How Does Remodeling Of Junctions Happen?

Atrial remodeling is a persistent change in atrial structure or function that promotes the occurrence or maintenance of atrial fibrillation (AF) by acting on fundamental mechanisms. In 1967, Revel and Karnovsky first described an aggregate of membrane-associated particles that blocked extracellular space, allowing tracer mechano-transduction events during remodeling of endothelial adherens junctions. Gap junction remodeling in cardiac disease involves changes in connexin expression, resulting in altered gap junction density and functional coupling.

Anchoring cell-cell junctions (desmosomes, fascia adherens) play crucial roles in maintaining mechanical integrity of cardiac muscle cells and tissue. Genetic factors, transjunctional voltage, (H+) i6 and (Ca 2+) i, the phosphorylation state of connexins, and extracellular factors all contribute to tight junction remodeling at multiple scales.

Epithelial and endothelial cell-cell contacts are established and maintained by several intercellular junctional complexes. Any persistent change in atrial structure or function constitutes atrial remodeling. Cell junctions between dividing cells and their neighbors are progressively remodeled, with constriction of the cytokinetic ring in the dividing cell acting as a mechanical signal that promotes local dismantling of E-cad-Catenin complexes, and thus AJs, at the ingressing membrane.

Junctional remodeling and barrier function preservation are facilitated by the recruitment of membrane from the lateral border recycling compartment (LBRC), a process that involves the trafficking of proteins to the TJ. This review article provides an integrated view of mechanosensing mechanisms that regulate cell-cell contact composition, geometry, and integrity under tension and stress.

How does bone remodeling occur?

Bones are constantly changing throughout their lifespan, a process known as bone remodeling. This process protects the structural integrity of the skeletal system and contributes to the body’s calcium and phosphorus balance. Bone remodeling involves the resorption of old or damaged bone and the deposition of new bone material. German anatomist and surgeon Julius Wolff developed a law explaining how bones adapt to mechanical loading. An increase in loading strengthens the internal, spongy bone architecture, followed by the strengthening of the cortical layer.

Conversely, a decrease in stress weakens these layers. The duration, magnitude, and rate of forces applied to the bone dictate how the bone’s integrity is altered. Osteoclasts and osteoblasts are the primary cells responsible for both resorption and deposition phases of bone remodeling. The activity of these cells, particularly osteoclasts, is influenced by hormonal signals, creating potential pathophysiological consequences.

How does cardiac remodeling occur?

Cardiac remodeling is a process involving the activation of the sympathetic and renin-angiotensin-aldosterone systems. These systems stimulate protein synthesis, leading to cellular hypertrophy and fibrosis. Other effects include growth factors activation, hemodynamic overload, increased oxidative stress, and direct cytotoxic effects, resulting in cellular death. Blocking these systems is crucial for preventing or attenuating cardiac remodeling.

Pharmacological treatment of cardiac remodeling can be divided into consolidated, promising, and potential strategies, including Angiotensin-converting-enzyme (ACE) and Angiotensin receptor blockers (ARBs).

How do anchoring junctions work?

Cell junctions are essential for cell-cell and cell-matrix contact in tissues, particularly in epithelia. Anchoring junctions mechanically attach cells to their neighbors or the extracellular matrix, while communicating junctions mediate the passage of chemical or electrical signals. These junctions are best visualized using conventional or freeze-fracture electron microscopy, revealing the specialized plasma membranes and intercellular space in these regions.

Cell junctions can be classified into three functional groups: occlusing junctions, which seal cells together in an epithelium, and communicating junctions, which mediate the passage of chemical or electrical signals.

How do gap junctions occur?

Gap junctions are clusters of intercellular channels that allow direct diffusion of ions and small molecules between adjacent cells. They are formed by head-to-head docking of hexameric assemblies of tetraspan integral membrane proteins, connexins (Cx). Initially described as low-resistance ion pathways joining excitable cells, gap junctions are found in virtually all cells in solid tissues. Their long evolutionary history has allowed adaptation of gap-junctional intercellular communication to various functions, with multiple regulatory mechanisms.

Gap-junctional channels are composed of hexamers of medium-sized families of integral proteins, such as connexins in chordates and innexins in precordates. Studies have explored the functions of gap junctions in various species, revealing a wide diversity of function in tissue and organ biology.

What proteins form tight junctions?

Epithelia and endothelia are essential organs that separate compartments within an organism and regulate the exchange of substances. The tight junction (TJ) acts as a barrier for the passage of ions and molecules through the paracellular pathway and the movement of proteins and lipids between the apical and basolateral domains of the plasma membrane. Over 40 different proteins have been discovered at TJs of epithelia, endothelia, and myelinated cells, changing our view of TJs from a paracellular barrier to a complex structure involved in signaling cascades controlling cell growth and differentiation.

Both cortical and transmembrane proteins integrate TJs, including scaffolding proteins, tumor suppressors, transcription factors, and proteins involved in vesicle transport. Two components of TJ filaments have been identified: occludin and claudin, which are integral proteins capable of interacting adhesively with complementary molecules on adjacent cells and co-polymerizing laterally. These advancements in understanding TJ molecular structure support previous physiological models that showed TJ as dynamic structures with distinct permeability and morphological characteristics in different tissues and response to changing conditions.

What holds tight junctions together?

The interaction of claudins with a partner group on the opposite cell membrane is responsible for the formation of a tight binding force that holds cells at a tight junction together.

How does anchoring work?

The anchoring effect is a cognitive bias that refers to the tendency to rely too heavily on the first piece of information offered during decision-making. This bias occurs when individuals use an initial piece of information to make subsequent judgments, adjusting away from it and interpreting other information around it. In negotiations, the anchoring effect often occurs, but goal setting can affect the end result. Negotiation scholars Deborah Zetik and Alice Stuhlmacher found that setting specific, challenging goals consistently outperforms those who set lower or vague goals.

Performance improves when negotiators are given rewards for reaching a goal, such as a $10, 000 bonus for billing 2, 000 hours. However, setting ambitious goals can also have potential drawbacks, such as the potential for failure to reach the goal to affect satisfaction with the overall outcome. Researchers Adam Galinsky, Victoria Medvec, and Thomas Mussweiler found that high-achieving negotiators were less satisfied with their outcomes than their peers.

What causes gap junctions to close?

Extracellular Ca2+ levels are around 10-3 mol/L, while intracellular levels are around 10-6 mol/L. When a cell is damaged, Ca2+ rushes in, increasing intracellular Ca2+. Gap junction channels close if intracellular Ca2+ reaches 10-3 mol/L, preventing damage spread. Copyright © 2024 Elsevier B. V., its licensors, and contributors. All rights reserved, including those for text and data mining, AI training, and similar technologies.

What is the difference between tight and anchoring junctions?

Cell junctions are divided into three main groups: tight junctions, which prevent molecule leakage between cells, and anchoring junctions, where neighboring cell membranes are supported by cytoskeletal elements like actin or. ScienceDirect uses cookies and cookies are used by the site. All rights are reserved for text and data mining, AI training, and similar technologies, and for open access content, Creative Commons licensing terms apply.

How are tight junctions formed?

Bicellular tight junctions, found between the lateral membrane surfaces of two adjacent cells, are primarily formed by claudin strands. A model for claudin assembly into tight junction strands has been recently proposed from the crystal structures of mouse claudin-15. The formation of linear claudin polymers is initiated by intermolecular interactions between adjacent claudin monomers through residues on their extracellular loops.

A conserved hydrophobic residue on the extracellular helix of one monomer docks at the hydrophobic pocket formed by conserved residues in transmembrane segment 3 and extracellular segment 2 of a second monomer.

The two contact surfaces facilitate chain-like association of other monomers at newly-formed ends, resulting in a linear polymer. Higher order assemblies occur by the association of two linear polymers, resulting in an antiparallel double row. Claudin molecules in the two chains interact with each other via their extracellular palms (beta-sheet structures), which is stabilized by the formation of hydrogen bonds and leads to the formation of a ‘half-pipe’-shaped continuous beta-sheet structure across the double row. The final step in tight junction formation involves the association of two claudin double rows on adjacent membranes, leading to the formation of the paracellular channel pores.

What protein makes gap junctions?

Gap junctions are protein complexes that connect cells using connexins, which include over 26 types and at least 12 non-connexin components. These components include the tight junction protein ZO-1, sodium channels, and aquaporin. Next-generation sequencing has led to the discovery of more gap junction proteins, with innexins being used to differentiate invertebrate connexins. There are over 20 known innexins, along with unnexins in parasites and vinnexins in viruses.

Electrical synapses are gap junctions that transmit action potentials between neurons, creating bidirectional continuous-time electrical coupling between neurons. Connexon pairs act as generalized regulated gates for ions and smaller molecules between cells, while semichannel connexons form channels to the extracellular environment.