scholarly journals UNUSUAL DEVELOPMENT OF BASEMENT MEMBRANE ABOUT SMALL BLOOD VESSELS

1965 ◽  
Vol 26 (2) ◽  
pp. 669-672 ◽  
Author(s):  
W. E. Stehbens ◽  
M. D. Silver
2006 ◽  
Vol 14 (3-4) ◽  
pp. 126-130 ◽  
Author(s):  
Tijana Vujasinovic ◽  
Marko Buta ◽  
Milan Markicevic ◽  
Dragica Nikolic-Vukosavljevic

Angiogenesis, or neovascularization, is a complex process leading to formation of new blood vessels from the pre-existing vascular network of the tissue. Angiogenesis plays a central role in various physiological and pathological conditions, including embryonic development, reproduction, inflammation and wound healing, infertility, heart diseases, ulcers, rheumatoid arthritis, diabetic blindness and cancer. It is a multistep process involving EC activation, basement membrane and extracellular matrix (ECM) degradation, EC proliferation, migration and differentiation, synthesis of new basement membrane and maturation of new blood vessels. Tumor vasculature is considered to be of an "immature" nature with series of structural abnormalities. There are reciprocal paracrine interactions between ECs, tumor cells, stroma and ECM. Angiogenesis plays a key role in transformation of normal to malignant cell, tumor progression and metastasis. It is similar to the metastatic process in that it requires EC attachment, proteolysis, and locomotion to proceed. A close relationship exists between the tumor and ECs invasiveness of the tissue. The switch to the angiogenic phenotype involves a change in the local equilibrium between positive and negative regulators of the growth of microvessels. Basic fibroblast growth factor (bFGF) and vas?cular endothelial growth factor (VEGF) are positive regulators of angiogenesis. Intimate cross-talk exists among bFGF and the different members of the VEGF family during angiogenesis, lymphangiogenesis, and vasculogenesis. A substantial body of experimental evidence supports the hypothesis that angiogenesis and angiogenic factors may be strong prognostic and predictive factors in breast carcinoma. This article reviews the current knowledge on angiogenesis and its positive regulators: bFGF and VEGF. .


Diabetologia ◽  
2008 ◽  
Vol 51 (7) ◽  
pp. 1181-1191 ◽  
Author(s):  
I. Virtanen ◽  
M. Banerjee ◽  
J. Palgi ◽  
O. Korsgren ◽  
A. Lukinius ◽  
...  

1961 ◽  
Vol 11 (3) ◽  
pp. 571-605 ◽  
Author(s):  
G. Majno ◽  
G. E. Palade

The mechanism, whereby histamine and serotonin increase the permeability of blood vessels, was studied in the rat by means of the electron microscope. The drugs were injected subcutaneously into the scrotum, whence they diffused into the underlying (striated) cremaster muscle. An intravenous injection of colloidal HgS was also given, in order to facilitate the identification of leaks by means of visible tracer particles. After intervals varying from 1 minute to 57 days the animals were killed; the cremaster was fixed, embedded in methacrylate, and examined with the electron microscope. One to 12 minutes after the injection, the blood vessels of the smallest caliber (3 to 5 micra as measured on electron micrographs) appeared intact. Numerous endothelial openings were present in blood vessels with a diameter of 7 to 8 micra or more. These gaps were 0.1 to 0.8 micra in width; portions of intercellular junctions were often present in one or both of the margins. The underlying basement membrane was morphologically intact. An accumulation of tracer particles and chylomicra against the basement membrane indicated that the latter behaved as a filter, allowing fluid to escape but retaining and concentrating suspended particulate matter of the size used. Uptake of tracer particles by endothelial vesicles was minimal. Phagocytosis by endothelial cells became more prominent at 3 hours, but as a secondary occurrence; the pericytes were actively phagocytic at all stages. At the 3-hour stage no leaks were found. The changes induced by histamine and serotonin were indistinguishable, except that the latter was more potent on a mole-to-mole basis. In control animals only small accumulations of tracer particles were found in the wall of a number of blood vessels. With regard to the pathogenesis of the endothelial leaks, the electron microscopic findings suggested that the endothelial cells become partially disconnected along the intercellular junctions. Supporting evidence was provided at the level of the light microscope, by demonstrating—in the same preparation—the leaks with appropriate tracer particles1, and the intercellular junctions by the silver nitrate method. The lipid nature of the chylomicron deposits observed in electron micrographs was also confirmed at the level of the light microscope, using cremasters fixed in formalin and stained in toto with sudan red.


2004 ◽  
Vol 127 (5) ◽  
pp. 592-597 ◽  
Author(s):  
Kouji Chiba ◽  
Wenli Zhao ◽  
Jiang Chen ◽  
Jingxin Wang ◽  
Hong Yan Cui ◽  
...  

2014 ◽  
Vol 5 (1) ◽  
pp. 71-73
Author(s):  
Ana Maria Abreu Velez ◽  
Vickie M. Brown ◽  
Michael S. Howard

1982 ◽  
Vol 94 (3) ◽  
pp. 597-606 ◽  
Author(s):  
F Grinnell ◽  
J R Head ◽  
J Hoffpauir

The rat endometrium during pregnancy was used as a model system to study fibronectin in vivo. Fibronectin distribution on stromal fibroblasts, as determined by indirect immunofluorescence staining, was studied in relationship to cell shape during decidual transformation. Fibroblasts of the estrus endometrial stroma were elongated cells with a fibrillar pattern of fibronectin on their surfaces. During days 1-6 of pregnancy, as these elongated cells acquired a round morphology, fibronectin changed first to a patched distribution on the cells'a surfaces and then disappeared. The change in fibronectin was specific for the fibroblasts since over the same time period there was no decrease in fibronectin found associated with blood vessels or in the epithelial-stromal basement membrane. These results support the proposed relationship between cell surface fibronectin and cell shape that has been inferred from in vitro experiments. After implantation, fibronectin distribution was studied in relationship to the position of the conceptus. In the stroma proximal to the implanting conceptus, fibronectin was absent except around blood vessels, which may help explain how decidual tissue could act as a barrier to trophoblast invasion. Finally, fibronectin distribution was studied in the uterus after parturition. Debris in the uterine lumen was coated with fibronectin, which may be important in the rapid removal of this material by phagocytic cells. Also, fibronectin associated with the epithelial-stromal basement membrane was reorganized after reepithelialization had occurred.


mBio ◽  
2015 ◽  
Vol 6 (5) ◽  
Author(s):  
Bruce Chesebro ◽  
James Striebel ◽  
Alejandra Rangel ◽  
Katie Phillips ◽  
Andrew Hughson ◽  
...  

ABSTRACT Aggregation of misfolded host proteins in the central nervous system is believed to be important in the pathogenic process in several neurodegenerative diseases of humans, including prion diseases, Alzheimer's disease, and Parkinson's disease. In these diseases, protein misfolding and aggregation appear to expand through a process of seeded polymerization. Prion diseases occur in both humans and animals and are experimentally transmissible orally or by injection, thus providing a controllable model of other neurodegenerative protein misfolding diseases. In rodents and ruminants, prion disease has a slow course, lasting months to years. Although prion infectivity has been detected in brain tissue at 3 to 4 weeks postinfection (p.i.), the details of early prion replication in the brain are not well understood. Here we studied the localization and quantitation of PrPSc generation in vivo starting at 30 min postmicroinjection of scrapie into the brain. In C57BL mice at 3 days p.i., generation of new PrPSc was detected by immunohistochemistry and immunoblot assays, and at 7 days p.i., new generation was confirmed by real-time quaking-induced conversion assay. The main site of new PrPSc generation was near the outer basement membrane of small and medium blood vessels. The finding and localization of replication at this site so early after injection have not been reported previously. This predominantly perivascular location suggested that structural components of the blood vessel basement membrane or perivascular astrocytes might act as cofactors in the initial generation of PrPSc. The location of PrPSc replication at the basement membrane also implies a role for the brain interstitial fluid drainage in the early infection process. IMPORTANCE Neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, and prion diseases, of humans are characterized by misfolding and aggregation of certain proteins, resulting in the destruction of brain tissue. In these diseases, the damage process spreads progressively within the central nervous system, but only prion diseases are known to be transmissible between individuals. Here we used microinjection of infectious prion protein (PrPSc) into the mouse brain to model early events of iatrogenic prion transmission via surgical instruments or tissue grafts. At 3 and 7 days postinjection, we detected the generation of new PrPSc, mostly on the outer walls of blood vessels near the injection site. This location and very early replication were surprising and unique. Perivascular prion replication suggested the transport of injected PrPSc via brain interstitial fluid to the basement membranes of blood vessels, where interactions with possible cofactors made by astrocytes or endothelia might facilitate the earliest cycles of prion infection.


Author(s):  
Rudradev Meyur ◽  
Anirban Sadhu ◽  
Hironmoy Mondal ◽  
Santanu Kumar Khanra

Background: Eclampsia is one of the leading causes of maternal and consequent foetal mortality in India. Studies on the histology of eclampsia are relatively uncommon, more so in the eastern region of India. The present study therefore is an attempt to analyse the changes which occur in placentae of eclamptic mothers with the help of light microscope as it is considered to be the epicentre of the disease. These findings are useful to understand the pathology of the killer disease and improve morbidity and mortality.Methods: 60 cases were selected for the study. 30 were non-eclamptic and 30 were eclamptic. Abnormalities in blood vessels, villi and basement membrane of placentae were searched for after routine H and E staining.Results: Eclamptic cases recorded with higher incidences of fibrinoid necrosis of villi, cytotrophoblastic proliferation, increased syncytial knots, hypo vascular villi and thickening of basement membrane. Non-eclamptic cases recorded only fibrinoid necrosis. Other features were not observed in the latter cases.Conclusions: Light microscopic changes observed in eclamptic placentae may contribute to the pathogenesis of the condition and serve as the baseline for further studies.


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