cells. The immunoprecipitated CSPG is totally susceptible to chondroitinase ABC digestion and possesses a core glycoprotein of Mr approximately 400-500 KD. By use of immunofluorescence light microscopy and immunogold electron microscopy, the PG recognized by this Mab was shown to be deposited in the extracellular matrix of monkey arterial smooth muscle cell cultures in clusters which were not part of other fibrous matrix components and not associated with the cell's plasma membrane. With similar immunolocalization techniques, the CSPG antigen was found enriched in the intima and present in the medial portions of normal blood vessels, as well as in the interstitial matrix of thickened intimal lesions of atherosclerotic vessels. Immunoelectron microscopy revealed that this CSPG was confined principally to the space within the extracellular matrix not occupied by other matrix components, such as collagen and elastic fibers. These results indicate that this particular proteoglycan has a specific but restricted distribution in the extracellular matrix of arterial tissue.

Neutrophil migration through in vitro interstitial matrix

1992 ◽  
Vol 50 (1) ◽  
pp. 894-895
Author(s):  
J. Roemer ◽  
S.R. Simon
Keyword(s):  
Extracellular Matrix ◽  
Smooth Muscle ◽  
Cell Migration ◽  
Smooth Muscle Cells ◽  
Inflammatory Cell ◽  
Neutrophil Migration ◽  
Culture Conditions ◽  
Aortic Smooth Muscle ◽  
Specific Culture

We are developing an in vitro interstitial extracellular matrix (ECM) system for study of inflammatory cell migration. Falcon brand Cyclopore membrane inserts of various pore sizes are used as a support substrate for production of ECM by R22 rat aortic smooth muscle cells. Under specific culture conditions these cells produce a highly insoluble matrix consisting of typical interstitial ECM components, i.e.: types I and III collagen, elastin, proteoglycans and fibronectin.

Sign in / Sign up

Export Citation Format

Share Document