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Cell Adhesion Molecules
Introduction
Cells are independent units of life. However, when a cell becomes part of an organism, it becomes part of a tissue and organ system. Cells in a tissue are joined to each other and to the extracellular matrix (ECM) by cell junctions. There are three kinds of cell junctions: Occluding junctions, anchoring junctions and communication junctions. Occluding junctions occur in the epithelium where the adjacent cells are so tightly sealed together that even small molecules cannot pass. Communicating junctions allow the exchange of chemical and electrical signals between cells. Anchoring junctions are the ones which attach a cell either to its neighbor or to the extracellular matrix. Formation of an anchoring junction requires the cells to stick to each other. Various molecules mediate adhesion between cells following which the cytoskeleton forms a structure around them. The anchoring junctions thus formed can be of four types- desmosomes, hemidesmosomes, focal adhesions and adherens junctions. In order for a proper tissue to form, it is important for the cells of the tissue to bind together. It is equally important to prevent the invasion and binding of other cells. Thus, cell adhesion has to be specific. This is where the cell adhesion molecules come into play (Alberts et al. 2002).
Cell Adhesion Molecules (CAMs) Adhesion of cells to other cells and to the ECM is mediated by certain proteins on the
The maximum cell density of the naked mole rat cells was found to be three times lower than the mouse sample. This result shows that naked mole-rat cells are hypersensitive to contact inhibition, also known as early contact inhibition. Researchers attempted to determine whether this early contact inhibition was caused by cell contact or secreted factors by replacing the media of naked mole-rat fibroblasts. The replacement increased the maximum cell density but not enough to reach the same level as the mouse sample showing that contact is the cause of the contact inhibition. Naked mole-rat and mouse fibroblasts were infected with oncoproteins which disable Rb and p53 in different samples to determine their role in early contact inhibition. The results showed that both Rb and p53 both played a role in preventing cell proliferation but Rb is more important in the regulation of early contact inhibition. Naked mole-rat fibroblasts were compared to human, mouse and a mutated naked mole-rat fibroblast without early contact inhibition by analyzing for p27 using Western blot. The naked mole-rat sample was the only sample that expressed little p27. When the same process was repeated for p16, the naked mole-rat sample was the only sample expressing high levels of p16. This result shows how p16 is the early contact inhibitor in the naked mole rat and p27 serves as a backup. GFP
Epithelial-mesenchymal transition (EMT) is a cellular process that is essential for normal processes in many organisms, including embryonic development and wound healing, and is recapitulated in human disease, contributing to organ fibrosis and cancer progression (Thiery et al. 2009; Yang and Weinberg 2008). EMT describes the conversion of a cell with an epithelial phenotype to one with mesenchymal characteristics and can be a partial or complete transformation. Epithelial cells form the borders of tissues and organs, and are characterized by apical-basal polarity, contact with a basement membrane, and strong adherence to other epithelial cells through intercellular junctions including adherens junctions, tight junctions, and desmosomes. Conversely, mesenchymal cells have front-rear polarity and generally lack cell-cell contact, allowing them to be motile. During human embryonic development, EMT is essential for the formation of a variety of tissues, including mesoderm, neural crest, somites, palate, pancreas, liver, reproductive tracts, and heart valves (Thiery et al. 2009; Yang and Weinberg 2008). After development, partial EMT also contributes to wound healing (Thiery et al. 2009). However, EMT can also play a more insidious role by factoring into tumour progression.
N-cadherin is a protein encoded by the CDH2 gene. It interacts with the cellular cytoskeleton, and is often involved in cardiac muscle, as well as certain cancers. Being calcium dependent, it helps to maintain cellular structure and integrity. For example, it plays a role in trans-endothelial migration, which involves cell-cell adhesion [3]. The endothelial layer contains many different fibers, as well as pathways that allow attachment for the cadherin protein. Some cancer cells can eventually pass through the endothelium, causing the cancer to become malignant and spread. Cadherins in this case can be used to identify and track the spread of the cells, and further identify common routes of travel through the human vasculature.
The next two molecules, α6β4 integrin, and collagen XVII extend beyond the basal keratinocyte membrane and into the lamina lucida layer of the basement membrane zone and hence they are known as transmembrane molecules. These latter two molecules can be found within the outer plaque of the hemidesmosome. The last molecule, CD151, the most recently discovered molecule, is closely associated with α6β4 Integrin, and resides at or near the surface of the basal cell plasma membrane. The intermediate filaments attach to BPAG1 and plectin, which compose the hemidesmosome inner plaque. Both plectin and BPAG1 belong to the plakin family of proteins, and share significant sequence homology.[14]
The muscles and the sensory organs also show changes such as shrinkage of cells, thickening
One protein mentioned called RhoA is said to force cells into shape. Another protein called Rac1 can maintain myosin phosphorylation to put a controlling influence on entotic
In the meanwhile, in the cytoplasm, the hemagglutinin and neuraminidase have undergone glycosylation, polymerization, and acylation. The hemagglutinin, neuraminidase, and the matrix protein two (M2) all travel together to the plasma membrane. There the proteins meet with the other matrix protein (M1), and begin the
Four ways that large molecules and substances are transported across a membrane include phagocytosis, pinocytosis, receptor-mediated endocytosis and receptor proteins. During phagocytosis, the cell engulfs a particle by wrapping pseudopodia around the particle and packing the particle within the food vacuole (membranous sac). Once the food vacuole integrates with a lysosome (w/ hydrolytic enzyme), the particle will be digested. The second way is pinocytosis, in which the cell takes in “droplets” of extracellular fluid and packs it into tiny vesicles; after this, the tiny vesicles are then transported into the cell because the molecules dissolved in the droplets are the main factors that the cells need. The third process is known as receptor-mediated endocytosis which the cells takes in large quantities of specific substances of all concentration in the Extracellular (EC) fluid; the membranes of the cell vesicle are embedded with proteins that has certain receptor sites that are exposed to the EC fluid in which ligand binds to. Then, the last step is that the receptor proteins cluster in regions of the membrane known as coated pits which contain fuzzy layer of coat proteins on the exterior; then, each coated pit forms a vesicle which contains the ligand molecules and after the ingested material is released from the vesicle, the vesicles then recycle the receptors to the plasma
Tissues are defined as groups of cells with a common structure and function. However, there are four different main categories in the human body: epithelial tissue, connective tissue, muscle tissue, and nervous tissue. Even within the four main categories, there are different types of cells assembled in a different formation. For example, the cells in the epithelial tissue are joined closely together with little material in between them. There are different types of epithelium tissues, including the simple epithelium and stratified epithelium. A simple epithelium has a single layer of cells and a stratified epithelium has multiple layers of cells. Just within the epithetical tissue, the cells connect to each other in a different structure
The effects of integrin’s vary from the type of protein they are and how they affect a certain part of the body. They are usually surface receptors that will interact with extracellular matrix. There is a family of alpha and beta classes which would usually form heterodimers. They are used for adhesion purposes most of the time and can also transduce a biochemical signal into or out of the cell. This process is called bidirectional, where the can transmit information from in and out of a cell. There are different structures that integrin’s play a role in. Integrin’s can bind to a ligand, where it will form a complex with a biological molecule that will usually serve as a purpose. They can go through a process called activation, where they would have a conformational change of the receptor. They can also trigger a cascade effect, which can change a receptors shape.
a. Poke Weed Mitogen act as lectins which are cell membrane binding proteins. Lectins allow cells to stick together. These do not associate with the immune system so cell to cell interaction occurs once the cells are bound together by these proteins. This allows the number of cells that are stuck together to be counted which
Bacterial cells eukaryotes have a cell wall that provides protection to the bacterial cells. Targeting of the cell wall would result in interruption of bacterial cell structure which would result in an osmotic imbalance resulting into cell
Tight junctions function as barriers in epithelial cells through the formation of protein complexes between neighboring cells. Made up of three transmembrane protein families including the occludin proteins, the claudin proteins, and the junctional adhesion molecules (JAMs), tight junctions are able to maintain the distinction between the apical and basolateral regions of the cell as well as maintain the endothelial and epithelial cell sheet barrier. Tight junctions are found to work based on properties such as size selectivity, ion permeability, concentration gradients, sensitivity to pH, and other transport mechanisms (Tang and Goodenough, 2003). This becomes important when recognizing that tight junctions work to prevent molecules from permeating the epithelial sheet and transport them through a paracellular pathway. Permeation of pathogenic bacteria may cause disruption of tight junctions which plainly leads to malfunction of the epithelium which serves to absorb food and water and protect the body against foreign antigens. Since the discovery that disruption could occur due to reception of certain bacteria such as enterohaemorrhagic E. coli (EHEC) and enteropathogenic E. coli, much research has been done on the bacterial disruption and effects on tight junctions due to the perceived relationship that some pathogens cause symptoms such as diarrhea that are due to various
INTRODUCTION: If a cell is to perform its functions it must maintain a steady state in the midst of an ever changing environment. This steadiness is maintained by the regulation of movement of materials into and out of the cell. To achieve this control, cells are bounded by a delicate membrane that differentiates between different substances, slowing down the movement of some while allowing others to pass through. The membrane is said to be differentially permeable since not all substances penetrate equally well. Selective permeability is a characteristic of healthy, intact cells. When a cell is seriously damaged, the membrane becomes permeable to virtually to everything and substances can move freely in and out of the cell. (Marieb 2013)
These barrier-forming cells are called "endothelial cells". You can think of "endothelial" as a synonym for "lining" or even just "barrier".