scholarly journals Loss of surface and cyst epithelial basement membranes and preneoplastic morphologic changes in prophylactic oophorectomies

Cancer ◽  
2003 ◽  
Vol 98 (12) ◽  
pp. 2607-2623 ◽  
Author(s):  
Isabelle H. Roland ◽  
Wan-Lin Yang ◽  
Dong-Hua Yang ◽  
Mary B. Daly ◽  
Robert F. Ozols ◽  
...  
Development ◽  
2001 ◽  
Vol 128 (6) ◽  
pp. 883-894 ◽  
Author(s):  
B.E. Vogel ◽  
E.M. Hedgecock

him-4 mutations cause a novel syndrome of tissue fragility, defective cell migration and chromosome instability in Caenorhabditis elegans. Null mutants have abnormal escape reflex, mispositioning of the vas deferens and uterus, and mitotic chromosome loss and multinucleate cells in the germline. The him-4 gene product, hemicentin, is a conserved extracellular matrix protein with 48 tandem immunoglobulin repeats flanked by novel terminal domains. Secreted from skeletal muscle and gonadal leader cells, hemicentin assembles into fine tracks at specific sites, where it contracts broad regions of cell contact into oriented linear junctions. Some tracks organize hemidesmosomes in the overlying epidermis. Hemicentin tracks facilitate mechanosensory neuron anchorage to the epidermis, gliding of the developing gonad along epithelial basement membranes and germline cellularization.


2018 ◽  
Vol 46 (12) ◽  
pp. 2027-2031 ◽  
Author(s):  
Chisato Sakuma ◽  
Hideto Imura ◽  
Tomohiro Yamada ◽  
Toshio Sugahara ◽  
Azumi Hirata ◽  
...  

2000 ◽  
Vol 148 (3) ◽  
pp. 615-624 ◽  
Author(s):  
Naohiko Koshikawa ◽  
Gianluigi Giannelli ◽  
Vincenzo Cirulli ◽  
Kaoru Miyazaki ◽  
Vito Quaranta

Laminin-5 (Ln-5) is an extracellular matrix substrate for cell adhesion and migration, which is found in many epithelial basement membranes. Mechanisms eliciting migration on Ln-5 need to be elucidated because of their relevance to tissue remodeling and cancer metastasis. We showed that exogenous addition of activated matrix metalloprotease (MMP) 2 stimulates migration onto Ln-5 in breast epithelial cells via cleavage of the γ2 subunit. To investigate the biological scope of this proteolytic mechanism, we tested a panel of cells, including colon and breast carcinomas, hepatomas, and immortalized hepatocytes, selected because they migrated or scattered constitutively in the presence of Ln-5. We found that constitutive migration was inhibited by BB94 or TIMPs, known inhibitors of MMPs. Limited profiling by gelatin zymography and Western blotting indicated that the ability to constitutively migrate on Ln-5 correlated with expression of plasma membrane bound MT1-MMP metalloprotease, rather than secretion of MMP2, since MMP2 was not produced by three cell lines (one breast and two colon carcinomas) that constitutively migrated on Ln-5. Moreover, migration on Ln-5 was reduced by MT1-MMP antisense oligonucleotides both in MMP2+ and MMP2− cell lines. MT1-MMP directly cleaved Ln-5, with a pattern similar to that of MMP2. The hemopexin-like domain of MMP2, which interferes with MMP2 activation, reduced Ln-5 migration in MT1-MMP+, MMP2+ cells, but not in MT1-MMP+, MMP2− cells. These results suggest a model whereby expression of MT1-MMP is the primary trigger for migration over Ln-5, whereas MMP2, which is activated by MT1-MMP, may play an ancillary role, perhaps by amplifying the MT1-MMP effects. Codistribution of MT1-MMP with Ln-5 in colon and breast cancer tissue specimens suggested a role for this mechanism in invasion. Thus, Ln-5 cleavage by MMPs may be a widespread mechanism that triggers migration in cells contacting epithelial basement membranes.


2007 ◽  
Vol 299 (7) ◽  
pp. 337-343 ◽  
Author(s):  
Yannis Dalezios ◽  
Babis Papasozomenos ◽  
Petros Petrou ◽  
Georges Chalepakis

2019 ◽  
Vol 8 (5) ◽  
pp. 716 ◽  
Author(s):  
Andrzej Grzybowski ◽  
Piotr Kanclerz ◽  
Valentín Huerva ◽  
Francisco J. Ascaso ◽  
Raimo Tuuminen

Diabetes mellitus is one of the most prevalent chronic diseases worldwide. Diabetic patients are at risk of developing cataract and present for surgery at an earlier age than non-diabetics. The aim of this study was to review the problems associated with cataract surgery in a diabetic patient. Corneal complications in diabetic patients include delayed wound healing, risk of developing epithelial defects or recurrent erosions due to the impairment of epithelial basement membranes and epithelial–stromal interactions. Diabetic patients present lower endothelial cell density and their endothelium is more susceptible to trauma associated with cataract surgery. A small pupil is common in diabetic patients making cataract surgery technically challenging. Finally diabetic patients have an increased risk for developing postoperative pseudophakic cystoid macular edema, posterior capsule opacification or endophthalmitis. In patients with pre-proliferative or proliferative diabetic retinopathy, diabetic macular edema or iris neovascularization adjunctive therapy such as an intravitreal anti-vascular endothelial growth factor injection, can inhibit exacerbation related to cataract surgery.


1997 ◽  
Vol 272 (14) ◽  
pp. 9531-9538 ◽  
Author(s):  
Barbara Gayraud ◽  
Bianca Höpfner ◽  
Ali Jassim ◽  
Monique Aumailley ◽  
Leena Bruckner-Tuderman

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