scholarly journals Extracellular matrix: key structural and functional meshwork in health and disease

FEBS Journal ◽  
2019 ◽  
Vol 286 (15) ◽  
pp. 2826-2829
Author(s):  
Nikos K. Karamanos
Keyword(s):  
Extracellular Matrix ◽  
Health And Disease

scholarly journals The role of extracellular matrix on liver stem cell fate: A dynamic relationship in health and disease

2019 ◽  
Vol 106 ◽  
pp. 49-56 ◽  
Author(s):  
Natalia Sánchez-Romero ◽  
Pilar Sainz-Arnal ◽  
Iris Pla-Palacín ◽  
Pablo Royo Dachary ◽  
Helen Almeida ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Stem Cell ◽  
Cell Fate ◽  
Stem Cell Fate ◽  
Dynamic Relationship ◽  
Health And Disease

scholarly journals Skin proteomics – analysis of the extracellular matrix in health and disease

2020 ◽  
Vol 17 (5) ◽  
pp. 377-391
Author(s):  
Jörn Dengjel ◽  
Leena Bruckner-Tuderman ◽  
Alexander Nyström
Keyword(s):  
Extracellular Matrix ◽  
Proteomics Analysis ◽  
Health And Disease

scholarly journals Neurons, Glia, Extracellular Matrix and Neurovascular Unit: A Systems Biology Approach to the Complexity of Synaptic Plasticity in Health and Disease

2020 ◽  
Vol 21 (4) ◽  
pp. 1539 ◽  
Author(s):  
Ciro De Luca ◽  
Anna Maria Colangelo ◽  
Assunta Virtuoso ◽  
Lilia Alberghina ◽  
Michele Papa
Keyword(s):  
Extracellular Matrix ◽  
Synaptic Plasticity ◽  
Systems Biology ◽  
Synapse Formation ◽  
Neurovascular Unit ◽  
Synaptic Cleft ◽  
Adult Brain ◽  
Molecular Networks ◽  
Maladaptive Plasticity ◽  
Health And Disease

The synaptic cleft has been vastly investigated in the last decades, leading to a novel and fascinating model of the functional and structural modifications linked to synaptic transmission and brain processing. The classic neurocentric model encompassing the neuronal pre- and post-synaptic terminals partly explains the fine-tuned plastic modifications under both pathological and physiological circumstances. Recent experimental evidence has incontrovertibly added oligodendrocytes, astrocytes, and microglia as pivotal elements for synapse formation and remodeling (tripartite synapse) in both the developing and adult brain. Moreover, synaptic plasticity and its pathological counterpart (maladaptive plasticity) have shown a deep connection with other molecular elements of the extracellular matrix (ECM), once considered as a mere extracellular structural scaffold altogether with the cellular glue (i.e., glia). The ECM adds another level of complexity to the modern model of the synapse, particularly, for the long-term plasticity and circuit maintenance. This model, called tetrapartite synapse, can be further implemented by including the neurovascular unit (NVU) and the immune system. Although they were considered so far as tightly separated from the central nervous system (CNS) plasticity, at least in physiological conditions, recent evidence endorsed these elements as structural and paramount actors in synaptic plasticity. This scenario is, as far as speculations and evidence have shown, a consistent model for both adaptive and maladaptive plasticity. However, a comprehensive understanding of brain processes and circuitry complexity is still lacking. Here we propose that a better interpretation of the CNS complexity can be granted by a systems biology approach through the construction of predictive molecular models that enable to enlighten the regulatory logic of the complex molecular networks underlying brain function in health and disease, thus opening the way to more effective treatments.

The neurovascular extracellular matrix in health and disease

2020 ◽  
pp. 153537022097719
Author(s):  
Aric F Logsdon ◽  
Elizabeth M Rhea ◽  
May Reed ◽  
William A Banks ◽  
Michelle A Erickson
Keyword(s):  
Extracellular Matrix ◽  
Systemic Circulation ◽  
Endothelial Glycocalyx ◽  
Normal Brain ◽  
First Line ◽  
Brain Functions ◽  
Disease States ◽  
Health And Disease ◽  
Genetic And Environmental Factors ◽  
Main Component

The blood–brain barrier (BBB) is a vital interface that supports normal brain functions. Endothelial cells (ECs) are the main component of the BBB and are highly specialized to govern the transfer of substances into brain. The EC lumen is enmeshed with an extracellular matrix (ECM), known as the endothelial glycocalyx layer (EGL). The lumen-facing EGL is primarily comprised of proteoglycans (PGs) and glycosaminoglycans (GAGs), which function as the first line of defense for blood-to-brain transfer of substances. Circulating factors must first penetrate the EGL before interacting with the EC. The abundance and composition of the PG and GAGs can dictate EGL function, and determine which circulating substances communicate with the ECs. The EGL can interact with circulating factors through physio-chemical interactions with the EC. Some disease states reveal a “thinning” of the EGL that may increase EC interactions with components of the systemic circulation and alter BBB function. EGL changes may also contribute to the cognitive complications of systemic diseases, such as sepsis and diabetes. For decades, researchers have measured how genetic and environmental factors influence the peripheral EGL constituents; however, much less is known about the neurovascular EGL. In this mini-review, we introduce components of the EGL and innovative ways to measure their abundance and composition that may contribute to BBB dysfunction.

scholarly journals Workshop on cardiovascular extracellular matrix in health and disease in Baeza, Spain

2015 ◽  
Vol 8 (1) ◽  
pp. 2
Author(s):  
Enrique Lara-Pezzi ◽  
Elke Dworatzek ◽  
Fernando Rodríguez-Pascual
Keyword(s):  
Extracellular Matrix ◽  
Health And Disease

scholarly journals Cysteine Peptidases of Mammals: Their Biological Roles and Potential Effects in the Oral Cavity and Other Tissues in Health and Disease

2002 ◽  
Vol 13 (3) ◽  
pp. 238-275 ◽  
Author(s):  
D.P. Dickinson
Keyword(s):  
Extracellular Matrix ◽  
Oral Cavity ◽  
Cell Function ◽  
Human Saliva ◽  
Protective Function ◽  
Cysteine Peptidases ◽  
Genes Encoding ◽  
Foreign Proteins ◽  
Health And Disease

Cysteine peptidases (CPs) are phylogenetically ubiquitous enzymes that can be classified into clans of evolutionarily independent proteins based on the structural organization of the active site. In mammals, two of the major clans represented in the genome are: the CA clan, whose members share a structure and evolutionary history with papain; and the CD clan, which includes the legumains and caspases. This review focuses on the properties of these enzymes, with an emphasis on their potential roles in the oral cavity. The human genome encodes at least (but possibly no more than) 11 distinct enzymes, called cathepsins, that are members of the papain family C1A. Ten of these are present in rodents, which also carry additional genes encoding other cathepsins and cathepsin-like proteins. Human cathepsins are best known from the ubiquitously expressed lysosomal cathepsins B, H, and L, and dipeptidyl peptidase I (DPP I), which until recently were considered to mediate primarily “housekeeping” functions in the cell. However, mutations in DPP I have now been shown to underlie Papillon-Lefèvre syndrome and pre-pubertal periodontitis. Other cathepsins are involved in tissue-specific functions such as bone remodeling, but relatively little is known about the functions of several recently discovered enzymes. Collectively, CPs participate in multiple host systems that are active in health and in disease. They are involved in tissue remodeling and turnover of the extracellular matrix, immune system function, and modulation and alteration of cell function. Intracellularly, CPs function in diverse processes including normal protein turnover, antigen and proprotein processing, and apoptosis. Extracellularly, they can contribute directly to the degradation of foreign proteins and the extracellular matrix. However, CPs can also participate in proteolytic cascades that amplify the degradative capacity, potentially leading to pathological damage, and facilitating the penetration of tissues by cancer cells. We know relatively little regarding the role of human CPs in the oral cavity in health or disease. Most studies to date have focused on the potential use of the lysosomal enzymes as markers for periodontal disease activity. Human saliva contains high levels of cystatins, which are potent CP inhibitors. Although these proteins are presumed to serve a protective function, their in vivo targets are unknown, and it remains to be discovered whether they serve to control any human CP activity.

scholarly journals Microglia as hackers of the matrix: sculpting synapses and the extracellular space

2021 ◽  
Author(s):  
Joshua D. Crapser ◽  
Miguel A. Arreola ◽  
Kate I. Tsourmas ◽  
Kim N. Green
Keyword(s):  
Extracellular Matrix ◽  
Extracellular Space ◽  
The Other ◽  
Perineuronal Nets ◽  
Normal Brain ◽  
The Matrix ◽  
Health And Disease ◽  
Synapse Model ◽  
Brain Homeostasis

AbstractMicroglia shape the synaptic environment in health and disease, but synapses do not exist in a vacuum. Instead, pre- and postsynaptic terminals are surrounded by extracellular matrix (ECM), which together with glia comprise the four elements of the contemporary tetrapartite synapse model. While research in this area is still just beginning, accumulating evidence points toward a novel role for microglia in regulating the ECM during normal brain homeostasis, and such processes may, in turn, become dysfunctional in disease. As it relates to synapses, microglia are reported to modify the perisynaptic matrix, which is the diffuse matrix that surrounds dendritic and axonal terminals, as well as perineuronal nets (PNNs), specialized reticular formations of compact ECM that enwrap neuronal subsets and stabilize proximal synapses. The interconnected relationship between synapses and the ECM in which they are embedded suggests that alterations in one structure necessarily affect the dynamics of the other, and microglia may need to sculpt the matrix to modify the synapses within. Here, we provide an overview of the microglial regulation of synapses, perisynaptic matrix, and PNNs, propose candidate mechanisms by which these structures may be modified, and present the implications of such modifications in normal brain homeostasis and in disease.

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