Sus scrofa
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PROVIDER: PRJNA144155 | ENA |
REPOSITORIES: ENA
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Project description:The arterial endothelium’s response to its flow environment is critical to vascular homeostasis. The endothelial glycocalyx has been shown to play a major role in mechanotransduction, but the extent to which the components of the glycocalyx affect the overall function of the endothelium remains unclear. The objective of this study was to further elucidate the role of heparan sulfate as a mechanosensor on the surface of the arterial endothelium, by (1) expanding the variety of shear waveforms investigated, (2) continuously suppressing heparan sulfate expression rather than using a pre-flow batch treatment, and (3) performing microarray analysis on post-flow samples. Porcine aortic endothelial cells were exposed to non-reversing, reversing, and oscillatory shear waveforms for 24 hours with or without continuous heparan sulfate suppression with heparinase. All shear waveforms significantly increased the amount of heparan sulfate on the surface of the endothelium. Suppression of heparan sulfate to less than 25% of control levels did not inhibit shear-induced cell alignment or nitric oxide production, or alter gene expression, for any of the shear waveforms investigated. We infer that heparan sulfate on the surface of porcine aortic endothelial cells is not the primary mechanosensor for many shear-responsive endothelial cell functions in this species.
2011-07-22 | GSE30843 | GEO
Project description:The arterial endothelium’s response to its flow environment is critical to vascular homeostasis. The endothelial glycocalyx has been shown to play a major role in mechanotransduction, but the extent to which the components of the glycocalyx affect the overall function of the endothelium remains unclear. The objective of this study was to further elucidate the role of heparan sulfate as a mechanosensor on the surface of the arterial endothelium, by (1) expanding the variety of shear waveforms investigated, (2) continuously suppressing heparan sulfate expression rather than using a pre-flow batch treatment, and (3) performing microarray analysis on post-flow samples. Porcine aortic endothelial cells were exposed to non-reversing, reversing, and oscillatory shear waveforms for 24 hours with or without continuous heparan sulfate suppression with heparinase. All shear waveforms significantly increased the amount of heparan sulfate on the surface of the endothelium. Suppression of heparan sulfate to less than 25% of control levels did not inhibit shear-induced cell alignment or nitric oxide production, or alter gene expression, for any of the shear waveforms investigated. We infer that heparan sulfate on the surface of porcine aortic endothelial cells is not the primary mechanosensor for many shear-responsive endothelial cell functions in this species. Porcine aortic endothelial cells were exposed to 3 different shear waveforms for 24 hours with or without the addition of 300 mU/ml heparinase III to the flow media. The shear waveforms inculded Non-reversing (15 ± 15 dyne/cm2, 1 Hz), Steady (15 dyne/cm2), or Oscillatory (0 ± 15 dyne/cm2, 1 Hz) shear. Four replicates of each condition were performed for a total of 24 experiments. Each experimental sample was hybridized to an oligonucleotide array along with a standard reference sample (static cells).
2011-07-21 | E-GEOD-30843 | biostudies-arrayexpress
Project description:Sepsis patients are at increased risk for hospital-acquired pulmonary infections, potentially due to post-septic immunosuppression known as the compensatory anti-inflammatory response syndrome (CARS). CARS has been attributed to leukocyte dysfunction, with an unclear role for endothelial cells. The pulmonary circulation is lined by an endothelial glycocalyx, a heparan sulfate-rich layer essential to pulmonary homeostasis. Heparan sulfate degradation occurs early in sepsis, leading to lung injury. Endothelial synthesis of new heparan sulfates subsequently allows for glycocalyx reconstitution and endothelial recovery. We hypothesized that remodeling of the reconstituted endothelial glycocalyx, mediated by alterations in the endothelial machinery responsible for heparan sulfate synthesis, contributes to CARS. Our experimental animal model of CARS recapitulated post-septic immunosuppression, coincidentally with structural remodeling of endothelial glycocalyx heparan sulfate. We used microarray to identify which heparan sulfate modifying enzyme is responsible for the remodeling of post-septic reconstituted glycocalyx, characterized with enrichment of heparan sulfate disaccharides sulfated at the 6-O position of glucosamine.
2019-04-14 | GSE129775 | GEO
Project description:Giantsos-Adams2013 - Growth of glycocalyx
under static conditions
This model is described in the article:
Heparan Sulfate Regrowth
Profiles Under Laminar Shear Flow Following Enzymatic
Degradation.
Giantsos-Adams KM, Koo AJ, Song S,
Sakai J, Sankaran J, Shin JH, Garcia-Cardena G, Dewey CF.
Cell Mol Bioeng 2013 Jun; 6(2):
160-174
Abstract:
The local hemodynamic shear stress waveforms present in an
artery dictate the endothelial cell phenotype. The observed
decrease of the apical glycocalyx layer on the endothelium in
atheroprone regions of the circulation suggests that the
glycocalyx may have a central role in determining
atherosclerotic plaque formation. However, the kinetics for the
cells' ability to adapt its glycocalyx to the environment have
not been quantitatively resolved. Here we report that the
heparan sulfate component of the glycocalyx of HUVECs increases
by 1.4-fold following the onset of high shear stress, compared
to static cultured cells, with a time constant of 19 h.
Cell morphology experiments show that 12 h are required
for the cells to elongate, but only after 36 h have the
cells reached maximal alignment to the flow vector. Our
findings demonstrate that following enzymatic degradation,
heparan sulfate is restored to the cell surface within
12 h under flow whereas the time required is 20 h
under static conditions. We also propose a model describing the
contribution of endocytosis and exocytosis to apical heparan
sulfate expression. The change in HS regrowth kinetics from
static to high-shear EC phenotype implies a differential in the
rate of endocytic and exocytic membrane turnover.
This model is hosted on
BioModels Database
and identified by:
MODEL1609100001.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2016-09-28 | MODEL1609100001 | BioModels
Project description:Giantsos-Adams2013 - Growth of glycocalyx
under static conditions
This model is described in the article:
Heparan Sulfate Regrowth
Profiles Under Laminar Shear Flow Following Enzymatic
Degradation.
Giantsos-Adams KM, Koo AJ, Song S,
Sakai J, Sankaran J, Shin JH, Garcia-Cardena G, Dewey CF.
Cell Mol Bioeng 2013 Jun; 6(2):
160-174
Abstract:
The local hemodynamic shear stress waveforms present in an
artery dictate the endothelial cell phenotype. The observed
decrease of the apical glycocalyx layer on the endothelium in
atheroprone regions of the circulation suggests that the
glycocalyx may have a central role in determining
atherosclerotic plaque formation. However, the kinetics for the
cells' ability to adapt its glycocalyx to the environment have
not been quantitatively resolved. Here we report that the
heparan sulfate component of the glycocalyx of HUVECs increases
by 1.4-fold following the onset of high shear stress, compared
to static cultured cells, with a time constant of 19 h.
Cell morphology experiments show that 12 h are required
for the cells to elongate, but only after 36 h have the
cells reached maximal alignment to the flow vector. Our
findings demonstrate that following enzymatic degradation,
heparan sulfate is restored to the cell surface within
12 h under flow whereas the time required is 20 h
under static conditions. We also propose a model describing the
contribution of endocytosis and exocytosis to apical heparan
sulfate expression. The change in HS regrowth kinetics from
static to high-shear EC phenotype implies a differential in the
rate of endocytic and exocytic membrane turnover.
This model is hosted on
BioModels Database
and identified by:
MODEL1609100001.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2019-10-09 | BIOMD0000000830 | BioModels
Project description:To study the genomic changes in senescent porcine coronary arterial endothelial cells by multiple passaging in vitro
| PRJNA102429 | ENA
Project description:Our specific aim is to examine differential expression of sulf-1 and sulf-2, enzymes involved in heparan sulfate biosynthesis, as well as Wnt ligands and Wnt signaling mediators during corneal wound healing using a mouse corneal scratch model. The specific structural features of heparan sulfate underlie its role in modulating cellular responses to growth factors such as the Wnts. Heparan sulfate 6-O-endosulfatases (sulf-1 and sulf-2) remove 6-O sulfate group from trisulfated disaccharides present on heparan sulfate chains. Our preliminary results suggest that sulf-1 is upregulated at the protein level in the epithelial cells of wounded mouse corneas, as compared to the undamaged contralateral eye. Modulation of heparan sulfate proteoglycan expression and/or structural modifications of its chains might be an important aspect of the regulation of epithelial cell migration and proliferation during wound healing.
2011-04-29 | GSE28931 | GEO
Project description:The general area of research interests of my lab is the glycobiology of HSPGs in cell-cell/cell-matrix interactions and growth factor signalling. Heparan sulfate binding proteins in neural development and differentiation. We used the Glyco-gene Chips to study the gene expression responses of mouse neural cells to heparin-binding growth factors. The experimental systems studied is in vivo (developing mouse brain). The goal is to examine the global responses of neural cells to particular growth factors during differentiation in terms of effects on HS biosynthetic enzymes and proteoglycan core proteins, as well as growth factors and their receptors. Analysis of A) P1 mouse brain wild type for Heparan sulfate 2-O sulfotransferase (HS2ST) and B) heterozygous for Heparan sulfate 2-O sulfotransferase (HS2ST) loss of function mutation.
2010-12-11 | E-GEOD-26010 | biostudies-arrayexpress
Project description:Large White and Meishan pigs were either non-treated or injected with mammalian 1-24 ACTH (Immediate Synachten, Novartis France) at the dose of 250 µg per animal. Pigs were sacrificed either immediately after capture from their home cage (non-treated animals) or 1 hour following ACTH injection. Adrenal glands were immediately collected from pigs and frozen on dry ice and then stored at -80°C until RNA isolation. Keywords: stress response, adrenal, gene expression, pig
2008-01-07 | GSE8377 | GEO
Project description: Not available
| S-EPMC7006094 | biostudies-literature