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If you google visceral and parietal you get: The parietal layers of the membranes line the walls of the body cavity (pariet- refers to a cavity wall). The visceral layer of the membrane covers the organs (the viscera).
but the first image that pops up is this :
I don't understand how the inner layer is covering and the outer is lining ?
Yes, the parietal pleura is on the wall of the thorax. That picture isn't great. Each lung has its own pleural cavity, ie its own visceral+parietal. Another important thing is the folding over. Imagine the parietal pleura running along the inside of the ribcage… when it gets to the middle of the chest (the mediastinum), it folds over, or "turns the corner", and is now the visceral pleural running along the surface of the lungs. The pericardium functions similarly, and so does the peritoneum/mesentery. Here's another diagram that could help:
Use of Mesothelial Cells and Biological Matrices for Tissue Engineering of Simple Epithelium Surrogates
Tissue-engineering technologies have progressed rapidly through last decades resulting in the manufacture of quite complex bioartificial tissues with potential use for human organ and tissue regeneration. The manufacture of avascular monolayered tissues such as simple squamous epithelia was initiated a few decades ago and is attracting increasing interest. Their relative morphostructural simplicity makes of their biomimetization a goal, which is currently accessible. The mesothelium is a simple squamous epithelium in nature and is the monolayered tissue lining the walls of large celomic cavities (peritoneal, pericardial, and pleural) and internal organs housed inside. Interestingly, mesothelial cells can be harvested in clinically relevant numbers from several anatomical sources and not less important, they also display high transdifferentiation capacities and are low immunogenic characteristics, which endow these cells with therapeutic interest. Their combination with a suitable scaffold (biocompatible, degradable, and non-immunogenic) may allow the manufacture of tailored serosal membranes biomimetics with potential spanning a wide range of therapeutic applications, principally for the regeneration of simple squamous-like epithelia such as the visceral and parietal mesothelium vascular endothelium and corneal endothelium among others. Herein, we review recent research progresses in mesothelial cells biology and their clinical sources. We make a particular emphasis on reviewing the different types of biological scaffolds suitable for the manufacture of serosal mesothelial membranes biomimetics. Finally, we also review progresses made in mesothelial cells-based therapeutic applications and propose some possible future directions.
Keywords: biological matrices biomaterials corneal endothelium epithelial surrogates mesothelial cells serosal membranes simple epithelia tissue engineering.
What is Omentum
Omentum is an abdominal structure derived from the visceral peritoneum, extending from the stomach and the proximal part of the duodenum to the other organs of the abdomen. Generally, the two main types of omenta are the greater omentum and the lesser omentum .
The greater omentum consists of four layers of the visceral peritoneum. It originates from the greater curvature of the stomach and the proximal part of the duodenum. It is attached to the anterior surface of the transverse colon by folding back up. Moreover, the ‘abdominal policemen’ refers to the greater omentum due to its role in immunity, preventing visceral infections. The three components of the greater omentum include the g astrocolic ligament, which is the largest component, the g astrosplenic ligament that extends up to the hilus of the spleen, and the g astrophrenic ligament.
Figure 1: The Greater Omentum
The lesser omentum , which is smaller than the greater omentum, consists of two layers of visceral peritoneum. I t originates from the lesser curvature of the stomach and to the proximal part of the duodenum. And, at the end, it is attached to the liver. Furthermore, the two components of the lesser omentum include the g astrohepatic ligament, which is flat and broad, and the h epatoduodenal ligament, which is the free edge. Moreover, the gastrohepatic ligament is attached to the left lobe of the liver, while the hepatoduodenal ligament contains the portal triad the portal vein, hepatic artery, and the common bile duct.
Figure 2: The Lesser Omentum
Autotaxin signaling governs phenotypic heterogeneity in visceral and parietal mesothelia
Mesothelia, which cover all coelomic organs and body cavities in vertebrates, perform diverse functions in embryonic and adult life. Yet, mesothelia are traditionally viewed as simple, uniform epithelia. Here we demonstrate distinct differences between visceral and parietal mesothelia, the most basic subdivision of this tissue type, in terms of gene expression, adhesion, migration, and invasion. Gene profiling determined that autotaxin, a secreted lysophospholipase D originally discovered as a tumor cell-motility-stimulating factor, was expressed exclusively in the more motile and invasive visceral mesothelia and at abnormally high levels in mesotheliomas. Gain and loss of function studies demonstrate that autotaxin signaling is indeed a critical factor responsible for phenotypic differences within mesothelia. Furthermore, we demonstrate that known and novel small molecule inhibitors of the autotaxin signaling pathway dramatically blunt migratory and invasive behaviors of aggressive mesotheliomas. Taken together, this study reveals distinct phenotypes within the mesothelial cell lineage, demonstrates that differential autotaxin expression is the molecular underpinning for these differences, and provides a novel target and lead compounds to intervene in invasive mesotheliomas.
Conflict of interest statement
Competing Interests: The authors have declared that no competing interests exist.
Figure 1. Visceral and parietal mesothelia have…
Figure 1. Visceral and parietal mesothelia have significantly different gene expression profiles.
Figure 2. Autotaxin is expressed at significantly…
Figure 2. Autotaxin is expressed at significantly higher levels in visceral mesothelia compared to parietal.
Figure 3. Autotaxin activity is significantly up-regulated…
Figure 3. Autotaxin activity is significantly up-regulated in visceral mesothelia and mesotheliomas.
Figure 4. Visceral mesothelial cells are more…
Figure 4. Visceral mesothelial cells are more adherent then their parietal counterparts.
Figure 5. Mesothelia have varying abilities to…
Figure 5. Mesothelia have varying abilities to migrate.
Visceral mesothelial (A), parietal mesothelial (B), pleural…
Figure 6. Autotaxin signaling regulates mesothelial and…
Figure 6. Autotaxin signaling regulates mesothelial and mesothelioma cell invasion.
Visceral mesothelial, parietal mesothelial, pleural…
Figure 7. Autotaxin signaling regulates mesothelial and…
Figure 7. Autotaxin signaling regulates mesothelial and mesothelioma cell migration.
The role of cell interactions in the differentiation of teratocarcinoma-derived parietal and visceral endoderm
Cell interactions have been implicated in the differentiation of visceral and parietal endoderm in the developing mouse embryo. Embryoid bodies formed from F9 embryonal carcinoma cells have been useful in characterizing the events which lead to endoderm formation. As part of our effort to specify the interactions which may be involved in this process we have isolated visceral endoderm-like cells (VE) from F9 embryoid bodies and cultured them under various conditions. Using a combination of immunoprecipitation and enzyme-linked immunosorbent assay, we demonstrate that monolayer culture of these cells on a number of different substrates leads to a dramatic decrease in the level of alphafetoprotein (AFP), a VE-specific marker. Northern blot analysis of AFP mRNA indicates very low levels of this message are present after 48 hr in monolayer culture. Coincident with the drop in AFP levels is an increase in the levels of the cytokeratin Endo C and tissue plasminogen activator, both markers for parietal endoderm (PE). Morphological evidence at the ultrastructural level supports a transition from VE to PE. In contrast, the VE phenotype can be maintained in vitro by interaction with aggregates, but not monolayers, of stem cells. In addition, culturing the cells on the curved surface of gelatin-coated dextran beads, but not on a flat gelatin surface facilitates AFP expression and the cells are morphologically intermediate between VE and PE cells. The potential role of junctional complexes and cell shape are discussed.
Regulation of the differentiation and behaviour of extra-embryonic endodermal cells by basement membranes
Both the extracellular matrix and parathyroid hormone-related peptide (PTHrP) have been implicated in the differentiation and migration of extra-embryonic endodermal cells in the pre-implantation mammalian blastocyst. In order to define the individual roles and interactions between these factors in endodermal differentiation, we have used embryoid bodies derived from Lamc1(-/-) embryonic stem cells that lack basement membranes. The results show that in the absence of basement membranes, increased numbers of both visceral and parietal endodermal cells differentiate, but they fail to form organised epithelia. Furthermore, although parietal endodermal cells only migrate away from control embryoid bodies in the presence of PTHrP, they readily migrate from Lamc1(-/-) embryoid bodies in the absence of PTHrP, and this migration is unaffected by PTHrP. Thus, the basement membrane between epiblast and extra-embryonic endoderm is required for the proper organisation of visceral and parietal endodermal cells and also restricts their differentiation to maintain the population of primitive endodermal stem cells. Moreover, this basement membrane inhibits migration of parietal endodermal cells, the role of PTHrP being to stimulate delamination of parietal endodermal cells from the basement membrane rather than promoting migration per se.
The addition of dibutyryl cyclic AMP (dbcAMP) to aggregate cultures of F9 cells in medium containing retinoic acid (RA) directs the pathway of differentiation into parietal endoderm instead of visceral endoderm. We examined the levels of some of the markers that characterize the two pathways and studied the time of commitment of cells to either direction of differentiation by using immunoprecipitation and enzyme-linked immunosorbent assays (ELISA). For either pathway, the levels and patterns of laminin, type IV collagen, and fibronectin are the same on the first day of differentiation, characterized by slightly decreased levels of laminin and type IV collagen synthesis and an increased level of fibronectin synthesis. These levels reverse on the second day of culture when the pathways diverge markedly. The differentiation pathway, however, can be redirected into the alternate one parietal endoderm cells become committed after 3 days, whereas visceral endoderm cells are able to change into parietal endoderm cells at any time. Thus, α-fetoprotein (AFP)-producing F9 embryoid bodies switched to dbcAMP-containing medium lose the capacity to synthesize AFP and start to express genes characteristic of parietal endoderm. Our results indicate that at least some visceral endoderm cells may redifferentiate into parietal endoderm cells. These phenomena thus mimic features of endoderm differentiation in the mouse embryo.
This work is supported by grants from the National Institutes of Health: HD 18782 and P30 CA 30199.
Department of Physiology, University of Thessaly Medical School, Mezourlo Hill, 41110, Larissa, Greece
Sotirios Zarogiannis, Triantafyllia Deligiorgi, Paschalis Adam Molyvdas & Chrissi Hatzoglou
Department of Nephrology, University of Thessaly Medical School, Mezourlo Hill, 41110, Larissa, Greece
Ioannis Stefanidis & Vassilios Liakopoulos
Department of Respiratory Medicine, University of Thessaly Medical School, Mezourlo Hill, 41110, Larissa, Greece
Parietal Pleura lines the inside of the thoracic cavity or chest wall, while visceral pleura lines the outside of the lungs.
In between the parietal pleura and visceral pleura is the pleural space or pleural cavity.
The innervation of the parietal pleura and visceral pleura differs too. Parietal pleura is innervated by the phrenic and intercostal nerves, while the visceral pleura is innervated by the pulmonary plexus from the sympathetic trunk and vagus nerve.
Parietal pleura feels pressure, pain, and temperature. Visceral pleura only senses stretch, not touch, pain, or temperature.
Previous work by us and others has demonstrated that podocyte damage, apoptosis and podocyte loss are critical steps in the development of glomerulosclerosis [ 15–18 ]. The reason for podocyte damage can be a genetic defect leading to misexpression or loss of podocyte specific proteins, activation of TGF−β and/or a changed expression of extracellular or intracellular signalling modifiers [ 16–19 ]. As a result podocytes may dedifferentiate, detach and/or undergo apoptosis. As a logical consequence, the detached cells should be detectable in the urine. Many groups have tried to quantify excreted podocytes with various technical approaches in human disease. Hara et al . report excretion of podocytes detected with a PDX immunofluorescence technique on cytospins [ 5–7 , 14 ]. They report higher levels of PDX-positive cells in FSGS compared to MCD and MGN as well as in IgA and Henoch Schönlein Purpura. Vogelmann et al . describe excretion of viable PDX-positive cells in patients with active FSGS and active lupus nephritis [ 8 ]. Their results are similar but all related to the specificity of PDX as a podocyte specific marker. We can partially confirm their results however, with our method we cannot detect markers of mature differentiated podocytes (e.g. synaptopodin, WT-1 or nephrin) in the majority of the PDX-positive cells. Instead we detected by double immunofluorescence PGP9.5 a marker of PECs and CK8–18, a cytokeratin, that is regularly not expressed on mature podocytes. When we stained the corresponding biopsies of patients for these markers, we found that the majority of the detected cells originate from the parietal side of the glomerulus rather than the visceral epithelium. Nevertheless we find a strong relationship between the number of excreted PDX-positive cells and disease activity in patients with FSGS, MGN and MPGN. Strikingly, we never detected PDX-positive cells in the urine of patients with active MCD. These results would indicate that PDX-positive cells might be a good non-invasive marker for disease activity in FSGS, MGN and MPGN and could be used for monitoring of treatment success in these patients. This is especially of interest since detachment of the cells might be a more specific marker of ongoing glomerular damage than proteinuria, as proteinuria can also be the expression of residual scarring processes rather than active disease. A similar finding was described by Yu and co-workers in three different rodent models of glomerular disease [ 3 ]. They demonstrated persistent proteinuria despite remission of podocyturia. Since the rate of PDX-positive cell excretion reflects disease activity, but not the disease type, monitoring of these cells cannot replace a biopsy however, it might be a very helpful tool for the differentiation of MCD and FSGS. Excretion of these cells certainly reflects better on both organs and all glomeruli, whereas a biopsy might miss early stages of a focal disease. Interestingly, we can obtain similar results if we just quantify the total amount of cells that adhere in our urine cultures overnight, since the total amount of intact cells correlates highly with the amount of PDX-positive cells. PDX was initially described as a podocyte-associated membrane protein. Later it was also detected on endothelial cells [ 20–23 ]. Our results suggest that PECs express PDX as well. We used two different antibodies: a polyclonal antibody (R&D Systems) and a monoclonal antibody (gift from Dontscho Kerjaschki). Both antibodies resulted in positive staining of PECs on kidney biopsies in a concentration dependent effect: after serial dilutions with both antibodies, we can only detect PDX staining on podocytes whereas endothelial cells and PECs are negative (data not shown). Therefore PDX staining of PECs can be easily missed when the research focus is on podocytes. Interestingly Bariety et al . describe ‘parietal podocytes’ in normal kidney samples [ 24 ]. They found cells expressing podocyte specific proteins lining Bowman's capsule and demonstrated PDX staining along the circumference of Bowman's capsule. The other cell population we detected is the PDX-positive cells in the urine that do not co-express cytokeratin. These cells cannot be attributed to a specific cell type. They might originate from either the visceral or the parietal side, and thus these cells might have been podocytes. PDX staining seems to persist in various disease states, whereas other markers have been described to get lost with dedifferentiation [ 14 , 25 ]. Podocytes might undergo phenotypic changes before, during or after detachment from the glomerular basement membrane [ 26–28 ]. This might be the same for other glomerular cells that are shed into the urine.
Therefore the identification of glomerular cells detected in the urine sediment will always carry the risk of describing artificially expressed marker proteins. In the present study we present evidence that PDX-positive cells are excreted in active glomerular diseases. We demonstrate that a significant amount of cells originate from the parietal epithelial cell layer, indicating that in active glomerular disease parietal epithelial cells might react with proliferation and shedding. The number of cells reflects the disease activity however, it is not a tool to differentiate between various glomerular diseases. Nevertheless, in paediatric patients these cells might help with decision making of taking a biopsy since we could not detect the cells in active MCD. Further studies are on the way to validate our data in other glomerular diseases and in prospective studies.
Since PECs are found in high amounts in the urine in active disease states, this could be interpreted as reaction secondary to ongoing tissue damage. Therefore our data provide evidence for a significant crosstalk of glomerular cells in active disease. The question arises why PECs shed in the urine in high amounts and why this correlates with disease activity. There is recent evidence that PECs can transdifferentiate to podocytes and repopulate the glomerulus in animal models (personnel communication Marcus Moeller, Aachen). In addition there is evidence that a subset of PECs coexpresses stem cell markers CD24 and CD133 as well as the stem cell specific transcription factors Oct-4 and BmI-1 [ 29 ]. It is an intriguing hypothesis that the PDX-positive cells that we are detecting in the urine are not a read-out of ongoing cell damage, but instead are a read-out of ongoing regeneration. However a more detailed characterization of the urinary cells is necessary to prove that they truly originate from the parietal epithelial cell layer. With our overnight cultures we might have selected out this specific subfraction of cells, whereas the detached and dying podocytes are not detected using our method. We are in the process of analyzing expression of stem cell markers in our cell population and characterizing the transdifferentiation potential of the PDX-positive cells isolated from patient urine in vitro . Further analysis and understanding of this ‘parietal epithelial shedding’ in the urine might help to understand disease progression in glomerular disease.
We would like to thank Heike Lührs for excellent technical assistance. This work was supported by grant support from the German Research Council (Emmy Noether Fellowship Grant Schi 587/2) to M.S.
Conflict of interest statement. None declared. The results presented in this paper have not been published previously in whole or part, except in abstract format.