scholarly journals Involvement of follicular basement membrane and vascular endothelium in blood–follicle barrier formation of mice revealed by ‘in vivo cryotechnique’

Reproduction ◽  
2007 ◽  
Vol 134 (2) ◽  
pp. 307-317 ◽  
Author(s):  
Hong Zhou ◽  
Nobuhiko Ohno ◽  
Nobuo Terada ◽  
Sei Saitoh ◽  
Yasuhisa Fujii ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Blood Vessels ◽  
Vascular Endothelium ◽  
Serum Proteins ◽  
Vascular Endothelial Cells ◽  
Follicular Development ◽  
Basement Membranes ◽  
In Vivo Cryotechnique ◽  
Quick Freezing

The molecular sieve with size- and charge selectivity in ovarian follicles, the so-called blood–follicle barrier (BFB), was examined during follicular development under physiological conditions to reveal ovarian structures responsible for the BFB by using our ‘in vivocryotechnique’ (IVCT). Mouse ovary specimens were prepared with different methods including IVCT, immersion, or perfusion chemical fixation and quick-freezing following resection or perfusion. Their paraffin sections or cryosections were stained with hematoxylin–eosin or immunostained for serum proteins with different molecular weights: albumin, immunoglobulin (Ig) G1 heavy chain, inter-α-trypsin inhibitor (IαI), fibrinogen, and IgM. Their immunoreactivity was better preserved with IVCT. The immunostaining for albumin was clearly observed in blood vessels, interstitium, and developing follicles, but that of IgG1, IαI, or fibrinogen was significantly decreased inside the follicles. IgM was immunohistochemically decreased throughout the interstitium outside blood vessels. The immunoreactivities of IgG1 and IgM, as compared with albumin, were clearly changed along follicular basement membranes and around vascular endothelial cells respectively. These findings indicate that BFB functions throughout follicular development, and the follicular basement membrane and the vascular endothelium could play some significant roles in the permselectivity for such soluble proteins with intermediate and high molecular weight respectively.

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.

scholarly journals Permselectivity of blood follicle barriers in mouse ovaries of the mifepristone-induced polycystic ovary model revealed by in vivo cryotechnique

Reproduction ◽  
2008 ◽  
Vol 136 (5) ◽  
pp. 599-610 ◽  
Author(s):  
Hong Zhou ◽  
Nobuhiko Ohno ◽  
Nobuo Terada ◽  
Sei Saitoh ◽  
Ichiro Naito ◽  
...  
Keyword(s):  
Blood Flow ◽  
Blood Vessels ◽  
Histopathological Examination ◽  
Polycystic Ovary ◽  
Basement Membranes ◽  
In Vivo Cryotechnique ◽  
Preparation Methods ◽  
Perfusion Fixation ◽  
Pco Syndrome

Despite the potential association of polycystic ovary (PCO) syndrome with hemodynamic changes, follicular microenvironment and the involvement of blood follicle barriers (BFB), a histopathological examination has been hampered by artifacts caused by conventional preparation methods. In this study, mouse ovaries of a mifepristone-induced PCO model were morphologically and immunohistochemically examined byin vivocryotechnique (IVCT), which prevents those technical artifacts. Ovarian specimens of PCO model mice were prepared by IVCT or the conventional perfusion fixation after s.c. injection of mifepristone. Their histology and immunolocalization of plasma proteins, including albumin (molecular mass, 69 kDa), immunoglobulin G (IgG, 150 kDa), inter-α-trypsin inhibitor (ITI, 220 kDa), fibrinogen (340 kDa), and IgM (900 kDa), were examined. In the PCO model, enlarged blood vessels with abundant blood flow were observed in addition to cystic follicles with degenerative membrana granulosa. The immunolocalization of albumin and IgM in the PCO model were similar to those in normal mice. Albumin immunolocalized in the blood vessels, interstitium or follicles, and IgM was mostly restricted within the blood vessels. In contrast, immunolocalization of IgG, ITI, and fibrinogen changed in the PCO model. Both IgG and ITI were clearly blocked by follicular basement membranes, and hardly observed in the membrana granulosa, though fibrinogen was mostly observed within blood vessels. These findings suggest that increased blood flow and enhanced selectivity of molecular permeation through the BFB are prominent features in the PCO ovaries, and changes in hemodynamic conditions and permselectivity of BFB are involved in the pathogenesis and pathophysiology of PCO syndrome.

scholarly journals Evaluation of Extension of Blood Vessels during Static Stretching Using Ultrasound 2D Speckle Tracking Imaging

2017 ◽  
Vol 9 (8) ◽  
pp. 1
Author(s):  
Hiromi Shinno ◽  
Satoshi Kurose ◽  
Yutaka Yamanaka ◽  
Yaeko Fukushima ◽  
Hiromi Tsutsumi ◽  
...  
Keyword(s):  
Blood Vessels ◽  
Speckle Tracking ◽  
Vascular Endothelial Cells ◽  
Ulnar Artery ◽  
General Purpose ◽  
Speckle Tracking Imaging ◽  
Static Stretching ◽  
Maximum Angle ◽  
2D Speckle Tracking

BACKGROUND: During static stretching, a muscle extends longitudinally, and blood vessels seem to extend simultaneously. However, it is difficult to visualize, and few findings have seen. The recent progress with ultrasonography enables measurements of movement in vivo using 2D speckle tracking imaging, as well as detailed evaluation of extension in tissues at the same site. The aim of this study is to evaluate longitudinal extension of blood vessels during static stretching using this methodology.METHODS: Participants were 10 healthy female volunteers (age of 39.4±11.6). They extended their right wrist with elbow extended. Then the ulnar artery was measured by using 2D speckle tracking imaging with a general-purpose ultrasound instrument. Tissue extension per unit time at the stretching site was calculated from before stretching to maximum of stretching. Simultaneous changes in the caliber of blood vessels during stretching were measured using ultrasound M-mode.RESULTS: The maximum angle of wrist extension was 0 to 83.6±12.5°. The muscle extended by 3.80±1.65% per unit time during stretching, and blood vessels simultaneously extended by 3.20±1.96%. These changes were significant compared to measurements before stretching (p<0.01) and shows the correlation between muscles and blood vessels (r=0.56, p=0.1). The calibers of blood vessels per unit time before and during stretching were 2.24±0.27 and 1.64±0.53 mm with a significant decrease during stretching (p<0.01).CONCLUSIONS: Imaging of static stretching showed extension of both the muscle/skeletal system and blood vessels longitudinally. The finding suggests that endothelial function might be activated by mechanical stress on vascular endothelial cells.

In vivo biosynthesis and turnover of glomerular basement membrane in diabetic rats

1982 ◽  
Vol 242 (4) ◽  
pp. F385-F389
Author(s):  
M. P. Cohen ◽  
M. L. Surma ◽  
V. Y. Wu
Keyword(s):  
Basement Membrane ◽  
Glomerular Basement Membrane ◽  
Diabetic Rats ◽  
Basement Membranes ◽  
Membrane Turnover ◽  
Proline Incorporation ◽  
Basement Membrane Collagen ◽  
Osmotic Lysis ◽  
Specific Activities

Glomerular basement membrane (GBM) was labeled in vivo by the injection of tracer amounts of tritiated proline into normal and streptozotocin-diabetic rats. Basement membrane biosynthesis and turnover were determined from the specific activities of proline and hydroxyproline in samples purified following osmotic lysis of glomeruli isolated 4 h to 12 days after injection. Peak radiolabeling of normal and diabetic GBM occurred within 24-48 h and 48-72 h, respectively, and, when corrected for differences in the serum proline specific activities, [3H]proline incorporation was greater in diabetic than in normal samples. In contrast to the subsequent time-dependent progressive decline in radiolabeling in basement membranes from normal animals, specific activities of proline and hydroxyproline in diabetic glomerular basement membrane did not change significantly over the same period of observation. Renal cortical mass and glomerular basement membrane collagen content were preserved in diabetic animals despite loss of body weight. The findings are compatible with prolongation of glomerular basement membrane turnover in experimental diabetes, and suggest that diminished degradation contributes to the accumulation of glomerular basement membrane that is characteristic of chronic diabetes.

Zebrafish mutants identify an essential role for laminins in notochord formation

Development ◽  
2002 ◽  
Vol 129 (13) ◽  
pp. 3137-3146 ◽  
Author(s):  
Michael J. Parsons ◽  
Steven M. Pollard ◽  
Leonor Saúde ◽  
Benjamin Feldman ◽  
Pedro Coutinho ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Positional Cloning ◽  
Essential Role ◽  
Basement Membranes ◽  
Form Complex ◽  
Organ Formation ◽  
Notochord Cells ◽  
Laminin 1

Basement membranes are thought to be essential for organ formation, providing the scaffold on which individual cells organize to form complex tissues. Laminins are integral components of basement membranes. To understand the development of a simple vertebrate organ, we have used positional cloning to characterize grumpy and sleepy, two zebrafish loci known to control notochord formation, and find that they encode laminin β1 and laminin γ1, respectively. Removal of either chain results in the dramatic loss of laminin 1 staining throughout the embryo and prevents formation of the basement membrane surrounding the notochord. Notochord cells fail to differentiate and many die by apoptosis. By transplantation, we demonstrate that, for both grumpy and sleepy, notochord differentiation can be rescued by exogenous sources of the missing laminin chain, although notochordal sources are also sufficient for rescue. These results demonstrate a clear in vivo requirement for laminin β1 and laminin γ1 in the formation of a specific vertebrate organ and show that laminin or the laminin-dependent basement membrane is essential for the differentiation of chordamesoderm to notochord.

scholarly journals EXPERIMENTAL NONTHROMBOCYTOPENIC VASCULAR PURPURA: A REVIEW OF THE JAPANESE LITERATURE, WITH PRELIMINARY CONFIRMATORY REPORT

Blood ◽  
1950 ◽  
Vol 5 (4) ◽  
pp. 320-328 ◽  
Author(s):  
WILLIAM G. CLARK ◽  
EDITH JACOBS
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Blood Vessels ◽  
Vascular Endothelium ◽  
Blood Platelets ◽  
Japanese Literature ◽  
Mouse Bone Marrow ◽  
Aqueous Fraction ◽  
Made In

Abstract Antisera were produced against guinea pig and mouse blood platelets, guinea pig and mouse spleen, mouse bone marrow, spleen, marrow plus spleen ("antireticulocytotoxic" serum), aqueous fraction of guinea pig adipose tissue rich in nonmuscular blood vessels, guinea pig choroid plexi rich in capillaries, whole guinea pig blood vessels, guinea pig smooth muscle, whole guinea pig blood vessel antiserum absorbed with guinea pig smooth muscle, and dog vascular endothelium. In all cases except the last named there were positive agglutinin and/or complement fixation titers, which were slightly enhanced anamnestically by whole adrenal cortical extract, but not by "Lipoadrenal" extract presumably high in "carbohydrate" factor. In no case was there a nonthrombocytopenic vascular purpura produced in vivo except by the anti-vascular endothelium serum. These preliminary observations are considered to confirm and extend observations made in previous reports in Japanese language periodicals, which are reviewed.

scholarly journals Morphological study by an 'in vivo cryotechnique' of the shape of erythrocytes circulating in large blood vessels

1998 ◽  
Vol 193 (1) ◽  
pp. 73-79 ◽  
Author(s):  
MEI XUE ◽  
YASUKO KATO ◽  
NOBUO TERADA ◽  
YASUHISA FUJII ◽  
TAKESHI BABA ◽  
...  
Keyword(s):  
Blood Vessels ◽  
Morphological Study ◽  
In Vivo Cryotechnique

scholarly journals The netrin receptor DCC focuses invadopodia-driven basement membrane transmigration in vivo

2013 ◽  
Vol 201 (6) ◽  
pp. 903-913 ◽  
Author(s):  
Elliott J. Hagedorn ◽  
Joshua W. Ziel ◽  
Meghan A. Morrissey ◽  
Lara M. Linden ◽  
Zheng Wang ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Cancer Metastasis ◽  
Normal Development ◽  
Basement Membranes ◽  
Membrane Interface ◽  
Anchor Cell ◽  
Membrane Components ◽  
Invasive Cell ◽  
Basement Membrane Components

Though critical to normal development and cancer metastasis, how cells traverse basement membranes is poorly understood. A central impediment has been the challenge of visualizing invasive cell interactions with basement membrane in vivo. By developing live-cell imaging methods to follow anchor cell (AC) invasion in Caenorhabditis elegans, we identify F-actin–based invadopodia that breach basement membrane. When an invadopodium penetrates basement membrane, it rapidly transitions into a stable invasive process that expands the breach and crosses into the vulval tissue. We find that the netrin receptor UNC-40 (DCC) specifically enriches at the site of basement membrane breach and that activation by UNC-6 (netrin) directs focused F-actin formation, generating the invasive protrusion and the cessation of invadopodia. Using optical highlighting of basement membrane components, we further demonstrate that rather than relying solely on proteolytic dissolution, the AC’s protrusion physically displaces basement membrane. These studies reveal an UNC-40–mediated morphogenetic transition at the cell–basement membrane interface that directs invading cells across basement membrane barriers.

scholarly journals Basement membrane assembly of the integrin α8β1 ligand nephronectin requires Fraser syndrome–associated proteins

2012 ◽  
Vol 197 (5) ◽  
pp. 677-689 ◽  
Author(s):  
Daiji Kiyozumi ◽  
Makiko Takeichi ◽  
Itsuko Nakano ◽  
Yuya Sato ◽  
Tomohiko Fukuda ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Direct Consequence ◽  
Basement Membranes ◽  
Dystrophic Epidermolysis Bullosa ◽  
Membrane Assembly ◽  
Fraser Syndrome ◽  
Basement Membrane Protein ◽  
Integrin Binding Site ◽  
Associated Proteins

Dysfunction of the basement membrane protein QBRICK provokes Fraser syndrome, which results in renal dysmorphogenesis, cryptophthalmos, syndactyly, and dystrophic epidermolysis bullosa through unknown mechanisms. Here, we show that integrin α8β1 binding to basement membranes was significantly impaired in Qbrick-null mice. This impaired integrin α8β1 binding was not a direct consequence of the loss of QBRICK, which itself is a ligand of integrin α8β1, because knock-in mice with a mutation in the integrin-binding site of QBRICK developed normally and do not exhibit any defects in integrin α8β1 binding. Instead, the loss of QBRICK significantly diminished the expression of nephronectin, an integrin α8β1 ligand necessary for renal development. In vivo, nephronectin associated with QBRICK and localized at the sublamina densa region, where QBRICK was also located. Collectively, these findings indicate that QBRICK facilitates the integrin α8β1–dependent interactions of cells with basement membranes by regulating the basement membrane assembly of nephronectin and explain why renal defects occur in Fraser syndrome.

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