Effects of soluble factors and extracellular matrix components on vascular cell behavior in vitro and in vivo: Models of de-endothelialization and repair

1991 ◽  
Vol 45 (2) ◽  
pp. 123-130 ◽  
Author(s):  
Joseph A. Madri ◽  
Martin Marx ◽  
June R. Merwin ◽  
Craig Basson ◽  
Christian Prinz ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Cell Behavior ◽  
Soluble Factors ◽  
Vascular Cell ◽  
In Vivo Models ◽  
Extracellular Matrix Components ◽  
Matrix Components

scholarly journals Regulation of Tissue Fibrosis by the Biomechanical Environment

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Wayne Carver ◽  
Edie C. Goldsmith
Keyword(s):  
Extracellular Matrix ◽  
Intracellular Signaling ◽  
Mechanical Load ◽  
Mechanical Force ◽  
Mechanical Signals ◽  
Organ Systems ◽  
Extracellular Matrix Components ◽  
Matrix Components

The biomechanical environment plays a fundamental role in embryonic development, tissue maintenance, and pathogenesis. Mechanical forces play particularly important roles in the regulation of connective tissues including not only bone and cartilage but also the interstitial tissues of most organs.In vivostudies have correlated changes in mechanical load to modulation of the extracellular matrix and have indicated that increased mechanical force contributes to the enhanced expression and deposition of extracellular matrix components or fibrosis. Pathological fibrosis contributes to dysfunction of many organ systems. A variety ofin vitromodels have been utilized to evaluate the effects of mechanical force on extracellular matrix-producing cells. In general, application of mechanical stretch, fluid flow, and compression results in increased expression of extracellular matrix components. More recent studies have indicated that tissue rigidity also provides profibrotic signals to cells. The mechanisms whereby cells detect mechanical signals and transduce them into biochemical responses have received considerable attention. Cell surface receptors for extracellular matrix components and intracellular signaling pathways are instrumental in the mechanotransduction process. Understanding how mechanical signals are transmitted from the microenvironment will identify novel therapeutic targets for fibrosis and other pathological conditions.

scholarly journals Salmonella Extracellular Matrix Components Influence Biofilm Formation and Gallbladder Colonization

2016 ◽  
Vol 84 (11) ◽  
pp. 3243-3251 ◽  
Author(s):  
Haley E. Adcox ◽  
Erin M. Vasicek ◽  
Varun Dwivedi ◽  
Ky V. Hoang ◽  
Joanne Turner ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Typhoid Fever ◽  
Salmonella Enterica ◽  
Biofilm Formation ◽  
Bacterial Survival ◽  
Content Type ◽  
Extracellular Matrix Components ◽  
Matrix Components

Salmonella enterica serovar Typhi, the causative agent of typhoid fever in humans, forms biofilms encapsulated by an extracellular matrix (ECM). Biofilms facilitate colonization and persistent infection in gallbladders of humans and mouse models of chronic carriage. Individual roles of matrix components have not been completely elucidated in vitro or in vivo . To examine individual functions, strains of Salmonella enterica serovar Typhimurium, the murine model of S . Typhi, in which various ECM genes were deleted or added, were created to examine biofilm formation, colonization, and persistence in the gallbladder. Studies show that curli contributes most significantly to biofilm formation. Expression of Vi antigen decreased biofilm formation in vitro and virulence and bacterial survival in vivo without altering the examined gallbladder pro- or anti-inflammatory cytokines. Oppositely, loss of all ECM components (Δ wcaM Δ csgA Δ yihO Δ bcsE ) increased virulence and bacterial survival in vivo and reduced gallbladder interleukin-10 (IL-10) levels. Colanic acid and curli mutants had the largest defects in biofilm-forming ability and contributed most significantly to the virulence increase of the Δ wcaM Δ csgA Δ yihO Δ bcsE mutant strain. While the Δ wcaM Δ csgA Δ yihO Δ bcsE mutant was not altered in resistance to complement or growth in macrophages, it attached and invaded macrophages better than the wild-type (WT) strain. These data suggest that ECM components have various levels of importance in biofilm formation and gallbladder colonization and that the ECM diminishes disseminated disease in our model, perhaps by reducing cell attachment/invasion and dampening inflammation by maintaining/inducing IL-10 production. Understanding how ECM components aid acute disease and persistence could lead to improvements in therapeutic treatment of typhoid fever patients.

Megakaryocytes Contribute To The Establishment Of The Bone Marrow Environment By Expressing Extracellular Matrix proteins

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 3695-3695
Author(s):  
Alessandro Malara ◽  
Cristian Gruppi ◽  
Manuela Currao ◽  
Alessandra Balduini
Keyword(s):  
Bone Marrow ◽  
Extracellular Matrix ◽  
Type Iv Collagen ◽  
Extracellular Matrix Component ◽  
Matrix Component ◽  
Type Iv ◽  
Extracellular Matrix Components ◽  
Matrix Components

Abstract Introduction the bone marrow microenvironment consists of various types of cells and their secreted extracellular matrix components that surround capillary-venous sinusoids, and plays a key role in the regulation of hematopoiesis. In general, extracellular matrix components interact with each other to form a structural framework that supports tissue organization and positional cues that regulate cellular processes. Megakaryocytes are rare cells in the bone marrow and, besides platelet release, growing evidences attribute new functions to these cells in the generation and maintenance of the bone marrow cell niche. Recent evidences, by our group, demonstrated that megakaryocytes are involved in matrix deposition and remodeling, as demonstrated by their role in fibronectin fibrillogenesis and the expression of matrix cross-linking enzymes, such as factor XIIIa, essential in the dynamic of megakaryocyte-matrix component interactions. Interestingly, individual extracellular matrix components were demonstrated to play a role in the regulation of megakaryocytes development in vitro. Fibronectin was shown to regulate megakaryocyte maturation and proplatelet extension, while type III and type IV collagens were demonstrated to support proplatelet formation in vitro. In contrast, type I collagen is an important physiological inhibitor of platelet release in vitro. However, little is known about the exact localization as well as function of these matrix components in vivo. Results in this work we have analyzed the spatial distribution of megakaryocytes and extracellular matrix components by immunofluorescence in murine femur sections. We found that megakaryocytes were predominantly located in the femur diaphysis with only 20% of megakaryocytes within 50μm from the endosteal surface and more than 80% of megakaryocytes located less than 50 μm from a sinusoid. Correlation between megakaryocyte distance from sinusoids and dimension suggested a gradient of maturing megakaryocytes towards the vascular niche. Next, we deciphered bone marrow extracellular matrix component composition by western blotting and mapped the location in situ of different collagens (I, III, IV, VI) and glycoproteins (fibronectin, laminin). We found that all these proteins were differently located in the endosteal and sinusoidal districts supporting the concept that regulation of hemopoiesis, in the bone marrow, may also depend from matrix distribution. Further, we showed, for the first time, that megakaryocytes were surrounded by a pericellular matrix mainly composed of fibronectin, laminin and type IV collagen. Interestingly, these three proteins were also demonstrated to promote thrombopoietin-dependent megakaryocyte differentiation in in vitro cultures of bone marrow hemopoietic progenitor cells. Finally, fibronectin, laminin and type IV collagen were also demonstrated to be expressed and synthesized by differentiated megakaryocytes in vitro as demonstrated by PCR and western blotting analysis. Most importantly, megakaryocyte expression of these extracellular matrix components was up-regulated in vivo during bone marrow reconstitution upon drug induced myelosuppression and, at a lesser extent, thrombocytopenia. Conclusions all together these results suggested that megakaryocytes are important extracellular matrix component-producing bone marrow cells and that released extracellular matrix components support megakaryopoiesis and concur to the generation of bone marrow niches. Disclosures: No relevant conflicts of interest to declare.

Cell-extracellular matrix interactions under in vivo conditions during interstitial cell migration in Hydra vulgaris

Development ◽  
1994 ◽  
Vol 120 (2) ◽  
pp. 425-432 ◽  
Author(s):  
X. Zhang ◽  
M.P. Sarras
Keyword(s):  
Extracellular Matrix ◽  
Cell Migration ◽  
Synthetic Peptide ◽  
Interstitial Cell ◽  
Extracellular Matrix Components ◽  
Matrix Interactions ◽  
Apical Half ◽  
Matrix Components ◽  
Extracellular Matrix Interactions

Interstitial cell (I-cell) migration in hydra is essential for establishment of the regional cell differentiation pattern in the organism. All previous in vivo studies have indicated that cell migration in hydra is a result of cell-cell interactions and chemotaxic gradients. Recently, in vitro cell adhesion studies indicated that isolated nematocytes could bind to substrata coated with isolated hydra mesoglea, fibronectin and type IV collagen. Under these conditions, nematocytes could be observed to migrate on some of these extracellular matrix components. By modifying previously described hydra grafting techniques, two procedures were developed to test specifically the role of extracellular matrix components during in vivo I-cell migration in hydra. In one approach, the extracellular matrix structure of the apical half of the hydra graft was perturbed using beta-aminopropionitrile and beta-xyloside. In the second approach, grafts were treated with fibronectin, RGDS synthetic peptide and antibody to fibronectin after grafting was performed. In both cases, I-cell migration from the basal half to the apical half of the grafts was quantitatively analyzed. Statistical analysis indicated that beta-aminopropionitrile, fibronectin, RGDS synthetic peptide and antibody to fibronectin all were inhibitory to I-cell migration as compared to their respective controls. beta-xyloside treatment had no effect on interstitial cell migration. These results indicate the potential importance of cell-extracellular matrix interactions during in vivo I-cell migration in hydra.

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