Role of microRNAs in regulation of urothelial permeability
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ABSTRACT:
REPOSITORIES: ENA
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Project description:Vascular permeability is frequently associated with inflammation and it is triggered by chemokines and by a cohort of secreted permeability factors, such as VEGF. In contrast, here we showed that the physiological vascular permeability that precedes implantation is directly controlled by progesterone receptor (PR) and it is independent of VEGF. Both global and endothelial-specific deletion of PR block physiological vascular permeability in the uterus while misexpression of PR in the endothelium of other organs results in ectopic vascular leakage. Integration of genome-wide transcriptional profile of endothelium and ChIP-sequencing revealed that PR induces a NR4A1 (Nur77/TR3) specific transcriptional program that broadly regulates vascular permeability in response to progesterone. This program triggers concurrent suppression of several junctional proteins and leads to an effective, timely and venule-specific regulation of vascular barrier function. Silencing NR4A1 blocks PR-mediated permeability responses indicating a direct link between PR and NR4A1. These results reveal a previously unknown function for progesterone receptor on endothelial cell biology with consequences to physiological vascular permeability and implications to the clinical use of progestins and anti-progestins on blood vessel integrity. Examination of PR binding sites in HUVEC cells using ChIP-seq (non-infected-negative control, PR infected followed by ligand treatment-PR+P or vehicle PR)
2014-01-01 | E-GEOD-43786 | biostudies-arrayexpress
Project description:Vascular permeability is frequently associated with inflammation and it is triggered by chemokines and by a cohort of secreted permeability factors, such as VEGF. In contrast, here we showed that the physiological vascular permeability that precedes implantation is directly controlled by progesterone receptor (PR) and it is independent of VEGF. Both global and endothelial-specific deletion of PR block physiological vascular permeability in the uterus while misexpression of PR in the endothelium of other organs results in ectopic vascular leakage. Integration of genome-wide transcriptional profile of endothelium and ChIP-sequencing revealed that PR induces a NR4A1 (Nur77/TR3) specific transcriptional program that broadly regulates vascular permeability in response to progesterone. This program triggers concurrent suppression of several junctional proteins and leads to an effective, timely and venule-specific regulation of vascular barrier function. Silencing NR4A1 blocks PR-mediated permeability responses indicating a direct link between PR and NR4A1. These results reveal a previously unknown function for progesterone receptor on endothelial cell biology with consequences to physiological vascular permeability and implications to the clinical use of progestins and anti-progestins on blood vessel integrity. Examination of PR target genes in human umbilical vein endothelial cells (HUVECs) using RNA-seq (PR infected only -PR only and PR infected followed by ligand treatment-PR+P)
2014-01-01 | E-GEOD-43788 | biostudies-arrayexpress
Project description:In this study, we aimed to determine the overall effect of TNFα on transcriptomic profile of urothelial cells using RNA sequencing. Our study represents a reference database that could lead to a better understanding of the role of urothelial cells in IC/BPS pathology and more importantly, sets grounds for future studies exploring potential biomarkers and therapeutic targets for IC/PBS diagnosis and treatment.
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Project description:Proctor2017- Role of microRNAs in osteoarthritis (miR140 in osteoarthritis)
This model is described in the article:
Computer simulation models
as a tool to investigate the role of microRNAs in
osteoarthritis.
Proctor CJ, Smith GR.
PLoS ONE 2017; 12(11): e0187568
Abstract:
The aim of this study was to show how computational models
can be used to increase our understanding of the role of
microRNAs in osteoarthritis (OA) using miR-140 as an example.
Bioinformatics analysis and experimental results from the
literature were used to create and calibrate models of gene
regulatory networks in OA involving miR-140 along with key
regulators such as NF-?B, SMAD3, and RUNX2. The individual
models were created with the modelling standard, Systems
Biology Markup Language, and integrated to examine the overall
effect of miR-140 on cartilage homeostasis. Down-regulation of
miR-140 may have either detrimental or protective effects for
cartilage, indicating that the role of miR-140 is complex.
Studies of individual networks in isolation may therefore lead
to different conclusions. This indicated the need to combine
the five chosen individual networks involving miR-140 into an
integrated model. This model suggests that the overall effect
of miR-140 is to change the response to an IL-1 stimulus from a
prolonged increase in matrix degrading enzymes to a pulse-like
response so that cartilage degradation is temporary. Our
current model can easily be modified and extended as more
experimental data become available about the role of miR-140 in
OA. In addition, networks of other microRNAs that are important
in OA could be incorporated. A fully integrated model could not
only aid our understanding of the mechanisms of microRNAs in
ageing cartilage but could also provide a useful tool to
investigate the effect of potential interventions to prevent
cartilage loss.
This model is hosted on
BioModels Database
and identified by:
MODEL1705170005.
To cite BioModels Database, please use:
Chelliah V et al. BioModels: ten-year
anniversary. Nucl. Acids Res. 2015, 43(Database
issue):D542-8.
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.
| MODEL1705170005 | BioModels
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Project description:To elucidate the role of Protein Kinase C in Urothelial Bladder Carcinoma.
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Project description:Proctor2017- Role of microRNAs in
osteoarthritis (Negative Feedback By MicroRNA)
This model is described in the article:
Computer simulation models
as a tool to investigate the role of microRNAs in
osteoarthritis.
Proctor CJ, Smith GR.
PLoS ONE 2017; 12(11): e0187568
Abstract:
The aim of this study was to show how computational models
can be used to increase our understanding of the role of
microRNAs in osteoarthritis (OA) using miR-140 as an example.
Bioinformatics analysis and experimental results from the
literature were used to create and calibrate models of gene
regulatory networks in OA involving miR-140 along with key
regulators such as NF-?B, SMAD3, and RUNX2. The individual
models were created with the modelling standard, Systems
Biology Markup Language, and integrated to examine the overall
effect of miR-140 on cartilage homeostasis. Down-regulation of
miR-140 may have either detrimental or protective effects for
cartilage, indicating that the role of miR-140 is complex.
Studies of individual networks in isolation may therefore lead
to different conclusions. This indicated the need to combine
the five chosen individual networks involving miR-140 into an
integrated model. This model suggests that the overall effect
of miR-140 is to change the response to an IL-1 stimulus from a
prolonged increase in matrix degrading enzymes to a pulse-like
response so that cartilage degradation is temporary. Our
current model can easily be modified and extended as more
experimental data become available about the role of miR-140 in
OA. In addition, networks of other microRNAs that are important
in OA could be incorporated. A fully integrated model could not
only aid our understanding of the mechanisms of microRNAs in
ageing cartilage but could also provide a useful tool to
investigate the effect of potential interventions to prevent
cartilage loss.
This model is hosted on
BioModels Database
and identified by:
MODEL1610100001.
To cite BioModels Database, please use:
Chelliah V et al. BioModels: ten-year
anniversary. Nucl. Acids Res. 2015, 43(Database
issue):D542-8.
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.
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Project description:The Notch signaling pathway controls cell fates through interactions between neighboring cells by positively or negatively affecting, in a context-dependent manner, processes of proliferation, differentiation, and apoptosis1. It has been implicated in human cancer both as an oncogene and a tumor suppressor2. Here we report, for the first time, novel inactivating mutations in the Notch pathway components in over forty percent of the human bladder cancers examined. Bladder cancer is the fourth most commonly diagnosed malignancy in the US male population3. Thus far, driver mutations in the FGFR3 and less commonly RAS proteins have been identified4,5. We show that Notch activation in bladder cancer cells suppresses proliferation both in vitro and in vivo by directly upregulating dual specificity phosphatases (DUSPs), thus reducing ERK1/2 phosphorylation. In mouse models, genetic inactivation of Notch signaling leads to ERK1/2 phosphorylation resulting in tumorigenesis in the urinary tract. In recent years, the tumor suppressor role of Notch has been recognized by loss-of-function mutations identified in myeloid cancers6 as well as squamous cell carcinomas of the skin, lung7, and the head and neck8,9. Of the 4 Notch receptors (N1-4), only N1 and 2 have been implicated in human cancer. two biological replicates from normal and tumor urothelial tissue were hybridized on Affymetrix mm 430 2.0 chips
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