The extracellular matrix (ECM) serves diverse functions and is a major component of the cellular microenvironment. The ECM is a highly dynamic structure, constantly undergoing a remodeling process where ECM components are deposited, degraded, or otherwise modified. ECM dynamics are indispensible during restructuring of tissue architecture. ECM remodeling is an important mechanism whereby cell differentiation can be regulated, including processes such as the establishment and maintenance of stem cell niches, branching morphogenesis, angiogenesis, bone remodeling, and wound repair. In contrast, abnormal ECM dynamics lead to deregulated cell proliferation and invasion, failure of cell death, and loss of cell differentiation, resulting in congenital defects and pathological processes including tissue fibrosis and cancer. Understanding the mechanisms of ECM remodeling and its regulation, therefore, is essential for developing new therapeutic interventions for diseases and novel strategies for tissue engineering and regenerative medicine.

/pdf/extracellular-matrix-degradation-and-remodeling-in-32jsm155da.pdf

Extracellular Matrix Degradation and Remodeling in Development and Disease

This review aims at presenting state-of-the-art knowledge on the composition and functions of the endothelial glycocalyx. The endothelial glycocalyx is a network of membrane-bound proteoglycans and glycoproteins, covering the endothelium luminally. Both endothelium- and plasma-derived soluble molecules integrate into this mesh. Over the past decade, insight has been gained into the role of the glycocalyx in vascular physiology and pathology, including mechanotransduction, hemostasis, signaling, and blood cell–vessel wall interactions. The contribution of the glycocalyx to diabetes, ischemia/reperfusion, and atherosclerosis is also reviewed. Experimental data from the micro- and macrocirculation alludes at a vasculoprotective role for the glycocalyx. Assessing this possible role of the endothelial glycocalyx requires reliable visualization of this delicate layer, which is a great challenge. An overview is given of the various ways in which the endothelial glycocalyx has been visualized up to now, including first data from two-photon microscopic imaging.

/pdf/the-endothelial-glycocalyx-composition-functions-and-37k47dm9fs.pdf

The endothelial glycocalyx: composition, functions, and visualization

Heparan sulfate proteoglycans are found at the cell surface and in the extracellular matrix, where they interact with a plethora of ligands. Over the last decade, new insights have emerged regarding the mechanism and biological significance of these interactions. Here, we discuss changing views on the specificity of protein-heparan sulfate binding and the activity of HSPGs as receptors and coreceptors. Although few in number, heparan sulfate proteoglycans have profound effects at the cellular, tissue, and organismal level.

/pdf/heparan-sulfate-proteoglycans-52vws5lyzu.pdf

Heparan Sulfate Proteoglycans

This article summarizes the recent progress in the design and synthesis of hydrogels as tissue-engineering scaffolds. Hydrogels are attractive scaffolding materials owing to their highly swollen network structure, ability to encapsulate cells and bioactive molecules, and efficient mass transfer. Various polymers, including natural, synthetic and natural/synthetic hybrid polymers, have been used to make hydrogels via chemical or physical crosslinking. Recently, bioactive synthetic hydrogels have emerged as promising scaffolds because they can provide molecularly tailored biofunctions and adjustable mechanical properties, as well as an extracellular matrix-like microenvironment for cell growth and tissue formation. This article addresses various strategies that have been explored to design synthetic hydrogels with extracellular matrix-mimetic bioactive properties, such as cell adhesion, proteolytic degradation and growth factor-binding.

Design properties of hydrogel tissue-engineering scaffolds

Bioactive modification of poly(ethylene glycol) hydrogels for tissue engineering

Introduction. In the following all semigroups are of finite order. One semigroup S, is said to divide another semigroup S2, written SlIS2, if S, is a homomorphic image of a subsemigroup of S2. The semidirect product of S2 by Sl, with connecting homomorphism Y, is written S2 X y Sl. See Definition 1.6. A semigroup S is called irreducible if for all finite semigroups S2 and Si and all connecting homomorphisms Y, S I (S2 X Y SJ) implies S I S2 or S I S1. It is shown that S is irreducible if and only if either:

/pdf/algebraic-theory-of-machines-i-prime-decomposition-theorem-322rynatn9.pdf

Algebraic theory of machines. I. Prime decomposition theorem for finite semigroups and machines

The extracellular matrix plays a number of important roles, among them providing structural support and information to cellular structures such as blood vessels imbedded within it. As more complex organisms have evolved, the matrix ability to direct signalling towards the vasculature and remodel in response to signalling from the vasculature has assumed progressively greater importance. This review will focus on the molecules of the extracellular matrix, specifically relating to vessel formation and their ability to signal to the surrounding cells to initiate or terminate processes involved in blood vessel formation.

The extracellular matrix and blood vessel formation: not just a scaffold

The kernel of monoid morphisms

This paper is concerned with the many deep and far reaching consequences of Ash's positive solution of the type II conjecture for finite monoids. After rewieving the statement and history of the problem, we show how it can be used to decide if a finite monoid is in the variety generated by the Malcev product of a given variety and the variety of groups. Many interesting varieties of finite monoids have such a description including the variety generated by inverse monoids, orthodox monoids and solid monoids. A fascinating case is that of block groups. A block group is a monoid such that every element has at most one semigroup inverse. As a consequence of the cover conjecture - also verified by Ash - it follows that block groups are precisely the divisors of power monoids of finite groups. The proof of this last fact uses earlier results of the authors and the deepest tools and results from global semigroup theory. We next give connections with the profinite group topologies on finitely generated free monoids and free groups. In particular, we show that the type II conjecture is equivalent with two other conjectures on the structure of closed sets (one conjecture for the free monoid and another one for the free group). Now Ash's theorem implies that the two topological conjectures are true and independently, a direct proof of the topological conjecture for the free group has been recently obtained by Ribes and Zalesskii. An important consequence is that a rational subset of a finitely generated free group G is closed in the profinite topology if and only if it is a finite union of sets of the form gH1H2... Hn, where each Hi is a finitely generated subgroup of G. This significantly extends classical results by M. Hall. Finally we return to the roots of this problem and give connections with the complexity theory of finite semigroups. We show that the largest local complexity function in the sense of Rhodes and Tilson is computable.

https://hal.archives-ouvertes.fr/hal-00019815/document

Ash's type II theorem, profinite topology and Malcev products

Heparan sulfate (HS) regulates the activity of various ligands and is involved in molecular recognition events on the cell surface and in the extracellular matrix. Specific binding of HS to different ligand proteins depends on the sulfation pattern of HS. For example, the interaction between antithrombin and a particular 3-O sulfated HS motif is thought to modulate blood coagulation. However, a recent study of mice defective for this modification suggested that 3-O sulfation plays other biological roles. Here, we show that Drosophila melanogaster HS 3-O sulfotransferase-b (Hs3st-B), which catalyzes HS 3-O sulfation, is a novel component of the Notch pathway. Reduction of Hs3st-B function by transgenic RNA interference compromised Notch signaling, producing neurogenic phenotypes. We also show that levels of Notch protein on the cell surface were markedly decreased by loss of Hs3st-B. These findings suggest that Hs3st-B is involved in Notch signaling by affecting stability or intracellular trafficking of Notch protein.

/pdf/regulation-of-notch-signaling-by-drosophila-heparan-sulfate-4whnqy9j4h.pdf

Regulation of Notch signaling by Drosophila heparan sulfate 3-O sulfotransferase.

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