Transforming growth factor-β, basement membrane components and heparan sulphate proteoglycans in experimental hepatic schistosomiasis mansoni

1998 ◽  
Vol 292 (1) ◽  
pp. 101-106 ◽  
Author(s):  
W. Jacobs ◽  
S. Kumar-Singh ◽  
J. Bogers ◽  
K. Van de Vijver ◽  
A. Deelder ◽  
...  
Keyword(s):  
Growth Factor ◽  
Basement Membrane ◽  
Transforming Growth Factor ◽  
Heparan Sulphate ◽  
Transforming Growth Factor Β ◽  
Schistosomiasis Mansoni ◽  
Heparan Sulphate Proteoglycans ◽  
Membrane Components ◽  
Basement Membrane Components

Differential deposition of basement membrane components during formation of the caudal neural tube in the mouse embryo

Development ◽  
1987 ◽  
Vol 99 (4) ◽  
pp. 509-519
Author(s):  
K.S. O'Shea
Keyword(s):  
Basement Membrane ◽  
Type Iv Collagen ◽  
Heparan Sulphate ◽  
Heparan Sulphate Proteoglycan ◽  
Sulphate Proteoglycan ◽  
Secondary Neurulation ◽  
Type Iv ◽  
Posterior Neuropore ◽  
Membrane Components ◽  
Basement Membrane Components

The distribution of basement membrane and extracellular matrix components laminin, fibronectin, type IV collagen and heparan sulphate proteoglycan was examined during posterior neuropore closure and secondary neurulation in the mouse embryo. During posterior neuropore closure, these components were densely deposited in basement membranes of neuroepithelium, blood vessels, gut and notochord; although deposition was sparse in the midline of the regressing primitive streak. During secondary neurulation, mesenchymal cells formed an initial aggregate near the dorsal surface, which canalized and merged with the anterior neuroepithelium. With aggregation, fibronectin and heparan sulphate proteoglycan were first detected at the base of a 3- to 4-layer zone of radially organized cells. With formation of a lumen within the aggregate, laminin and type IV collagen were also deposited in the forming basement membrane. During both posterior neuropore closure and secondary neurulation, fibronectin and heparan sulphate proteoglycan were associated with the most caudal portion of the neuroepithelium, the region where newly formed epithelium merges with the consolidated neuroepithelium. In regions of neural crest migration, the deposition of basement membrane components was altered, lacking laminin and type IV collagen, with increased deposition of fibronectin and heparan sulphate proteoglycan.

118. CHARACTERISATION OF HEPARAN SULPHATE PROTEOGLYCANS IN THE MATURING CUMULUS OOCYTE COMPLEX

2009 ◽  
Vol 21 (9) ◽  
pp. 37
Author(s):  
L. N. Watson ◽  
M. Sasseville ◽  
R. B. Gilchrist ◽  
D. L. Russell
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Cell Surface ◽  
Transforming Growth Factor ◽  
Heparan Sulphate ◽  
Cumulus Cells ◽  
Receptor Interaction ◽  
Heparan Sulphate Proteoglycans ◽  
Tgfβ Superfamily

Many growth factors including members of the transforming growth factor beta (TGFβ) superfamily and epidermal growth factor (Egf)-like ligands signal via interactions with heparan sulphate proteoglycans (HSPGs). Cell surface HSPGs can act by sequestering ligands at their site of action, by presenting a ligand to its signalling receptor, or by preventing ligand-receptor interaction. The oocyte secreted factors (OSF) growth differentiation factor 9 and bone morphogenetic protein 15 are members of the TGFβ superfamily that act selectively on cumulus cells. Conversely Egf-like ligands are secreted by mural granulosa cells and transmit LH-induced signals to cumulus cells. We investigated the possibility that HSPGs contribute to the spatially restricted responses these signals exert on cumulus cells. Syndecan-1 and Glypican-1 are cell surface HSPGs that are involved in numerous biological processes, including growth factor regulation, cell proliferation and differentiation. Microarray analysis showed Syndecan-1 and Glypican-1 mRNA expression induced 6-fold (P=10-9) and 3-fold (P=10-7) respectively in Egf+FSH stimulated cumulus oocyte complexes (COCs). Furthermore, Syndecan-1 and Glypican-1 mRNA were induced 27- and 16-fold respectively in COCs after hCG treatment of mice. Syndecan-1 and Glypican-1 protein was localised specifically to the COC through immunohistochemical analysis. In Vitro Maturation (IVM) of oocytes is a valuable alternative to gonadotropin mediated superovulation, but IVM COCs are less competent than those matured in vivo. Several components of the COC have been shown to be altered in IVM, including the chondroitin sulphate proteoglycan Versican. COCs from mice that underwent IVM in the presence of Egf+FSH and cilostamide for 16 hours had >16 fold reduced mRNA for Syndecan-1 when compared with In Vivo matured COCs. The lack of Syndecan-1 in IVM COCs could reduce signalling capacity of growth factors including OSFs. This may contribute to the reduced capacity of IVM oocytes to fertilise and produce a healthy embryo, and ultimately, a healthy offspring.

scholarly journals A Case of Transforming Growth Factor-β-Induced Gene-Related Oculorenal Syndrome: Granular Corneal Dystrophy Type II with a Unique Nephropathy

2016 ◽  
Vol 6 (3) ◽  
pp. 106-113 ◽  
Author(s):  
Yoichi Iwafuchi ◽  
Tetsuo Morioka ◽  
Yuko Oyama ◽  
Kandai Nozu ◽  
Kazumoto Iijima ◽  
...  
Keyword(s):  
Growth Factor ◽  
Basement Membrane ◽  
Transforming Growth Factor ◽  
Kidney Diseases ◽  
Renal Involvement ◽  
Transforming Growth Factor Β ◽  
Corneal Dystrophy ◽  
Renal Diseases ◽  
Type Ii ◽  
Granular Corneal Dystrophy

Many types of inherited renal diseases have ocular features that occasionally support a diagnosis. The following study describes an unusual example of a 40-year-old woman with granular corneal dystrophy type II complicated by renal involvement. These two conditions may coincidentally coexist; however, there are some reports that demonstrate an association between renal involvement and granular corneal dystrophy type II. Granular corneal dystrophy type II is caused by a mutation in the transforming growth factor-β-induced (TGFBI) gene. The patient was referred to us because of the presence of mild proteinuria without hematuria that was subsequently suggested to be granular corneal dystrophy type II. A kidney biopsy revealed various glomerular and tubular basement membrane changes and widening of the subendothelial space of the glomerular basement membrane by electron microscopy. However, next-generation sequencing revealed that she had no mutation in a gene that is known to be associated with monogenic kidney diseases. Conversely, real-time polymerase chain reaction, using a simple buccal swab, revealed TGFBI heteromutation (R124H). The TGFBI protein plays an important role in cell-collagen signaling interactions, including extracellular matrix proteins which compose the renal basement membrane. This mutation can present not only as corneal dystrophy but also as renal disease. TGFBI-related oculorenal syndrome may have been unrecognized. It is difficult to diagnose this condition without renal electron microscopic studies. To the best of our knowledge, this is the first detailed report of nephropathy associated with a TGFBI mutation.

Mechanisms of placental invasion of the uterus and their control

1992 ◽  
Vol 70 (10-11) ◽  
pp. 867-874 ◽  
Author(s):  
Charles H. Graham ◽  
Peeyush K. Lala
Keyword(s):  
Growth Factor ◽  
Basement Membrane ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Trophoblast Invasion ◽  
Trophoblast Cells ◽  
Decidual Cells ◽  
Cell Invasiveness ◽  
Malignant Trophoblast

Trophoblast cells of the placenta in many species have acquired mechanisms to invade the uterus, inclusive of its blood vessels, to establish efficient fetomaternal exchange of molecules. This invasion is strictly controlled both spatially and temporally and, in humans, usually continues until midgestation. Key mechanisms underlying various steps in trophoblast invasion are (i) the attachment to the basement membrane, most likely by binding to laminin; (ii) the detachment from the basement membrane matrix, a process requiring the presence of complex-type oligosaccharides on the cell surface; and (iii) the breakdown of basement membrane components, mediated by secretion of metalloproteases (such as type IV collagenases) and serine proteases (plasminogen activator). Activation of trophoblast-derived metalloproteases appears to be plasmin dependent. Trophoblast invasiveness in situ is controlled by the microenvironment, owing to local production of anti-invasive factors by the decidual tissue of the uterus. One of these factors is TIMP (tissue inhibitor of metalloproteases), which neutralizes metalloproteases in an equimolar ratio. Another is TGF-β (transforming growth factor-β), which has a dual effect: it induces TIMP-1 secretion by the trophoblast and decidual cells and promotes differentiation of invasive trophoblast cells into multinucleated giant cells, which are presumably noninvasive. Thus, TGF-β provides the key control of trophoblast invasiveness in situ. This control is lost in certain choriocarcinomas. In contrast to the response shown by the normal trophoblast, JAR and JEG-3 choriocarcinoma cell invasiveness does not seem to be inhibited by TGF-β. In fact, in preliminary studies, JAR cells responded to TGF-β by increased invasiveness. The reasons for the differential effects of TGF-β on normal versus malignant trophoblast cell invasiveness are currently under study.Key words: trophoblast, invasion, control, choriocarcinoma, transforming growth factor-β.

Transforming growth factor-β and Th17 responses in resistance to primary murine schistosomiasis mansoni

Cytokine ◽  
2009 ◽  
Vol 48 (3) ◽  
pp. 239-245 ◽  
Author(s):  
Hatem Tallima ◽  
Mohamed Salah ◽  
Fatem R. Guirguis ◽  
Rashika El Ridi
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Schistosomiasis Mansoni
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