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Molecular Mechanisms of Peritoneal Membrane Pathophysiology

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A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (1 April 2021) | Viewed by 42356

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Dr. Sotirios Zarogiannis

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Guest Editor

1. Faculty of Medicine, University of Thessaly, Larissa, Greece
2. Center for Pediatrics and Adolescent Medicine, Heidelberg, Germany
Interests: mesothelial physiology; mesothelial pathophysiology; mesothelioma; tight junctions; adherens junctions; ion transport; water transport; biomarkers; serosal effusions; computational biology
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Prof. Claus Peter Schmitt

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Guest Editor

Center for Pediatrics and Adolescent Medicine, Heidelberg, Germany
Interests: peritoneal dialysis; chronic kidney disease; mineral bone metabolism; cardiovascular disease; histidin dipeptide metabolism in kidney disease; children; reactive metabolites; European Research Consortium Improve PD; International Pediatric Dialysis Network; International Pediatric Peritoneal Biobank

Special Issue Information

Dear Colleagues,

The peritoneal membrane is the largest internal membrane of the human body, having a surface area that approximates the skin surface area. It vests the walls of the abdominal cavity (parietal peritoneum) and the surface of the internal organs (visceral peritoneum) and comprises a monolayer of mesothelial cells underneath of which there is connective tissue with blood vessels, nerves, lymphatics, and fibroblasts.

The peritoneal membrane has not been sufficiently studied despite the fact that several pathological conditions are linked to it, namely, the development of abdominal adhesions after surgery, peritoneal metastasis or primary peritoneal mesothelioma development, as well as abdominal infection leading to the development of peritonitis and ascites. Furthermore, the peritoneum serves as a semipermeable membrane in peritoneal dialysis—a widespread renal replacement therapy in patients with end-stage renal disease. However, the modality has limited efficacy and a finite technique survival rate due to progressive fibrosis and excessive angiogenesis ultimately leading to ultrafiltration failure.

The goal of this Special Issue is to attract original research articles as well as reviews that will broaden our current knowledge on the molecular mediators and mechanisms that govern the response of the peritoneum to infectious and non-infectious stimuli such as surgical complications and peritoneal dialysis, to malignancies and associated ascites formation. Molecular signatures, biomarkers, and therapeutic prospects are of particular interest. This Special Issue will give a comprehensive overview of current knowledge on peritoneal pathophysiology from different perspectives and disciplines to stimulate novel scientific approaches to understanding and treating the largest human serosal membrane.

Prof. Sotirios Zarogiannis
Prof. Claus Peter Schmitt
Guest Editors

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Keywords

peritoneum
mesothelium
abdominal adhesions
mesothelioma
peritoneal carcinoma
peritoneal dialysis
peritonitis
ascites
molecular signatures
biomarkers

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Published Papers (11 papers)

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Editorial

Jump to: Research, Review

5 pages, 204 KiB

Open AccessEditorial

Molecular Mechanisms of Peritoneal Membrane Pathophysiology

by Sotirios G. Zarogiannis and Claus Peter Schmitt

Biomolecules 2022, 12(6), 757; https://doi.org/10.3390/biom12060757 - 29 May 2022

Viewed by 1905

Abstract

The peritoneal membrane is the largest internal membrane of the human body, having a surface area that approximates the surface area of the skin [...] Full article

(This article belongs to the Special Issue Molecular Mechanisms of Peritoneal Membrane Pathophysiology)

Research

Jump to: Editorial, Review

10 pages, 1290 KiB

Open AccessArticle

Comparison of Isotonic Activation of Cell Volume Regulation in Rat Peritoneal Mesothelial Cells and in Kidney Outer Medullary Collecting Duct Principal Cells

by Galina S. Baturina, Liubov E. Katkova, Claus Peter Schmitt, Evgeniy I. Solenov and Sotirios G. Zarogiannis

Biomolecules 2021, 11(10), 1452; https://doi.org/10.3390/biom11101452 - 3 Oct 2021

Cited by 6 | Viewed by 1999

Abstract

In disease states, mesothelial cells are exposed to variable osmotic conditions, with high osmotic stress exerted by peritoneal dialysis (PD) fluids. They contain unphysiologically high concentrations of glucose and result in major peritoneal membrane transformation and PD function loss. The effects of isotonic entry of urea and myo-inositol in hypertonic (380 mOsm/kg) medium on the cell volume of primary cultures of rat peritoneal mesothelial cells and rat kidney outer medullary collecting duct (OMCD) principal cells were studied. In hypertonic medium, rat peritoneal mesothelial cells activated a different mechanism of cell volume regulation in the presence of isotonic urea (100 mM) in comparison to rat kidney OMCD principal cells. In kidney OMCD cells inflow of urea into the shrunken cell results in restoration of cell volume. In the shrunken peritoneal mesothelial cells, isotonic urea inflow caused a small volume increase and activated regulatory volume decrease (RVD). Isotonic myo-inositol activated RVD in hypertonic medium in both cell types. Isotonic application of both osmolytes caused a sharp increase of intracellular calcium both in peritoneal mesothelial cells and in kidney OMCD principal cells. In conclusion, peritoneal mesothelial cells exhibit RVD mechanisms when challenged with myo-inositol and urea under hyperosmolar isotonic switch from mannitol through involvement of calcium-dependent control. Myo-inositol effects were identical with the ones in OMCD principal cells whereas urea effects in OMCD principal cells led to no RVD induction. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Peritoneal Membrane Pathophysiology)

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21 pages, 2405 KiB

Open AccessArticle

Peritoneal Dialysis Fluid Supplementation with Alanyl-Glutamine Attenuates Conventional Dialysis Fluid-Mediated Endothelial Cell Injury by Restoring Perturbed Cytoprotective Responses

by Rebecca Herzog, Maria Bartosova, Silvia Tarantino, Anja Wagner, Markus Unterwurzacher, Juan Manuel Sacnun, Anton M. Lichtenauer, Lilian Kuster, Betti Schaefer, Seth L. Alper, Christoph Aufricht, Claus Peter Schmitt and Klaus Kratochwill

Biomolecules 2020, 10(12), 1678; https://doi.org/10.3390/biom10121678 - 15 Dec 2020

Cited by 20 | Viewed by 3395

Abstract

Long-term clinical outcome of peritoneal dialysis (PD) depends on adequate removal of small solutes and water. The peritoneal endothelium represents the key barrier and peritoneal transport dysfunction is associated with vascular changes. Alanyl-glutamine (AlaGln) has been shown to counteract PD-induced deteriorations but the effect on vascular changes has not yet been elucidated. Using multiplexed proteomic and bioinformatic analyses we investigated the molecular mechanisms of vascular pathology in-vitro (primary human umbilical vein endothelial cells, HUVEC) and ex-vivo (arterioles of patients undergoing PD) following exposure to PD-fluid. An overlap of 1813 proteins (40%) of over 3100 proteins was identified in both sample types. PD-fluid treatment significantly altered 378 in endothelial cells and 192 in arterioles. The HUVEC proteome resembles the arteriolar proteome with expected sample specific differences of mainly immune system processes only present in arterioles and extracellular region proteins primarily found in HUVEC. AlaGln-addition to PD-fluid revealed 359 differentially abundant proteins and restored the molecular process landscape altered by PD fluid. This study provides evidence on validity and inherent limitations of studying endothelial pathomechanisms in-vitro compared to vascular ex-vivo findings. AlaGln could reduce PD-associated vasculopathy by reducing endothelial cellular damage, restoring perturbed abundances of pathologically important proteins and enriching protective processes. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Peritoneal Membrane Pathophysiology)

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19 pages, 4114 KiB

Open AccessArticle

SGLT2 Inhibition by Intraperitoneal Dapagliflozin Mitigates Peritoneal Fibrosis and Ultrafiltration Failure in a Mouse Model of Chronic Peritoneal Exposure to High-Glucose Dialysate

by Michael S. Balzer, Song Rong, Johannes Nordlohne, Jan D. Zemtsovski, Sonja Schmidt, Britta Stapel, Maria Bartosova, Sibylle von Vietinghoff, Hermann Haller, Claus P. Schmitt and Nelli Shushakova

Biomolecules 2020, 10(11), 1573; https://doi.org/10.3390/biom10111573 - 19 Nov 2020

Cited by 45 | Viewed by 5273

Abstract

Peritoneal dialysis (PD) is limited by glucose-mediated peritoneal membrane (PM) fibrosis, angiogenesis, and ultrafiltration failure. Influencing PM integrity by pharmacologically targeting sodium-dependent glucose transporter (SGLT)-mediated glucose uptake has not been studied. In this study, wildtype C57Bl/6N mice were treated with high-glucose dialysate via an intraperitoneal catheter, with or without addition of selective SGLT2 inhibitor dapagliflozin. PM structural changes, ultrafiltration capacity, and peritoneal equilibration testing (PET) status for glucose, urea, and creatinine were analyzed. Expression of SGLT and facilitative glucose transporters (GLUT) was analyzed by real-time PCR, immunofluorescence, and immunohistochemistry. Peritoneal effluents were analyzed for cellular and cytokine composition. We found that peritoneal SGLT2 was expressed in mesothelial cells and in skeletal muscle. Dapagliflozin significantly reduced effluent transforming growth factor (TGF-β) concentrations, peritoneal thickening, and fibrosis, as well as microvessel density, resulting in improved ultrafiltration, despite the fact that it did not affect development of high-glucose transporter status. In vitro, dapagliflozin reduced monocyte chemoattractant protein-1 release under high-glucose conditions in human and murine peritoneal mesothelial cells. Proinflammatory cytokine release in macrophages was reduced only when cultured in high-glucose conditions with an additional inflammatory stimulus. In summary, dapagliflozin improved structural and functional peritoneal health in the context of high-glucose PD. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Peritoneal Membrane Pathophysiology)

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17 pages, 4895 KiB

Open AccessArticle

Alanyl-Glutamine Restores Tight Junction Organization after Disruption by a Conventional Peritoneal Dialysis Fluid

by Maria Bartosova, Rebecca Herzog, David Ridinger, Eszter Levai, Hanna Jenei, Conghui Zhang, Guadalupe T. González Mateo, Iva Marinovic, Thilo Hackert, Felix Bestvater, Michael Hausmann, Manuel López Cabrera, Klaus Kratochwill, Sotirios G. Zarogiannis and Claus Peter Schmitt

Biomolecules 2020, 10(8), 1178; https://doi.org/10.3390/biom10081178 - 13 Aug 2020

Cited by 21 | Viewed by 4188

Abstract

Understanding and targeting the molecular basis of peritoneal solute and protein transport is essential to improve peritoneal dialysis (PD) efficacy and patient outcome. Supplementation of PD fluids (PDF) with alanyl-glutamine (AlaGln) increased small solute transport and reduced peritoneal protein loss in a recent clinical trial. Transepithelial resistance and 10 kDa and 70 kDa dextran transport were measured in primary human endothelial cells (HUVEC) exposed to conventional acidic, glucose degradation products (GDP) containing PDF (CPDF) and to low GDP containing PDF (LPDF) with and without AlaGln. Zonula occludens-1 (ZO-1) and claudin-5 were quantified by Western blot and immunofluorescence and in mice exposed to saline and CPDF for 7 weeks by digital imaging analyses. Spatial clustering of ZO-1 molecules was assessed by single molecule localization microscopy. AlaGln increased transepithelial resistance, and in CPDF exposed HUVEC decreased dextran transport rates and preserved claudin-5 and ZO-1 abundance. Endothelial clustering of membrane bound ZO-1 was higher in CPDF supplemented with AlaGln. In mice, arteriolar endothelial claudin-5 was reduced in CPDF, but restored with AlaGln, while mesothelial claudin-5 abundance was unchanged. AlaGln supplementation seals the peritoneal endothelial barrier, and when supplemented to conventional PD fluid increases claudin-5 and ZO-1 abundance and clustering of ZO-1 in the endothelial cell membrane. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Peritoneal Membrane Pathophysiology)

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12 pages, 1714 KiB

Open AccessArticle

Fibrinogen Fucosylation as a Prognostic Marker of End-Stage Renal Disease in Patients on Peritoneal Dialysis

by Marko Baralić, Nikola Gligorijević, Voin Brković, Jaroslav Katrlík, Lucia Pažitná, Miloš Šunderić, Goran Miljuš, Ana Penezić, Zorana Dobrijević, Mirjana Laušević, Olgica Nedić and Dragana Robajac

Biomolecules 2020, 10(8), 1165; https://doi.org/10.3390/biom10081165 - 9 Aug 2020

Cited by 9 | Viewed by 3536

Abstract

Glycosylation may strongly affect protein structure and functions. A high risk of cardiovascular complications seen in patients with end-stage renal disease (ESRD) is, at least partly associated with delayed clot formation, increased clot strength, and delayed cloth lysis. Taking into consideration that fibrinogen mediates these processes, we isolated fibrinogen from the plasma from patients with ESRD on peritoneal dialysis (ESRD-PD), and examined glycosylation of native fibrinogen and its subunits by lectin-based microarray and lectin blotting. Compared to healthy controls, fibrinogen from patients had increased levels of A2BG2 and decreased levels of FA2 glycan. The distribution of glycans on individual chains was also affected, with the γ chain, responsible for physiological functions of fibrinogen (such as coagulation and platelet aggregation), being most prone to these alterations. Increased levels of multi-antennary N-glycans in ESRD-PD patients were also associated with the type of dialysis solutions, whereas an increase in the fucosylation levels was strongly related to the peritoneal membrane damage. Consequently, investigation of fibrinogen glycans can offer better insight into fibrinogen-related complications observed in ESRD-PD patients and, additionally, contribute to prognosis, choice of personalised therapy, determination of peritoneal membrane damage, and the length of utilization of peritoneum for dialysis. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Peritoneal Membrane Pathophysiology)

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13 pages, 2338 KiB

Open AccessArticle

Vibrational Spectroscopy of Peritoneal Dialysis Effluent for Rapid Assessment of Patient Characteristics

by Tom Grunert, Rebecca Herzog, Florian M. Wiesenhofer, Andreas Vychytil, Monika Ehling-Schulz and Klaus Kratochwill

Biomolecules 2020, 10(6), 965; https://doi.org/10.3390/biom10060965 - 26 Jun 2020

Cited by 6 | Viewed by 3451

Abstract

Peritoneal dialysis (PD) offers specific advantages over hemodialysis, enabling increased autonomy of patients with end-stage renal disease, but PD-related complications need to be detected in a timely manner. Fourier transform infrared (FTIR) spectroscopy could provide rapid and essential insights into the patients’ risk profiles via molecular fingerprinting of PD effluent, an abundant waste material that is rich in biological information. In this study, we measured FTIR spectroscopic profiles in PD effluent from patients taking part in a randomized controlled trial of alanyl-glutamine addition to the PD-fluid. Principal component analysis of FTIR spectra enabled us to differentiate between effluent samples from patients immediately after completion of instillation of the PD-fluid into the patients’ cavity and 4 h later as well as between patients receiving PD-fluid supplemented with 8 mM alanyl-glutamine compared with control. Moreover, feasibility of FTIR spectroscopy coupled to supervised classification algorithms to predict patient-, PD-, as well as immune-associated parameters were investigated. PD modality (manual continuous ambulatory PD (CAPD) vs. cycler-assisted automated PD (APD)), residual urine output, ultrafiltration, transport parameters, and cytokine concentrations showed high predictive potential. This study provides proof-of-principle that molecular signatures determined by FTIR spectroscopy of PD effluent, combined with machine learning, are suitable for cost-effective, high-throughput diagnostic purposes in PD. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Peritoneal Membrane Pathophysiology)

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18 pages, 3076 KiB

Open AccessFeature PaperArticle

Activation of General Control Nonderepressible-2 Kinase Ameliorates Glucotoxicity in Human Peritoneal Mesothelial Cells, Preserves Their Integrity, and Prevents Mesothelial to Mesenchymal Transition

by Theodoros Eleftheriadis, Georgios Pissas, Georgia Antoniadi, Evdokia Nikolaou, Spyridon Golfinopoulos, Vassilios Liakopoulos and Ioannis Stefanidis

Biomolecules 2019, 9(12), 832; https://doi.org/10.3390/biom9120832 - 5 Dec 2019

Cited by 3 | Viewed by 2822

Abstract

Along with infections, ultrafiltration failure due to the toxicity of glucose-containing peritoneal dialysis (PD) solutions is the Achilles’ heel of PD method. Triggered by the protective effect of general control nonderepressible-2 (GCN-2) kinase activation against high-glucose conditions in other cell types, we evaluated whether the same occurs in human peritoneal mesothelial cells. We activated GCN-2 kinase with halofuginone or tryptophanol, and assessed the impact of this intervention on glucose transporter-1, glucose transporter-3, and sodium-glucose cotransporter-1, glucose influx, reactive oxygen species (ROS), and the events that result in glucotoxicity. These involve the inhibition of glyceraldehyde 3-phosphate dehydrogenase and the diversion of upstream glycolytic products to the aldose pathway (assessed by D-sorbitol), the lipid synthesis pathway (assessed by protein kinase C activity), the hexosamine pathway (determined by O-linked β-N-acetyl glucosamine-modified proteins), and the advanced glycation end products generation pathway (assessed by methylglyoxal). Then, we examined the production of the profibrotic transforming growth factor-β1 (TGF-β1), the pro-inflammatory interleukin-8 (IL-8). Cell apoptosis was assessed by cleaved caspase-3, and mesothelial to mesenchymal transition (MMT) was evaluated by α-smooth muscle actin protein. High-glucose conditions increased glucose transporters, glucose influx, ROS, all the high-glucose-induced harmful pathways, TGF-β1 and IL-8, cell apoptosis, and MMT. Halofuginone and tryptophanol inhibited all of the above high glucose-induced alterations, indicating that activation of GCN-2 kinase ameliorates glucotoxicity in human peritoneal mesothelial cells, preserves their integrity, and prevents MMT. Whether such a strategy could be applied in the clinic to avoid ultrafiltration failure in PD patients remains to be investigated. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Peritoneal Membrane Pathophysiology)

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Review

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17 pages, 632 KiB

Open AccessReview

Post-Surgical Peritoneal Scarring and Key Molecular Mechanisms

by Sarah E. Herrick and Bettina Wilm

Biomolecules 2021, 11(5), 692; https://doi.org/10.3390/biom11050692 - 5 May 2021

Cited by 28 | Viewed by 4295

Abstract

Post-surgical adhesions are internal scar tissue and a major health and economic burden. Adhesions affect and involve the peritoneal lining of the abdominal cavity, which consists of a continuous mesothelial covering of the cavity wall and majority of internal organs. Our understanding of the full pathophysiology of adhesion formation is limited by the fact that the mechanisms regulating normal serosal repair and regeneration of the mesothelial layer are still being elucidated. Emerging evidence suggests that mesothelial cells do not simply form a passive barrier but perform a wide range of important regulatory functions including maintaining a healthy peritoneal homeostasis as well as orchestrating events leading to normal repair or pathological outcomes following injury. Here, we summarise recent advances in our understanding of serosal repair and adhesion formation with an emphasis on molecular mechanisms and novel gene expression signatures associated with these processes. We discuss changes in mesothelial biomolecular marker expression during peritoneal development, which may help, in part, to explain findings in adults from lineage tracing studies using experimental adhesion models. Lastly, we highlight examples of where local tissue specialisation may determine a particular response of peritoneal cells to injury. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Peritoneal Membrane Pathophysiology)

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36 pages, 2616 KiB

Open AccessFeature PaperReview

IL-17A as a Potential Therapeutic Target for Patients on Peritoneal Dialysis

by Vanessa Marchant, Antonio Tejera-Muñoz, Laura Marquez-Expósito, Sandra Rayego-Mateos, Raul R. Rodrigues-Diez, Lucia Tejedor, Laura Santos-Sanchez, Jesús Egido, Alberto Ortiz, Jose M. Valdivielso, Donald J. Fraser, Manuel López-Cabrera, Rafael Selgas and Marta Ruiz-Ortega

Biomolecules 2020, 10(10), 1361; https://doi.org/10.3390/biom10101361 - 24 Sep 2020

Cited by 15 | Viewed by 5253

Abstract

Chronic kidney disease (CKD) is a health problem reaching epidemic proportions. There is no cure for CKD, and patients may progress to end-stage renal disease (ESRD). Peritoneal dialysis (PD) is a current replacement therapy option for ESRD patients until renal transplantation can be achieved. One important problem in long-term PD patients is peritoneal membrane failure. The mechanisms involved in peritoneal damage include activation of the inflammatory and immune responses, associated with submesothelial immune infiltrates, angiogenesis, loss of the mesothelial layer due to cell death and mesothelial to mesenchymal transition, and collagen accumulation in the submesothelial compact zone. These processes lead to fibrosis and loss of peritoneal membrane function. Peritoneal inflammation and membrane failure are strongly associated with additional problems in PD patients, mainly with a very high risk of cardiovascular disease. Among the inflammatory mediators involved in peritoneal damage, cytokine IL-17A has recently been proposed as a potential therapeutic target for chronic inflammatory diseases, including CKD. Although IL-17A is the hallmark cytokine of Th17 immune cells, many other cells can also produce or secrete IL-17A. In the peritoneum of PD patients, IL-17A-secreting cells comprise Th17 cells, γδ T cells, mast cells, and neutrophils. Experimental studies demonstrated that IL-17A blockade ameliorated peritoneal damage caused by exposure to PD fluids. This article provides a comprehensive review of recent advances on the role of IL-17A in peritoneal membrane injury during PD and other PD-associated complications. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Peritoneal Membrane Pathophysiology)

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17 pages, 710 KiB

Open AccessReview

Unfavorable Effects of Peritoneal Dialysis Solutions on the Peritoneal Membrane: The Role of Oxidative Stress

by Stefanos Roumeliotis, Evangelia Dounousi, Marios Salmas, Theodoros Eleftheriadis and Vassilios Liakopoulos

Biomolecules 2020, 10(5), 768; https://doi.org/10.3390/biom10050768 - 14 May 2020

Cited by 48 | Viewed by 5217

Abstract

One of the main limitations to successful long-term use of peritoneal dialysis (PD) as a renal replacement therapy is the harmful effects of PD solutions to the structure and function of the peritoneal membrane (PM). In PD, the PM serves as a semipermeable membrane that, due to exposure to PD solutions, undergoes structural alterations, including peritoneal fibrosis, vasculopathy, and neoangiogenesis. In recent decades, oxidative stress (OS) has emerged as a novel risk factor for mortality and cardiovascular disease in PD patients. Moreover, it has become evident that OS plays a pivotal role in the pathogenesis and development of the chronic, progressive injury of the PM. In this review, we aimed to present several aspects of OS in PD patients, including the pathophysiologic effects on the PM, clinical implications, and possible therapeutic antioxidant strategies that might protect the integrity of PM during PD therapy. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Peritoneal Membrane Pathophysiology)

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