The effect of hydrostatic pressure in C. elegans
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ABSTRACT:
PROVIDER: PRJNA552290 | ENA |
REPOSITORIES: ENA
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Project description:We examined whether hydrostatic-pressure induced nuclear DAF-16 functions as a transcription factor. The expression changes were monitored by using DNA microarray analyses, after the WT adult hermaphrodites were exposed to a pressure of ≥30 MPa for 5 minutes. The results showed significant and reproducible increase of 31 genes after 30 minutes
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Project description:The role of pathological vascular degeneration in cirrhosis remains poorly understood. In this study, we engineered multidimensional vascular models to replicate the pathological characteristics of liver sinusoidal endothelial cells (LSECs) at various fibrosis stages. Our investigation revealed that LSEC response to hydrostatic pressure is matrix stiffness-dependent, with LSECs survival when cultured on soft matrices, while those cultured on hard matrices experiencing cellular damage. The biomimic vascular in vitro model enabled us to identify GPR116 as a crucial membrane receptor of LSECs to sense and respond to hydrostatic pressure. GPR116 is specifically expressed in liver endothelial cells, and silencing GPR116 effectively protected the endothelial cells from hydrostatic pressure-induced damage on hard matrix, consequently inhibiting hepatic stellate cell activation and collagen remodeling. Thus, our findings highlight GPR116 as an indispensable pressure sensor in hepatic sinusoidal endothelium, playing a pivotal role in vascular remodeling during cirrhosis.
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Project description:The role of pathological vascular degeneration in cirrhosis remains poorly understood. In this study, we engineered multidimensional vascular models to replicate the pathological characteristics of liver sinusoidal endothelial cells (LSECs) at various fibrosis stages. Our investigation revealed that LSEC response to hydrostatic pressure is matrix stiffness-dependent, with LSECs survival when cultured on soft matrices, while those cultured on hard matrices experiencing cellular damage. The biomimic vascular in vitro model enabled us to identify GPR116 as a crucial membrane receptor of LSECs to sense and respond to hydrostatic pressure. GPR116 is specifically expressed in liver endothelial cells, and silencing GPR116 effectively protected the endothelial cells from hydrostatic pressure-induced damage on hard matrix, consequently inhibiting hepatic stellate cell activation and collagen remodeling. Thus, our findings highlight GPR116 as an indispensable pressure sensor in hepatic sinusoidal endothelium, playing a pivotal role in vascular remodeling during cirrhosis.
2025-12-04 | GSE244720 | GEO
Project description:The role of pathological vascular degeneration in cirrhosis remains poorly understood. In this study, we engineered multidimensional vascular models to replicate the pathological characteristics of liver sinusoidal endothelial cells (LSECs) at various fibrosis stages. Our investigation revealed that LSEC response to hydrostatic pressure is matrix stiffness-dependent, with LSECs survival when cultured on soft matrices, while those cultured on hard matrices experiencing cellular damage. The biomimic vascular in vitro model enabled us to identify GPR116 as a crucial membrane receptor of LSECs to sense and respond to hydrostatic pressure. GPR116 is specifically expressed in liver endothelial cells, and silencing GPR116 effectively protected the endothelial cells from hydrostatic pressure-induced damage on hard matrix, consequently inhibiting hepatic stellate cell activation and collagen remodeling. Thus, our findings highlight GPR116 as an indispensable pressure sensor in hepatic sinusoidal endothelium, playing a pivotal role in vascular remodeling during cirrhosis.
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Project description:Transcription profiling of mouse oocytes treated with 20 MPa hydrostatic pressure for 60 minutes at 37 °C comparing control oocytes kept under identical conditions as pressure treated ones, except HHP treatment.
2012-01-06 | GSE28410 | GEO
Project description:In this study, we performed a global quantitative proteomic analysis under extreme temperatures, pH, hydrostatic pressure (HP) and salinity on an archaeal strain, Thermococcus eurythermalis A501. Here is the result of pressure adaptation: HP (40 MPa) tested under 85°C and 95°C, and the optimal culture condition (85°C, pH 7, 2.3% NaCl, 10 MPa) was used as the control.
2020-09-09 | PXD019007 | Pride
Project description:Transcription profiling of mouse oocytes treated with 20 MPa hydrostatic pressure for 60 minutes at 37 °C comparing control oocytes kept under identical conditions as pressure treated ones, except HHP treatment. One-condition experiment, HP treated oocytes vs. Control oocytes. Biological replicates: 4 HP treated replicates, 4 control replicates.
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Project description:The role of pathological vascular degeneration in cirrhosis remains poorly understood. In this study, we engineered multidimensional vascular models to replicate the pathological characteristics of liver sinusoidal endothelial cells (LSECs) at various fibrosis stages. Our investigation revealed that LSEC response to hydrostatic pressure is matrix stiffness-dependent, with LSECs survival when cultured on soft matrices, while those cultured on hard matrices experiencing cellular damage. The biomimic vascular in vitro model enabled us to identify GPR116 as a crucial membrane receptor of LSECs to sense and respond to hydrostatic pressure. GPR116 is specifically expressed in liver endothelial cells, and silencing GPR116 effectively protected the endothelial cells from hydrostatic pressure-induced damage on hard matrix, consequently inhibiting hepatic stellate cell activation and collagen remodeling. Thus, our findings highlight GPR116 as an indispensable pressure sensor in hepatic sinusoidal endothelium, playing a pivotal role in vascular remodeling during cirrhosis.
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Project description:Hydrostatic pressure is one of the main mechanical stimuli cartilage cells are submitted to during joint loading. If moderate hydrostatic pressure is known to be beneficial to cartilage differentiation, excessive pressure, on the other hand, induces changes in cartilage similar to those observed in osteoarthritic cartilage. Therefore, the purpose of the experiment is to identify new target genes of high hydrostatic pressure in chondrocyte precursor cells.
2017-12-02 | E-MTAB-5326 | biostudies-arrayexpress
Project description:We have identified differentially expressed genes according to hydrostatic pressure growth conditions in Desulfovibrio hydrothermalis. The transcriptomic datasets report the molecular mechanisms which could be involved in such adaptation and give information for the piezophile sulfate-reducing bacteria research communities. The data obtained pointed out a gradual response of D. hydrothermalis to an increase of hydrostatic pressure, with a threshold above 10 MPa and the involvement of a quite limited number of genes and/or pathways involved in the adaptation to hydrostatic pressure.
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