scholarly journals Immunocytochemical localization of fibronectin in limb tissues of the adult newt, Notophthalmus viridescens.

1981 ◽  
Vol 29 (8) ◽  
pp. 937-945 ◽  
Author(s):  
L A Repesh ◽  
L T Furcht ◽  
D Smith

This study describes the immunocytochemical localization of fibronectin, a defined connective tissue and plasma glycoprotein, and its relationship to collagen and reticulin in adult newt limb tissues. We have also isolated the plasma form of fibronectin in a related species, the adult mudpuppy. The insoluble form of fibronectin was detected with immunoperoxidase stain in basement membranes and loose connective tissue. The endoneurium and perineurium of nerve bundles and the connective tissue elements of striated muscle stained heavily for fibronectin. The dermis and blood vessel walls also reached positively with the immunoperoxidase stain. A similar distribution was observed for reticulin with conventional histologic techniques with the exception of the dermis where only trace amounts of the protein were observed. Fibronectin and collagen were codistributed in the tissues studies. Fibronectin appeared to be intercalated among larger collagenous fibers. Collagen and fibronectin form an extracellular connective tissue scaffold that abuts against many types of adherent cells in different tissues. This supports the possible role of fibronectin in cell-matrix interactions and normal cell and tissue organization.

1978 ◽  
Vol 147 (4) ◽  
pp. 1054-1064 ◽  
Author(s):  
S Stenman ◽  
A Vaheri

Fibronectin is a major surface-associated glycoprotein of cultured fibroblasts and it is also present in human plasma. Antiserum specific for human fibronectin was used to study the distribution of fibronectin in normal adult human tissues. The protein was detected (a) characteristically in various basement membranes including capillary walls: (b) around individual smooth muscle cells and in the sarcolemma of striated muscle fibers; and (c) in the stroma of lymphatic tissue and as thin fibers in loose connective tissue. The distribution of fibronectin was distinct from that of collagen and elastic fibers, but was very similar to reticulin, as demonstrated by conventional histological staining. The results indicate that fibronectin is a major component of connective tissue matrix. The distribution also indicates that most types of adherent cells abut fibronectin-containing structures. This supports the possible role of fibronectin in cell-cell and cell-matrix interactions in tissues.


1993 ◽  
Vol 11 (S1) ◽  
pp. S112-S114 ◽  
Author(s):  
M. Baccarani Contri ◽  
R. Tiozzo ◽  
M. A. Croce ◽  
T. Andreoli ◽  
A. De Paepe

1999 ◽  
Vol 112 (22) ◽  
pp. 3855-3867 ◽  
Author(s):  
U. Muller ◽  
A.W. Brandli

Functional analyses of cell-matrix interactions during kidney organogenesis have provided compelling evidence that extracellular-matrix glycoproteins and their receptors play instructive roles during kidney development. Two concepts are worthy of emphasis. First, matrix molecules appear to regulate signal transduction pathways, either by activating cell-surface receptors such as integrins directly or by modulating the activity of signaling molecules such as WNTs. Second, basement membranes are highly organized structures and have distinct molecular compositions, which are optimized for their diverse functions. The importance of these findings is highlighted by the fact that mutations affecting basement-membrane components lead to inherited forms of kidney disease.


2021 ◽  
Author(s):  
Iain Muntz ◽  
Michele Fenu ◽  
Gerjo J V M van Osch ◽  
Gijsje Koenderink

Abstract Living tissue is able to withstand large stresses in everyday life, yet it also actively adapts to dynamic loads. This remarkable mechanical behaviour emerges from the interplay between living cells and their non-living extracellular environment. Here we review recent insights into the biophysical mechanisms involved in the reciprocal interplay between cells and the extracellular matrix and how this interplay determines tissue mechanics, with a focus on connective tissues. We first describe the roles of the main macromolecular components of the extracellular matrix in regards to tissue mechanics. We then proceed to highlight the main routes via which cells sense and respond to their biochemical and mechanical extracellular environment. Next we introduce the three main routes via which cells can modify their extracellular environment: exertion of contractile forces, secretion and deposition of matrix components, and matrix degradation. Finally we discuss how recent insights in the mechanobiology of cell-matrix interactions are furthering our understanding of the pathophysiology of connective tissue diseases and cancer, and facilitating the design of novel strategies for tissue engineering.


1994 ◽  
Vol 124 (4) ◽  
pp. 619-626 ◽  
Author(s):  
SM Frisch ◽  
H Francis

Cell-matrix interactions have major effects upon phenotypic features such as gene regulation, cytoskeletal structure, differentiation, and aspects of cell growth control. Programmed cell death (apoptosis) is crucial for maintaining appropriate cell number and tissue organization. It was therefore of interest to determine whether cell-matrix interactions affect apoptosis. The present report demonstrates that apoptosis was induced by disruption of the interactions between normal epithelial cells and extracellular matrix. We have termed this phenomenon "anoikis." Overexpression of bcl-2 protected cells against anoikis. Cellular sensitivity to anoikis was apparently regulated: (a) anoikis did not occur in normal fibroblasts; (b) it was abrogated in epithelial cells by transformation with v-Ha-ras, v-src, or treatment with phorbol ester; (c) sensitivity to anoikis was conferred upon HT1080 cells or v-Ha-ras-transformed MDCK cells by reverse-transformation with adenovirus E1a; (d) anoikis in MDCK cells was alleviated by the motility factor, scatter factor. The results suggest that the circumvention of anoikis accompanies the acquisition of anchorage independence or cell motility.


Author(s):  
Marc Lenburg ◽  
Rulang Jiang ◽  
Lengya Cheng ◽  
Laura Grabel

We are interested in defining the cell-cell and cell-matrix interactions that help direct the differentiation of extraembryonic endoderm in the peri-implantation mouse embryo. At the blastocyst stage the mouse embryo consists of an outer layer of trophectoderm surrounding the fluid-filled blastocoel cavity and an eccentrically located inner cell mass. On the free surface of the inner cell mass, facing the blastocoel cavity, a layer of primitive endoderm forms. Primitive endoderm then generates two distinct cell types; parietal endoderm (PE) which migrates along the inner surface of the trophectoderm and secretes large amounts of basement membrane components as well as tissue-type plasminogen activator (tPA), and visceral endoderm (VE), a columnar epithelial layer characterized by tight junctions, microvilli, and the synthesis and secretion of α-fetoprotein. As these events occur after implantation, we have turned to the F9 teratocarcinoma system as an in vitro model for examining the differentiation of these cell types. When F9 cells are treated in monolayer with retinoic acid plus cyclic-AMP, they differentiate into PE. In contrast, when F9 cells are treated in suspension with retinoic acid, they form embryoid bodies (EBs) which consist of an outer layer of VE and an inner core of undifferentiated stem cells. In addition, we have established that when VE containing embryoid bodies are plated on a fibronectin coated substrate, PE migrates onto the matrix and this interaction is inhibited by RGDS as well as antibodies directed against the β1 integrin subunit. This transition is accompanied by a significant increase in the level of tPA in the PE cells. Thus, the outgrowth system provides a spatially appropriate model for studying the differentiation and migration of PE from a VE precursor.


Sign in / Sign up

Export Citation Format

Share Document