⚡ Role Stressors

Monday, October 11, 2021 6:23:36 AM

Role Stressors



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Creating a compassionate university

Tomlin, and Mary Anne P. The theory draws concepts from a variety of sources. Modeling recognizes that each patient has a unique perspective of his or her own world. These perspectives are called models. Role modeling is the process by which the nurse facilitates and nurtures the individual in attaining, maintaining, and promoting health. Hypoxia, inflammation, mechanical and chemical stress have been examined as to how they relate to perlecan expression. Hypoxia is a condition found in disease states and during injury and often results in a lack of endothelial cell proliferation.

This and perlecan's role as endorepellin prompted one study into the nature of perlecan expression regulation by endothelial cells during hypoxic conditions. The contention of this paper is that perlecan downregulation leads to a loss of FAK activation and thus less ERK signaling, leading to decreased cell proliferation. It does seem counterintuitive that endothelial cells would proliferate less quickly due to loss of perlecan and its endorepellin subunit.

It could be that these endothelial cells merely downregulated transcription of many genes in response to hypoxic conditions. In another study, hypoxia led to induction of genes associated with apoptosis and cell death, but repression of genes was not limited to proteins associated with a specific pathway. This difference between endothelial cells from the study in and the epithelial cell studied in these experiments is indicative of how varied the regulatory mechanisms of perlecan may be in different cell types. The development of beta-amyloid plaques on the brain is associated with onset of Alzheimer's disease. These plaques induce a constant state of inflammation in areas of accumulation, leading to expression of certain inflammation-related gene products, some of which perpetuate the inflammation in the brain context.

As previously mentioned, to investigate the effect of brain inflammation on expression levels of perlecan, needle stab wounds were created in mice brains, and after inflammation and variable periods of recovery, mRNA and protein levels were assessed via in situ hybridization and immunostaining. Perlecan levels were increased in the hippocampus but not in the striatum during the healing period, along with IL 1-alpha expression. This role for perlecan in beta-amyloid plaque generation is supported by an earlier study showing that perlecan and beta-amyloid treatment of rat brains led to formation of senile plaques, whereas treatment with beta-amyloid alone did not have the same effect.

At the organismic level, mechanical stress has a profound impact on extracellular matrix integrity and probably causes induction of a number of ECM genes for repair and remodeling of ECM in tissue stroma and basement membranes. One study examined the in vitro effects of pressure on global gene transcription using a microarray approach and a cell stretching system meant to simulate intraocular pressure in the lamina cribosa connective tissue of the optic nerve head.

Their findings were that perlecan and several other proteoglycans were upregulated in response to the stretching stimulus. Using a similar cell stretching mechanism to mimic arterial pressure, this investigation showed that perlecan production increased in response to mechanical strain. In this case, it seems that the molecule's signaling function is the operative upregulated factor, especially due to the increase in sulfation of the heparan sulfate chains. Chemical damage to organs can affect not only the cell's genetic and mechanical integrity but the extracellular matrix of the tissue. To study the effect of chemical damage on liver cells, wistar rats were treated with carbon tetrachloride for 48 hours prior to sacrificing.

Prior to treatment with CCl 4 , perlecan staining was limited to the bile duct and sinusoidal blood vessels of the liver. After treatment, perlecan staining was intense in areas of necrosis. This could have been due to the increase in capillarization of the liver as an attempt to regenerate damaged tissue. One of the resounding arguments against the validity of in vitro results of cell culture on 2D plastic plates is that the environment does not accurately reflect that of the cells in the organism.

This problem is being dealt with by developing 3D cell cultures using a wide variety of substrates as the scaffolds or environments for the cells. In this kind of setting the expression of ECM genes has the potential to more closely resemble that of the native expression profile. One such system has been developed to study skin development and basal membrane formation between keratinocytes and the stroma. Another system using a disorganized hydrated collagen I gel has been used to demonstrate that primary human corneal fibroblasts will eventually invade the gel and create a matrix consisting of collagen type I and perlecan, as well as several other sulfated matrix glycoproteins.

This mimics the in vivo corneal fibroblast's developmental program and response to injury. One of the long-term goals of creating 3D cell culture systems is to engineer tissues that can be used as replacements for patients with many types of disease. In tissue engineered heart valves created by seeding myofibroblasts onto collagen type I followed by endothelial cells, heparan sulfate proteoglycan expression has been verified, although no distinction between syndecan and perlecan has been made in these tissues.

Transplanted tissue must remain intact, which requires a pre-formed basement membrane. Collagen gels have promoted formation of a complete basement membrane by corneal epithelial cells in culture. Perlecan also holds promise to serve as a scaffold for plating cells in culture. Human salivary gland ductal and acinar cells have been successfully grown on a bioactive peptide containing a sequence repeated in domain IV of the perlecan protein. These cells reproduce acini-like structures similar to those found in the native gland and tight junctions, along with complete basement membranes in culture. While Perlecan suppression causes substantial inhibition of tumor growth and neovascularization in null mice, in contrast, when perlecan-null cells are injected into nude mice enhanced tumor growth is observed when compared to controls.

Cancer progression and pathogenesis is intimately linked to extracellular matrix composition and the role of perlecan and other ECM molecules in cancer is being studied by a large number of laboratories. Since the basement membrane is the first obstacle in the way of extravasating carcinoma cells, the functions of perlecan in this process are multiple. MeWo cells are characteristically less invasive than their clonal variant cell line 70W. One lab studied perlecan expression in 27 invasive melanomas and 26 of the 27 samples showed a significant increase in perlecan message when compared to normal tissue from the same patients.

They then used the MeWo and 70W cell lines to study if perlecan expression changed during treatment with neurotrophins, which can stimulate cell invasion through matrigel in vitro. The more invasive 70W cells began expressing perlecan message ten minutes after stimulation with the neurotrophins, and the MeWo cells did not produce any pln message regardless of treatment. This study took special note of the fact that perlecan upregulation occurred even before that of heparanase, an essential protein involved in the process of extravasation.

In ovarian cancer as in other cancers, perlecan expression occurs differently throughout progression of the disease. Perlecan staining is lost in ovarian basement membrane that has been breached by an invasive adenocarcinoma, which is in contrast to perlecan staining in the basement membranes of normal ovaries and those with benign tumors, where basement membrane is homogeneous and very similar in composition to that in other normal tissues.

RT cells with perlecan knocked down by antisense did not show tumor formation in this system, however cells expressing the antisense perlecan and a recombinant construct encoding domains I, II, and III of mouse perlecan did indeed show tumor formation. Thus in this system it does appear that tumor cell expression of perlecan is necessary for tumor aggregation. Several laboratories have studied in vitro tumor cell angiogenesis using antisense constructs to the perlecan message. The full-length reverse complement cDNA, driven by a strong promoter, is transfected into various cell types to completely eliminate perlecan expression. Antisense in colon carcinoma cells blocks perlecan translation, leading to decreased tumor growth and angiogenesis.

A ribozyme construct was created for use in knocking down perlecan translation levels. This ribozyme was targeted at a sequence coding domain I of the perlecan protein. What this disparity in results means for invasion is unknown, although it is true that perlecan is part of the extracellular matrix in mesenchymal tissue, and cells undergoing epithelial-mesenchymal transition EMT may upregulate perlecan expression as part of their EMT programming. Perlecan levels are decreased in many disease states - e. Perlecan has an important role in the maintenance of the glomerular filtration barrier. Perlecan expression is down regulated by many atherogenic stimuli and thus Perlecan is thought to play a protective role in atherosclerosis.

Synthesis of heparan sulfate was shown to decrease in the arteries of diabetics and in arteries developing atherosclerotic lesions. The mechanism by which heparan sulfate was downregulated in these lesions remained unknown for some time. One theory states that high glucose in circulation could lead to a decrease in GAG chain attachment to perlecan, but not necessarily a change in the synthetic pathway of the GAG chains or that of the core protein. After treatment of human aortic endothelial cells with high glucose medium, secreted perlecan contained less sulfate incorporation accompanied by less overall GAG chain incorporation. It is also noted that similar decreases in extracellular HS without a change in staining for the core protein chains occur in diabetic kidneys and in kidney cells in culture treated with high glucose.

Atherosclerosis is most often the culprit in coronary heart disease and other cardiovascular conditions, and a large aggregation of perlecan protein is symptomatic of advanced atherosclerotic plaques. VSMCs are the producers of the perlecan in this condition, meaning that a good deal of research has been focused on understanding the means of perlecan upregulation in this condition. In a test of the effect of circulating nonesterified fatty acids symptomatic of diabetes and atherogenesis on perlecan expression by VSMCs, expression did not change when compared to control cells.

This was in contrast to a fold increase in expression of other basement membrane proteoglycans. This concept is similar to previously mentioned studies showing that perlecan is only produced by VSMCs once they have ceased proliferation during development. Perlecan has been shown to interact with. From Wikipedia, the free encyclopedia. Chromosome 1 human [1]. Seeing the silver lining: cognitive reappraisal ability moderates the relationship between stress and depressive symptoms. Was this page helpful? Thanks for your feedback! Sign Up. What are your concerns? Article Sources. Verywell Mind uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read our editorial process to learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.

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