Behavior of fetal intestinal organ culture explanted onto a collagen substratum

Development ◽  
1990 ◽  
Vol 110 (2) ◽  
pp. 353-370
Author(s):  
G.G. Altmann ◽  
A. Quaroni
Keyword(s):  
Smooth Muscle ◽  
Epithelial Cells ◽  
Organ Culture ◽  
Smooth Muscle Cells ◽  
Collagen Type ◽  
Collagen Type I ◽  
Type I ◽  
The Matrix ◽  
P Cells

A model of organ culture of 18 day old fetal rat intestine (Quaroni, 1985) was modified and characterized in the present work with the purpose of developing an in vitro model for the study of intestinal epithelial cell behaviour. Fragments of this intestine were kept in suspension culture for 7 days and then explanted onto collagen (type I) matrix. Within a day, the fragments became anchored to the substratum and a circular monolayer grew out to about 1 cm diameter. In the fragments, an outer layer of absorptive epithelial cells came to enclose a stroma, which was polarized into a loose (mesenchymal) and a dense portion. The dense portion contained a mixture of smooth muscle cells and primitive stem-type epithelial cells (‘p-cells’). After explantation, at the contact point with the matrix, the epithelium broke up and the mesenchyme grew into the matrix and anchored the fragment. The epithelial edges now became continuous with the developing monolayer. Radioautography with tritiated thymidine indicated a constant cell renewal in epithelium and monolayer apparently from foci of p-cells, a reserve population of which was seen to be sequestered among the smooth muscle cells. Activated stem cells could differentiate into three mature epithelial phenotypes, each differentiation pathway apparently being determined by the type of underlying stroma. Immunohistochemistry using gold- and fluorescein-labeled monoclonal antibodies indicated that adult differentiation-specific markers (e.g. brush border enzymes) were present in the fragment epithelium but not in the monolayer cells. On the other hand, the monolayer cells could be induced to express some of these markers by contact with mesenchymal cells or by co-culturing with fibroblastic cell lines. Matrigel substratum mixed with collagen (type I) supported the appearance in monolayer of strands positive for amino-peptidase and lactase. The model thus appears to be suitable for the in vitro study of epithelial renewal and differentiation, and it has already provided some results in this respect.

In Vitro Growth of Human Urinary Tract Smooth Muscle Cells on Laminin and Collagen Type I-Coated Membranes under Static and Dynamic Conditions

2005 ◽  
Vol 11 (1-2) ◽  
pp. 161-171 ◽  
Author(s):  
Ulrich Hubschmid ◽  
Phaik-Mooi Leong-Morgenthaler ◽  
Aurelia Basset-Dardare ◽  
Sylvie Ruault ◽  
Peter Frey
Keyword(s):  
Smooth Muscle ◽  
Urinary Tract ◽  
Smooth Muscle Cells ◽  
Collagen Type ◽  
Muscle Cells ◽  
Collagen Type I ◽  
Type I ◽  
In Vitro Growth ◽  
Coated Membranes

scholarly journals Collagen degradation and platelet-derived growth factor stimulate the migration of vascular smooth muscle cells

2000 ◽  
Vol 113 (11) ◽  
pp. 2055-2064
Author(s):  
E. Stringa ◽  
V. Knauper ◽  
G. Murphy ◽  
J. Gavrilovic
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Cell ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cell ◽  
Collagen Type ◽  
Muscle Cells ◽  
Collagen Type I ◽  
Type I

Cell migration is a key event in many biological processes and depends on signals from both extracellular matrix and soluble motogenic factors. During atherosclerotic plaque development, vascular smooth muscle cells migrate from the tunica media to the intima through a basement membrane and interstitial collagenous matrix and proliferate to form a neointima. Matrix metalloproteinases have previously been implicated in neointimal formation and in this study smooth muscle cell adhesion and migration on degraded collagen have been evaluated. Vascular smooth muscle cells adhered to native intact collagen type I and to its first degradation by-product, 3/4 fragment (generated by collagenase-3 cleavage), unwound at 35 degrees C to mimic physiological conditions. PDGF-BB pre-treatment induced a fourfold stimulation of smooth muscle cell motility on the collagen 3/4 fragment whereas no increase in smooth muscle cell motility on collagen type I was observed. Cell migration on collagen type I was mediated by alpha2 integrin, whereas PDGF-BB-stimulated migration on the 3/4 collagen fragment was dependent on alphavbeta3 integrin. alphavbeta3 integrin was organised in clusters concentrated at the leading and trailing edges of the cells and was only expressed when cells were exposed to the 3/4 collagen fragment. Tyrphostin A9, an inhibitor of PDGF receptor-beta tyrosine kinase activity, resulted in complete abolition of migration of PDGF-BB treated cells on collagen type I and 3/4 fragment. These results strongly support the hypothesis that the cellular migratory response to soluble motogens can be regulated by proteolytic modification of the extracellular matrix.

scholarly journals Protein kinase C δ regulates the release of collagen type I from vascular smooth muscle cells via regulation of Cdc42

2012 ◽  
Vol 23 (10) ◽  
pp. 1955-1963 ◽  
Author(s):  
Justin Lengfeld ◽  
Qiwei Wang ◽  
Andrew Zohlman ◽  
Susana Salvarezza ◽  
Stephanie Morgan ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Smooth Muscle Cells ◽  
Arterial Wall ◽  
Collagen Type ◽  
Collagen Type I ◽  
Collagen I ◽  
Type I ◽  
Kinase C

Collagen type I is the most abundant component of extracellular matrix in the arterial wall. Mice knocked out for the protein kinase C δ gene (PKCδ KO) show a marked reduction of collagen I in the arterial wall. The lack of PKCδ diminished the ability of arterial smooth muscle cells (SMCs) to secrete collagen I without significantly altering the intracellular collagen content. Moreover, the unsecreted collagen I molecules accumulate in large perinuclear puncta. These perinuclear structures colocalize with the trans-Golgi network (TGN) marker TGN38 and to a lesser degree with cis-Golgi marker (GM130) but not with early endosomal marker (EEA1). Associated with diminished collagen I secretion, PKCδ KO SMCs exhibit a significant reduction in levels of cell division cycle 42 (Cdc42) protein and mRNA. Restoring PKCδ expression partially rescues Cdc42 expression and collagen I secretion in PKCδ KO SMCs. Inhibition of Cdc42 expression or activity with small interfering RNA or secramine A in PKCδ WT SMCs eliminates collagen I secretion. Conversely, restoring Cdc42 expression in PKCδ KO SMCs enables collagen I secretion. Taken together, our data demonstrate that PKCδ mediates collagen I secretion from SMCs, likely through a Cdc42-dependent mechanism.

SIRT1 deacetylates RFX5 and antagonizes repression of collagen type I (COL1A2) transcription in smooth muscle cells

2012 ◽  
Vol 428 (2) ◽  
pp. 264-270 ◽  
Author(s):  
Jun Xia ◽  
Xiaoyan Wu ◽  
Yuyu Yang ◽  
Yuhao Zhao ◽  
Mingming Fang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Collagen Type ◽  
Muscle Cells ◽  
Collagen Type I ◽  
Type I

Protein Kinase C Delta Is Necessary for the secretion of Collagen Type I from Vascular Smooth Muscle Cells

2008 ◽  
Vol 22 (S2) ◽  
pp. 609-609
Author(s):  
Andrew Zohlman ◽  
Kentaro Kamiya ◽  
Kaori Kato ◽  
Susana B Salvarezza ◽  
Stephen B Doty ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Collagen Type ◽  
Collagen Type I ◽  
Type I ◽  
Kinase C

Imbalance in the Synthesis of Collagen Type I and Collagen Type III in Smooth Muscle Cells Derived from Human Varicose Veins

2001 ◽  
Vol 38 (6) ◽  
pp. 560-568 ◽  
Author(s):  
Patricia Sansilvestri-Morel ◽  
Alain Rupin ◽  
Cécile Badier-Commander ◽  
Patrick Kern ◽  
Jean-Noël Fabiani ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Collagen Type ◽  
Varicose Veins ◽  
Muscle Cells ◽  
Collagen Type I ◽  
Type I ◽  
Collagen Type Iii ◽  
Type Iii

scholarly journals An In situ Collagen-HA Hydrogel System Promotes Survival and Preserves the Proangiogenic Secretion of hiPSC-derived Vascular Smooth Muscle Cells

2020 ◽  
Author(s):  
Biraja C. Dash ◽  
Kaiti Duan ◽  
Hao Xing ◽  
Themis R. Kyriakides ◽  
Henry C. Hsia
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Collagen Type ◽  
Muscle Cells ◽  
Collagen Type I ◽  
Type I ◽  
Hydrogel System

AbstractHuman induced pluripotent stem cell-derived vascular smooth muscle cells (hiPSC-VSMCs) with proangiogenic properties have huge therapeutic potential. While hiPSC-VSMCs have already been utilized for wound healing using a biomimetic collagen scaffold, an in situ forming hydrogel mimicking the native environment of skin offers the promise of hiPSC-VSMC mediated repair and regeneration. Herein, the impact of a collagen type-I-hyaluronic acid (HA) in situ hydrogel cross-linked using a PEG-based cross-linker on hiPSC-VSMCs viability and proangiogenic paracrine secretion was investigated. Our study demonstrated increases in cell viability, maintenance of phenotype and proangiogenic growth factor secretion, and proangiogenic activity in response to the conditioned medium. The optimally cross-linked and functionalized collagen type-I/HA hydrogel system developed in this study shows promise as an in situ hiPSC-VSMC carrier system for wound regeneration.

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