Peritoneal Injury by Methylglyoxal in Peritoneal Dialysis

2006 ◽  
Vol 26 (3) ◽  
pp. 380-392 ◽  
Author(s):  
Ichiro Hirahara ◽  
Eiji Kusano ◽  
Satoru Yanagiba ◽  
Yukio Miyata ◽  
Yasuhiro Ando ◽  
...  
Keyword(s):  
Peritoneal Dialysis ◽  
Basement Membrane ◽  
Structural Changes ◽  
Type Iv Collagen ◽  
Degradation Products ◽  
Abdominal Cocoon ◽  
Type Iv ◽  
Type Iv Collagen 7S ◽  
Peritoneal Function

Background Peritoneal dialysis (PD) is a common treatment for patients with reduced or absent renal function. Long-term PD leads to peritoneal injury with structural changes and functional decline, such as ultrafiltration loss. At worst, peritoneal injury leads to encapsulating peritoneal sclerosis, a serious complication of PD. Glucose degradation products contained in PD fluids contribute to the bioincompatibility of conventional PD fluids. Methylglyoxal (MGO) is an extremely toxic glucose degradation product. The present study examined the injurious effect of MGO on peritoneum in vivo. Methods Male Sprague–Dawley rats ( n = 6) were administered PD fluids (pH 5.0) containing 0, 0.66, 2, 6.6, or 20 mmol/L MGO every day for 21 days. On day 22, peritoneal function was estimated by the peritoneal equilibration test. Drained dialysate was analyzed for type IV collagen-7S, matrix metalloproteinase (MMP), and vascular endothelial growth factor (VEGF). Histological analysis was also performed. Results In rats receiving PD fluids containing more than 0.66 mmol/L MGO, peritoneal function decreased significantly and levels of type IV collagen-7S and MMP-2 in drained dialysate increased significantly. In the 20-mmol/L MGO-treated rats, loss of body weight, expression of VEGF, thickening of the peritoneum, and formation of abdominal cocoon were induced. MMP-2 and VEGF were produced by infiltrating cells in the peritoneum. Type IV collagen was detected in basement membrane of microvessels. Conclusion MGO induced not only peritoneal injury but also abdominal cocoon formation in vivo. The decline of peritoneal function may result from reconstitution of microvessel basement membrane or neovascularization.

scholarly journals SPARC Promotes Cell Invasion In Vivo by Decreasing Type IV Collagen Levels in the Basement Membrane

PLoS Genetics ◽  
2016 ◽  
Vol 12 (2) ◽  
pp. e1005905 ◽  
Author(s):  
Meghan A. Morrissey ◽  
Ranjay Jayadev ◽  
Ginger R. Miley ◽  
Catherine A. Blebea ◽  
Qiuyi Chi ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Cell Invasion ◽  
Type Iv Collagen ◽  
Type Iv

scholarly journals Characterization of the Hemorrhagic Reaction Caused by Vibrio vulnificus Metalloprotease, a Member of the Thermolysin Family

1998 ◽  
Vol 66 (10) ◽  
pp. 4851-4855 ◽  
Author(s):  
Shin-ichi Miyoshi ◽  
Hiromi Nakazawa ◽  
Koji Kawata ◽  
Ken-ichi Tomochika ◽  
Kazuo Tobe ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Type Iv Collagen ◽  
Vibrio Vulnificus ◽  
Vascular Endothelial Cells ◽  
Human Pathogen ◽  
Membrane Breakdown ◽  
Type Iv ◽  
Hemorrhagic Activity

ABSTRACT Vibrio vulnificus is an opportunistic human pathogen causing wound infections and septicemia, characterized by hemorrhagic and edematous damage to the skin. This human pathogen secretes a metalloprotease (V. vulnificus protease [VVP]) as an important virulence determinant. When several bacterial metalloproteases including VVP were injected intradermally into dorsal skin, VVP showed the greatest hemorrhagic activity. The level of the in vivo hemorrhagic activity of the bacterial metalloproteases was significantly correlated with that of the in vitro proteolytic activity for the reconstituted basement membrane gel. Of two major basement membrane components (laminin and type IV collagen), only type IV collagen was easily digested by VVP. Additionally, the immunoglobulin G antibody against type IV collagen, but not against laminin, showed sufficient protection against the hemorrhagic reaction caused by VVP. Capillary vessels are known to be stabilized by binding of the basal surface of vascular endothelial cells to the basement membrane. Therefore, specific degradation of type IV collagen may cause destruction of the basement membrane, breakdown of capillary vessels, and leakage of blood components including erythrocytes.

scholarly journals Basement membrane-like structures containing NTH α1(IV) are formed around the endothelial cell network in a novel in vitro angiogenesis model

2019 ◽  
Vol 317 (2) ◽  
pp. C314-C325
Author(s):  
Yongchol Shin ◽  
Akane Moriya ◽  
Yuta Tohnishi ◽  
Takafumi Watanabe ◽  
Yasutada Imamura
Keyword(s):  
Endothelial Cells ◽  
Basement Membrane ◽  
Blood Vessels ◽  
Type Iv Collagen ◽  
Vascular Endothelial Cells ◽  
Culture Dish ◽  
Cell Network ◽  
Type Iv

Angiogenesis is a process through which new blood vessels are formed by sprouting and elongating from existing blood vessels. Several methods have been used to replicate angiogenesis in vitro, including culturing vascular endothelial cells on Matrigel and coculturing with endothelial cells and fibroblasts. However, the angiogenesis elongation process has not been completely clarified in these models. We therefore propose a new in vitro model of angiogenesis, suitable for observing vascular elongation, by seeding a spheroid cocultured from endothelial cells and fibroblasts into a culture dish. In this model, endothelial cells formed tubular networks elongated from the spheroid with a lumen structure and were connected with tight junctions. A basement membrane (BM)-like structure was observed around the tubular network, similarly to blood vessels in vivo. These results suggested that blood vessel-like structure could be reconstituted in our model. Laminin and type IV collagen, main BM components, were highly localized around the network, along with nontriple helical form of type IV collagen α1-chain [NTH α1(IV)]. In an ascorbic acid-depleted condition, laminin and NTH α1(IV) were observed around the network but not the triple-helical form of type IV collagen and the network was unstable. These results suggest that laminin and NTH α1(IV) are involved in the formation of tubular network and type IV collagen is necessary to stabilize the network.

Extracellular matrix modulation of endothelial cell shape and motility following injury in vitro

1985 ◽  
Vol 73 (1) ◽  
pp. 19-32
Author(s):  
W.C. Young ◽  
I.M. Herman
Keyword(s):  
Extracellular Matrix ◽  
Basement Membrane ◽  
Fluorescence Microscopy ◽  
Type Iv Collagen ◽  
Type I ◽  
Post Injury ◽  
Type Iv ◽  
Interstitial Collagens

We utilized fluorescence microscopy and affinity-purified antibodies to probe the form and function of cytoplasmic actin in endothelial cells (EC) recovering from injury and grown on extracellular matrices in vitro. Bovine aortic EC were seeded onto glass microscope coverslips that had been coated with either BSA, fibronectin, type I and III (interstitial) collagens, type IV (basement membrane) collagen or gelatin. After EC that had been grown on glass, glass-BSA or extracellular matrix-coated coverslips reached confluence, a 300–400 micron zone of cells was mechanically removed to stimulate EC migration and proliferation. Post-injury EC movements were monitored with time-lapse, phase-contrast videomicrography before fixation for actin localization with fluorescence microscopy using affinity-purified antibodies. We found that the number of stress fibres within EC was inversely proportional to the rate of movement; and, the rates of movement for EC grown on glass or glass-BSA were approximately eight times faster than EC grown on gelatin or type IV collagen (X velocity = 0.5 micron/min versus 0.06 micron/min). EC movements on fibronectin and interstitial collagens were similar (X velocity = 0.2 micron/min). These results suggest that extracellular matrix molecules modulate EC stress fibre expression, thereby producing alterations in the cytoskeleton and the resultant EC movements that follow injury in vitro. Moreover, the induction of stress fibres in the presence of basement membrane (type IV) collagen may explain the failure of aortic EC to migrate and repopulate wounded regions of intima during atherogenesis in vivo.

scholarly journals SPARC promotes cell invasion in vivo by decreasing type IV collagen levels in the basement membrane

2016 ◽  
Author(s):  
Meghan A Morrissey ◽  
Ranjay Jayadev ◽  
Ginger R Miley ◽  
Catherine A Blebea ◽  
Qiuyi Chi ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Basement Membrane ◽  
Cell Invasion ◽  
Type Iv Collagen ◽  
Matrix Assembly ◽  
Dynamic Interactions ◽  
Cellular Processes ◽  
Type Iv ◽  
Cell Signaling Pathways

Overexpression of SPARC, a collagen-binding glycoprotein, is strongly associated with tumor invasion through extracellular matrix in many aggressive cancers. SPARC regulates numerous cellular processes including integrin-mediated cell adhesion, cell signaling pathways, and extracellular matrix assembly; however, the mechanism by which SPARC promotes cell invasion in vivo remains unclear. A main obstacle in understanding SPARC function has been the difficulty of visualizing and experimentally examining the dynamic interactions between invasive cells, extracellular matrix and SPARC in native tissue environments. Using the model of anchor cell invasion through the basement membrane (BM) extracellular matrix in Caenorhabditis elegans, we find that SPARC overexpression is highly pro-invasive and rescues BM transmigration in mutants with defects in diverse aspects of invasion, including cell polarity, invadopodia formation, and matrix metalloproteinase expression. By examining BM assembly, we find that overexpression of SPARC specifically decreases levels of BM type IV collagen, a crucial structural BM component. Reduction of type IV collagen mimicked SPARC overexpression and was sufficient to promote invasion. Tissue-specific overexpression and photobleaching experiments revealed that SPARC acts extracellularly to inhibit collagen incorporation into BM. By reducing endogenous SPARC, we also found that SPARC functions normally to traffic collagen from its site of synthesis to tissues that do not express collagen. We propose that a surplus of SPARC disrupts extracellular collagen trafficking and reduces BM collagen incorporation, thus weakening the BM barrier and dramatically enhancing its ability to be breached by invasive cells.

scholarly journals Dynamically remodeled hepatic extracellular matrix predicts prognosis of early-stage cirrhosis

2021 ◽  
Vol 12 (2) ◽  
Author(s):  
Yuexin Wu ◽  
Yuyan Cao ◽  
Keren Xu ◽  
Yue Zhu ◽  
Yuemei Qiao ◽  
...  
Keyword(s):  
Liver Cirrhosis ◽  
Basement Membrane ◽  
Type Iv Collagen ◽  
Patient Survival ◽  
Early Stage ◽  
Ecm Remodeling ◽  
Type Iv ◽  
Ecm Proteins ◽  
Stage Disease ◽  
Cirrhotic Patients

AbstractLiver cirrhosis remains major health problem. Despite the progress in diagnosis of asymptomatic early-stage cirrhosis, prognostic biomarkers are needed to identify cirrhotic patients at high risk developing advanced stage disease. Liver cirrhosis is the result of deregulated wound healing and is featured by aberrant extracellular matrix (ECM) remodeling. However, it is not comprehensively understood how ECM is dynamically remodeled in the progressive development of liver cirrhosis. It is yet unknown whether ECM signature is of predictive value in determining prognosis of early-stage liver cirrhosis. In this study, we systematically analyzed proteomics of decellularized hepatic matrix and identified four unique clusters of ECM proteins at tissue damage/inflammation, transitional ECM remodeling or fibrogenesis stage in carbon tetrachloride-induced liver fibrosis. In particular, basement membrane (BM) was heavily deposited at the fibrogenesis stage. BM component minor type IV collagen α5 chain expression was increased in activated hepatic stellate cells. Knockout of minor type IV collagen α5 chain ameliorated liver fibrosis by hampering hepatic stellate cell activation and promoting hepatocyte proliferation. ECM signatures were differentially enriched in the biopsies of good and poor prognosis early-stage liver cirrhosis patients. Clusters of ECM proteins responsible for homeostatic remodeling and tissue fibrogenesis, as well as basement membrane signature were significantly associated with disease progression and patient survival. In particular, a 14-gene signature consisting of basement membrane proteins is potent in predicting disease progression and patient survival. Thus, the ECM signatures are potential prognostic biomarkers to identify cirrhotic patients at high risk developing advanced stage disease.

Isolation and characterization of pepsin-solubilized human basement membrane (type IV) collagen peptides

Biochemistry ◽  
1983 ◽  
Vol 22 (21) ◽  
pp. 4940-4948 ◽  
Author(s):  
Robert S. MacWright ◽  
Virginia A. Benson ◽  
Katherine T. Lovello ◽  
Michel Van der Rest ◽  
Peter P. Fietzek
Keyword(s):  
Basement Membrane ◽  
Type Iv Collagen ◽  
Collagen Peptides ◽  
Type Iv ◽  
Isolation And Characterization ◽  
Membrane Type
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