PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Extracellular matrix”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources

A novel hydra matrix metalloproteinase (HMMP) functions in extracellular matrix degradation, morphogenesis and the maintenance of differentiated cells in the foot process.

As a member of Cnidaria, the body wall of hydra is structurally reduced to an epithelial bilayer with an intervening extracellular matrix (ECM). Biochemical and cloning studies have shown that the molecular composition of hydra ECM is similar to that seen in vertebrates and functional studies have demonstrated that cell-ECM interactions are important to developmental processes in hydra. Because vertebrate matrix metalloproteinases (MMPs) have been shown to have an important role in cell-ECM interactions, the current study was designed to determine whether hydra has homologues of these proteinases and, if so, what function these enzymes have in morphogenesis and cell differentiation in this simple metazoan. Utilizing a PCR approach, a single hydra matrix metalloproteinase, named HMMP was identified and cloned. The structure of HMMP was similar to that of vertebrate MMPs with an overall identity of about 35%. Detailed structural analysis indicated some unique features in (1) the cysteine-switch region of the prodomain, (2) the hinge region preceding the hemopexin domain, and (3) the hemopexin domain. Using a bacterial system, HMMP protein was expressed and folded to obtain an active enzyme. Substrate analysis studies indicated that recombinant HMMP could digest a number of hydra ECM components such as hydra laminin. Using a fluorogenic MMP substrate assay, it was determined that HMMP was inhibited by peptidyl hydroxamate MMP inhibitors, GM6001 and matlistatin, and by human recombinant TIMP-1. Whole-mount in situ studies indicated that HMMP mRNA was expressed in the endoderm along the entire longitudinal axis of hydra, but at relatively high levels at regions where cell-transdifferentiation occurred (apical and basal poles). Functional studies using GM6001 and TIMP-1 indicated that these MMP inhibitors could reversibly block foot regeneration. Blockage of foot regeneration was also observed using antisense thio-oligo nucleotides to HMMP introduced into the endoderm of the basal pole using a localized electroporation technique. Studies with adult intact hydra found that GM6001 could also cause the reversible de-differentiation or inhibition of transdifferentiation of basal disk cells of the foot process. Basal disk cells are adjacent to those endoderm cells of the foot process that express high levels of HMMP mRNA. In summary, these studies indicate that hydra has at least one MMP that is functionally tied to morphogenesis and cell transdifferentiation in this simple metazoan.

Amino Acid Sequence↗

Aortic endothelial cell proteoheparan sulfate. II. Modulation by extracellular matrix.

The effects of extracellular matrix components on proteoheparan sulfate biosynthesis was studied for bovine aortic endothelial cells in tissue culture. When the cells were maintained on a variety of different purified components of the extracellular matrix, the cells expressed the same three species of proteoheparan sulfates as the cells cultured on tissue culture plastic (HS I, HS II, and HS III). However, the amounts of the three species recovered from the tissue culture medium were found to be dependent on the substrate on which the cells are grown as well as on other factors. In comparison with plastic, much less HS I was found in the medium of cells maintained on substrates containing diverse matrix molecules, whereas the amounts of HS II and HS III essentially remained the same. In contrast, when bovine aortic organ cultures were analyzed under pulsatile flow, marked differences in the profile of proteoheparan sulfate biosynthesis were observed: HS I was found exclusively associated with the plasma membrane of the endothelial cells; HS II was localized only to the subendothelial matrix; and HS III represented the only proteoheparan sulfate species in the medium. This distribution is consistent with polarized secretion and deposition into the subcellular matrix of HS III and retention of HS I in the plasma membrane in the organ culture situation, a biosynthetic phenotype which can only be approximated at best by maintaining the endothelial cells on a substrate other than plastic. When aortic media (devoid of endothelial cells) was placed in organ culture, no HS III could be detected, which suggested that the vascular endothelial cell is the major cell type responsible for its synthesis in organ culture. Thus, the extracellular matrix, depending upon its composition and organization, may play an important role in stabilizing cell polarity and thereby contribute to maintenance of the differentiated phenotype appropriate for the endothelial cell.

Animals↗

Modeling extracellular matrix degradation balance with proteinase/transglutaminase cycle.

Extracellular matrix mass balance is implied in many physiological and pathological events, such as metastasis dissemination. Widely studied, its destructive part is mainly catalysed by extracellular proteinases. Conversely, the properties of the constructive part are less obvious, cellular neo-synthesis being usually considered as its only element. In this paper, we introduce the action of transglutaminase in a mathematical model for extracellular matrix remodeling. This extracellular enzyme, catalysing intermolecular protein cross-linking, is considered here as a reverse proteinase as far as the extracellular matrix physical state is concerned. The model is based on a proteinase/transglutaminase cycle interconverting insoluble matrix and soluble proteolysis fragments, with regulation of cellular proteinase expression by the fragments. Under "closed" (batch) conditions, i.e. neglecting matrix influx and fragment efflux from the system, the model is bistable, with reversible hysteresis. Extracellular matrix proteins concentration abruptly switches from low to high levels when transglutaminase activity exceeds a threshold value. Proteinase concentration usually follows the reverse complementary kinetics, but can become apparently uncoupled from extracellular matrix concentration for some parameter values. When matrix production by the cells and fragment degradation are taken into account, the dynamics change to sustained oscillations because of the emergence of a stable limit cycle. Transitions out of and into oscillation areas are controlled by the model parameters. Biological interpretation indicates that these oscillations could represent the normal homeostatic situation, whereas the other exhibited dynamics can be related to pathologies such as tumor invasion or fibrosis. These results allow to discuss the insights that the model could contribute to the comprehension of these complex biological events.

Animals↗

The role of the extracellular matrix in skeletal development.

The extracellular matrix of cartilage and bone is composed mostly of collagen with lesser amounts of other constituents such as proteoglycans. The focus of this brief review will be on the dynamic expression of collagens and proteoglycans in the cartilage and bone extracellular matrices. Recent research has shown the presence of different collagen types and proteoglycans that are differentially expressed in cartilage, in the transition from cartilage to bone, and in the bone extracellular matrices. These findings suggest the complexity of the skeletal extracellular matrix as well as its dynamic expression. Although the composition of both the cartilage and bone extracellular matrices are largely known, the function of each of the macromolecules composing these matrices and their developmental regulation is not well understood. Defects that modify the extracellular matrix, like the chicken chondrodysplasia, nanomelia, and tibial dyschondroplasia, have profound affects on skeletal structure. The poultry industry is currently confronting a high percentage of skeletal deformities due to selection for increased growth rate and needs to consider the effect of extracellular matrix modifications and how to maintain extracellular matrix integrity.

Animals↗

Receptor tyrosine phosphatase beta is expressed in the form of proteoglycan and binds to the extracellular matrix protein tenascin.

The extracellular domain of receptor type protein tyrosine phosphatase beta (RPTP beta) exhibits striking sequence similarity with a soluble, rat brain chondroitin sulfate proteoglycan (3F8 PG). Immunoprecipitation experiments of cells transfected with RPTP beta expression vector and metabolically labeled with [35S]sulfate and [35S]methionine indicate that the transmembrane form of RPTP beta is indeed a chondroitin sulfate proteoglycan. The 3F8 PG is therefore a variant form composed of the entire extracellular domain of RPTP beta probably generated by alternative RNA splicing. Previous immunohistochemical studies indicated that both RPTP beta and the extracellular matrix protein tenascin are localized in similar regions of the central nervous system. We have performed co-aggregation assays with red and green Co-vaspheres coated with tenascin and 3F8 PG, respectively, showing that the extracellular domain of RPTP beta (3F8 PG) binds specifically to tenascin. The interaction between a receptor tyrosine phosphatase and an extracellular matrix protein may have a role in development of the mammalian central nervous system.

Alternative Splicing↗

Transforming growth factor-beta 1 induces extracellular matrix formation in glomerulonephritis.

Extracellular matrices can be important in disease. Glomerulonephritis is an inflammation of the kidney that is characterized by the accumulation of extracellular matrix within the damaged glomeruli. We have shown that transforming growth factor-beta 1 (TGF-beta 1) is unique in regulating the production of proteoglycans and matrix glycoproteins by glomerular cells in vitro. In an experimental model of glomerulonephritis in rats, we found increased proteoglycan and fibronectin synthesis by cultured nephritic glomeruli, which was greatly reduced by the addition of antiserum to TGF-beta 1. Conditioned media from glomerular cultures, when added to normal cultured mesangial cells, induced elevated proteoglycan synthesis. The stimulatory activity of the conditioned media was blocked by addition of TGF-beta 1 antiserum. Glomerular histology showed mesangial matrix expansion in a time course that roughly paralleled the elevated proteoglycan synthesis by the nephritic glomeruli. At the same time there was an increased expression of TGF-beta 1 mRNA and TGF-beta 1 protein in the glomeruli. Administration of anti-TGF-beta 1 at the time of induction of glomerulonephritis suppressed the elevated extracellular matrix production and dramatically attenuated histological manifestations of the disease. A small proteoglycan, decorin, also inhibits the activity of TGF-beta, potentially providing an alternative format for the prevention of TGF-beta activity. Our results provide direct evidence for a causal role of TGF-beta 1 in the pathogenesis of the experimental disease and suggest a new approach to the therapy of glomerulonephritis.

Animals↗

The extracellular matrix and atherosclerosis.

The vascular extracellular matrix is a collection of vastly different macromolecules organized by entanglement and cross-linking into a biomechanically active polymer that imparts regional tensile strength, viscoelasticity, and compressibility to the atherosclerotic lesion. Each component of the extracellular matrix possesses unique structural properties that determine its separate roles during atherogenesis. Not only does this matrix provide the architectural framework that influences the structural integrity of the lesion, but it also provides the milieu for vascular cells and participates in the adhesive, proliferative, and migratory events that characterize lesion development. The fact that different components of the extracellular matrix selectively bind plasma proteins, growth factors, cytokines, and enzymes implicate these molecules in the regulation of key metabolic events in the formation of the atherosclerotic plaque. The extracellular matrix can no longer be thought of as simply an inert structural mass, but rather as a collection of molecules that possesses the capacity to 'instruct' and 'transduce the information' that 'drives' events central to the atherogenic process. A more thorough understanding of the nature and properties of the vascular extracellular matrix and the factors that regulate its accumulation would seem to be a reasonable goal if progress is to be made towards alleviating this disease.

Arteriosclerosis↗

The extracellular matrix and synapses.

Extracellular matrix (ECM) molecules, derived from both neurons and glial cells, are secreted and accumulate in the extracellular space to regulate various aspects of pre- and postsynaptic differentiation, the maturation of synapses, and their plasticity. The emerging mechanisms comprise interactions of agrin, integrin ligands, and reelin, with their cognate cell-surface receptors being coupled to tyrosine kinase activities. These may induce the clustering of postsynaptic receptors and changes in their composition and function. Furthermore, direct interactions of laminins, neuronal pentraxins, and tenascin-R with voltage-gated Ca(2+) channels, alpha-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid (AMPA), and gamma-aminobutyric acid(B) (GABA(B)) receptors, respectively, shape the organization and function of different subsets of synapses. Some of these mechanisms significantly contribute to the induction of long-term potentiation in excitatory synapses, either by the regulation of Ca(2+) entry via N-methyl-D-aspartate receptors or L-type Ca(2+) channels, or by the control of GABAergic inhibition.

Animals↗

An ultrastructural and immunohistochemical study of extracellular matrix in meningiomas.

Extracellular matrix of meningiomas was studied by light and electron microscopy with the aid of immunohistochemical techniques. Special attention was paid to the distribution of type I, III, IV, V collagens and laminin with a comparison between meningothelial and fibroblastic types. Connective tissue fibers and basement membrane were not found among the tumor cells in the meningothelial type, but were found in the fibroblastic type. The immunolocalizations were consistently demonstrated extracellularly, but were not within the cytoplasm. Type I, III and V collagens were usually demonstrated in the fibrous septum in the meningothelial type, while they were localized among the tumor cells in the fibroblastic type. Furthermore, type IV collagen and laminin were demonstrated within the vascular walls or around the syncytium in the meningothelial type, while they were localized among the tumor cells in the fibroblastic type. In both types the expression of type IV collagen and laminin was closely related to the distribution of basement membrane. Although meningothelial and fibroblastic meningiomas showed quite different distribution of extracellular matrices, the profile of collagen types expressed by these two basic types was essentially the same. The cellular derivation of meningiomas was discussed with particular attention to the structure of human arachnoid villi and meninges.

Collagen↗

The in vitro regulation of ovarian follicle development using alginate-extracellular matrix gels.

The extracellular matrix (ECM) provides a three-dimensional structure that promotes and regulates cell adhesion and provides signals that direct the cellular processes leading to tissue development. In this report, synthetic matrices that present defined ECM components were employed to investigate these signaling effects on tissue formation using ovarian follicle maturation as a model system. In vitro systems for follicle culture are being developed to preserve fertility for women, and cultures were performed to test the hypothesis that the ECM regulates follicle maturation in a manner that is dependent on both the ECM identity and the stage of follicle development. Immature mouse follicles were cultured within alginate-based matrices that were modified with specific ECM components (e.g., laminin) or RGD peptides. The matrix maintains the in vivo like morphology of the follicle and provides an environment that supports follicle development. The ECM components signal the somatic cells of the follicle, affecting their growth and differentiation, and unexpectedly also affect the meiotic competence of the oocyte. These effects depend upon both the identity of the ECM components and the initial stage of the follicle, indicating that the ECM is a dynamic regulator of follicle development. The development of synthetic matrices that promote follicle maturation to produce meiotically competent oocytes may provide a mechanism to preserve fertility, or more generally, provide design principles for scaffold-based approaches to tissue engineering.

Alginates↗

Biaxial strength of multilaminated extracellular matrix scaffolds.

Xenogeneic extracellular matrix (ECM) can be harvested and configured to function as a bioscaffold for tissue and organ reconstruction. The mechanical properties of the ECM vary depending upon the tissue from which it is harvested. Likewise, the manufacturing steps required to develop ECMs into medical grade devices will affect the surface morphology and the mechanical properties of the bioscaffold; important properties for constructive tissue remodeling. The present study compared the ball-burst strength of five different ECM scaffolds before and after treatment with peracetic acid (PAA): porcine small intestinal submucosa (SIS), porcine urinary bladder submucosa (UBS), porcine urinary bladder matrix (UBM), a composite of UBS + UBM, and canine stomach submucosa (SS). This study also compared the mechanical properties of 2- and 4-layer ECM scaffolds. Results showed 2-layer SS devices had the highest ball-burst value of all 2-layer ECM devices. Moreover, all 4-layer ECM devices had similar ball-burst strength except for 4-layer UBM devices which was the weakest. PAA-treatment decreased the ball-burst strength of SS and increased the ball-burst strength of UBS 2-layer devices. This study showed the material properties of the ECM scaffolds could be engineered to mimic those of native soft tissues (i.e. vascular, musculotendinous, etc) by varying the number of layers and modifying the disinfection/sterilization treatments used for manufacturing.

Absorbable Implants↗

Amelogenesis in vitro: a model for studies of epithelial postsecretory processing during tissue-specific extracellular matrix biomineralization.

The extracellular matrix (ECM) of developing mammalian enamel comprises a complex of unusual epithelial-derived proteins, which appear to function in concert to initiate and propagate tissue-specific biomineralization. Following enamel protein synthesis by ameloblast cells within the enamel organ, the subsequent steps of posttranslational modification, secretion, postsecretory processing and eventual removal of these proteins from forming enamel are largely unknown. To address this issue we have designed studies to investigate the hypothesis that enamel proteins are removed from enamel and translocated into the vasculature as relatively high-molecular-weight components. We examined enamel proteins recovered from serumless medium during prolonged organ culture of mouse capstage mandibular first molars. By 21 days in vitro the tooth crown formed and dentine and enamel biomineralization were apparent. At 31 days, explants retained metabolic activity and the enamel matrix showed extensive transformation. Immunologically identified enamel proteins of 26-18 k Da were produced by cultured tooth organs, translocated from tooth explants to the culture medium, recovered from the medium and then compared to control enamel protein from in vivo preparations. Comparable postsecretory processing of the 26-k Da amelogenin protein was observed in vitro and in vivo. We speculate that the pathway reported in the present studies is comparable to the processing of the enamel protein polypeptides of the maturing enamel which occurs in vivo. The in vitro organ culture model described in this report provides an approach with which to investigate the molecular events associated with epithelial-derived postsecretory processing of ECM molecules associated with tissue-specific biomineralization.

Ameloblasts↗

Electrospun scaffold tailored for tissue-specific extracellular matrix.

The natural extracellular matrix (ECM) is a complex structure that is built to meet the specific requirements of the tissue and organ. Primarily consisting of nanometer diameter fibrils, ECM may contain other vital substances such as proteoglycans, glycosaminoglycan and various minerals. Current research in tissue engineering involves trying to replicate the ECM such that it provides the environment for tissue regeneration. Electrospinning is a versatile process that results in nanofibers by applying a high voltage to electrically charge a liquid. A variety of polymers and other substances have been incorporated into the artificial nanofibrous scaffold. Surface modification and cross-linking of the nanofibers are some ways to improve the biocompatibility and stability of the scaffold. Electrospun scaffolds with oriented nanofibers and other assemblies can be constructed by modifying the electrospinning setup. Using electrospinning, researchers are able to specifically tailor the electrospun scaffold to meet the requirements of the tissue that they seek to regenerate. In vitro and in vivo experiments demonstrate that electrospun scaffolds hold great potential for tissue engineering applications.

Animals↗

Immunohistochemical study on phenotypical changes of hepatocytes in liver disease with reference to extracellular matrix composition.

AIMS/BACKGROUND: Extracellular matrix (ECM) may affect the function and phenotype of hepatocytes. Phenotypic changes of hepatocytes in diseased liver were investigated with reference to ECM composition. METHODS: Immunohistochemistry was performed on biopsied liver samples from chronic viral hepatitis (CVH), primary biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC) and normal patients, using monoclonal antibodies for laminin, type IV collagen, cytokeratin 19 (CK19) and epithelial glycoprotein (EGP), a protein homologous to nidogen. RESULTS: In normal controls, both EGP and CK 19 were expressed exclusively on biliary epithelia. Laminin and type IV collagen were expressed around portal bile ducts and blood vessels. Although type IV collagen was expressed in Disse's space, laminin was scarcely expressed. In all pathological livers, both EGP and CK 19 were expressed in proliferated bile ductules. In CVH with piecemeal necrosis, EGP was expressed on periportal hepatocytes, while CK19 expression was limited to a few hepatocytes. Laminin was expressed in Disse's space of periportal sinusoids, where EGP was expressed on hepatocytes. EGP expression on hepatocytes and laminin deposition in Disse's space were rare in PBC and PSC liver. CONCLUSION: These results suggest that hepatocytes transform into a phenotype similar to biliary epithelia and, laminin deposition in Disse's space (capillarization of sinusoids) may play a role in this phenotypic change.

Cholangitis, Sclerosing↗

Differential structural requirements for the induction of cell attachment, proliferation and differentiation by the extracellular matrix.

The subendothelial extracellular matrix (ECM) mediates the attachment of both human Ewing's sarcoma and colon carcinoma cells. Attachment and flattening of the sarcoma cells was sensitive to heat treatment but not to periodate oxidation of the ECM, whereas the colon carcinoma cells attached and flattened over heated but not periodate-treated ECM. Such differential sensitivity to heat treatment and periodate oxidation was also observed using purified fibronectin and laminin, respectively, but the inhibition of cell attachment was greater than with a similarly treated ECM. It is therefore conceivable that fibronectin and laminin specifically mediate the attachment and flattening of Ewing's sarcoma and colon carcinoma cells to the ECM, but that other constituents may support this attachment either directly or via interaction and stabilization of adhesive glycoproteins in the ECM. The ECM-mediated morphological differentiation of adult rat oligodendrocytes was sensitive to periodate oxidation to a much higher extent than to heat treatment of the ECM. In contrast, both treatments had only a small effect on the ECM-induced proliferation of vascular endothelial cells. These results indicate that different constituents of the ECM may be held responsible for its effects on different parameters of cell behavior, and that various cell types respond differently to a given modification of the ECM.

Animals↗

Extracellular matrix remodeling in the vascular wall.

The extracellular matrix provides a structural framework essential for the functional properties of vessel walls. The three dimensional organization of the extracellular matrix molecules--elastin, collagens, proteoglycans and structural glycoproteins--synthesized during fetal development--is optimal for these functions. Early in life, the vessel wall is subjected to injury: lipid deposition, hypoxia, enzyme secretion and reactive oxygen species production during inflammatory processes, and the extracellular matrix molecules are hydrolyzed by proteases--matrix metalloproteinases, leukocyte elastase, etc. In uninjured arteries and veins, some proteases are constitutively expressed, but through the control of their activation and/or their inhibition by inhibitors, these proteases have a very low activity. During the occurrence of vascular pathologies--atherosclerosis, hypertension, varicosis, restenosis, etc.--the balance between proteases and their inhibitors is temporally destroyed through the induction of matrix metalloproteinase gene expression or the secretion of enzymes by inflammatory cells. Smooth muscle cells, the most numerous cells in vascular walls, have a high ability to respond to injury through their ability to synthesize extracellular matrix molecules and protease inhibitors. However, the three dimensional organization of the newly synthesized extracellular matrix is never functionally optimal. In some other pathologies--aneurysm--the injury overcomes the responsive capacity of smooth muscle cells and the quantity of extracellular matrix decreases. In conclusion, care should be taken to maintain the vascular extracellular matrix reserve and any therapeutic manipulation of the protease/inhibitor balance must be perfectly controlled, because an accumulation of abnormal extracellular matrix may have unforeseen adverse effects.

Aneurysm↗

Genetic and biochemical evidence for involvement of HOTHEAD in the biosynthesis of long-chain alpha-,omega-dicarboxylic fatty acids and formation of extracellular matrix.

In plants, extracellular matrix polymers built from polysaccharides and cuticular lipids have structural and protective functions. The cuticle is found to be ten times thinner in Arabidopsis thaliana (L.) Heynh than in many other plants, and there is evidence that it is unusual in having a high content of alpha-,omega-dicarboxylic fatty acids (FAs) in its polyesters. We designated the new organ fusion mutant hth-12 after it appeared to be allelic to adhesion of calyx edges (ace) and hothead (hth), upon molecular cloning of the gene by transposon tagging. This mutant is deficient in its ability to oxidize long-chain omega-hydroxy FAs to omega-oxo FAs, which results in leaf polyesters in decreased alpha-,omega-dicarboxylic FAs and increased omega-hydroxy FAs. These chemical phenotypes lead to disorder of the cuticle membrane structure in hth-12. ACE/HTH is a single-domain protein showing sequence similarity to long-chain FA omega-alcohol dehydrogenases from Candida species, and we hypothesize that it may catalyze the next step after cytochrome P450 FA omega-hydroxylases in the omega-oxidation pathway. We show that ACE/HTH is specifically expressed in epidermal cells. It appears very likely therefore that the changes in the amount of alpha-,omega-dicarboxylic FAs in hth-12 reflect the different composition of cuticular polyesters. The ACE/HTH gene is also expressed in root epidermal cells which do not form a polyester membrane on the exterior surface, thereby making it possible that the end products of the pathway, alpha-,omega-dicarboxylic FAs, are generally required for the cross-linking that ensures the integrity of the outer epidermal cell wall.

Alleles↗

Laminin B1 expression is required for laminin deposition into the extracellular matrix of PC12 cells.

The extracellular matrix of rat pheochromocytoma PC12 cells was shown by indirect immunofluorescence to consist of a network of fibronectin. The matrix did not contain laminin. The cells synthesized messenger RNA for fibronectin, laminin B2, and s-laminin but not for entactin or the B1 and A chains of laminin. Laminin B2 but not laminin B1 was detectable in the culture medium and in cell lysates. A full-length cDNA clone for the B1 chain of laminin was constructed in the plasmid p-444, which contains the neomycin-resistance marker and human beta-actin promoter. PC12 cells were transfected with this recombinant plasmid, and stable neomycin-resistant clones were isolated and characterized. Clones that synthesized laminin B1 messenger RNA were found to deposit a laminin-containing matrix. In many of these clones the deposition of the fibronectin matrix was greatly diminished. The laminin matrix was predominantly localized in the intercellular spaces forming a honeycomb pattern. The morphology of the laminin-synthesizing transfected cells was markedly different from the parental cells. The cells grew in tight clusters that were resistant to dissociating agents. It is concluded that the B1 chain of laminin contains information that is required for the formation of a stable laminin-containing extracellular matrix network either by interaction with cell surface receptors or other extracellular matrix components. Furthermore, expression of the laminin B1 gene may be a central regulatory point in determining extracellular matrix composition during embryogenesis.

Animals↗