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TRPP2 and TRPV4 are mechanosensitive channels in the endocardium.Oscillatory flow modulates mechanosensitive klf2a expression through trpv4 and trpp2 during heart valve development.
TRPP2 utilizes TRPV4 to form a mechano- and thermosensitive molecular sensor in the cilium.
Age-dependence of heat-activated seizure susceptibility mimicks the mRNA expression of TRPV4 and glutamate receptors.
TRPV4 present in all sensory organs of adult zebrafish.
Study reports cloning of a zebrafish trpv4 cDNA and assaying its expression during embryogenesis; trpv4 is expressed as maternal mRNA in 4-cell embryos and later zygotic expression is first observed in the forming notochord at the one somite stage.
OS-9 regulates the secretory transport of TRPV4 and appears to protect TRPV4 subunits from the precocious ubiquitination and ER-associated degradation.
Wildtype and mutant TRPV4 channels were expressed in human coronary artery endothelial cells (HCAECs). AA-induced TRPV4 activation was blunted in the S824A mutant but was enhanced in the phosphomimetic S824E mutant, whereas the channel activation by the synthetic agonist GSK1016790A was not affected.
TRPV4 mediates Ca(2+) influx and nuclear accumulation of DDX3X in cells exposed to the Zika virus. Targeting of TRPV4 reduces infectivity of dengue, hepatitis C and Zika viruses. Our results highlight the role of TRPV4 in the regulation of DDX3X-dependent control of RNA metabolism and viral infectivity.
Results suggest that transient receptor potential vanilloid 4 (TRPV4) accelerates glioma migration and invasion through the AKT/Rac1 signaling, and TRPV4 might be considered as a potential target for glioma therapy.
study for the first time demonstrated an abnormal TRPV4-related mechanosensitive Ca(2+) signaling in Dilated cardiomyopathy induced-pluripotent stem cells-derived cardiomyocytes.
There is expression of TRPV4 channels on the nerve fibers of human dental pulp. Findings suggest upregulation of TRPV4 expression under inflammatory conditions in the pulp. The upregulation of TRPV4 channels may be associated with the exaggerated response of dental pulp to innocuous mechanical, thermal and osmotic stimuli under inflammatory conditions.
the antitumor effects caused by TRPV4 channel inhibition in hepatocellular carcinoma cell lines might be attributed to the suppression of epithelial-mesenchymal transition process and inactivation of phospho-ERK which induced subsequent cell apoptosis.
Hypothermia-mediated increase in AQP4 surface abundance on human astrocytes, which was blocked using either calmodulin antagonist; TRPV4 antagonist or calcium chelation. A TRPV4 agonist mimicked the effect of hypothermia compared with untreated normothermic astrocytes. Hypothermia increased surface localization of AQP4 in human astrocytes likely through TRPV4 calcium channels and calmodulin activation.
our study suggests a role for compound heterozygosity and loss-of-function as a potential novel disease mechanism for this group of disorders. Profound intellectual disability was also noted in both affected children, suggesting that TRPV4 may be necessary for normal brain development.
Findings indicate that TRPV4 channels function as a critical component of mechano-sensitive, Ca2+-signaling machinery within the trabecular meshwork (TM), and that TRPV4-dependent cytoskeletal remodeling regulates TM stiffness and outflow. Thus, TRPV4 is a potential IOP sensor within the conventional outflow pathway.
These results identify an essential role of TRPV4 in flow shear stress-induced early osteogenic differentiation of human mesenchymal stem cells.
axonal colocalization of TRPV4 and TRPC6 was found in the digital Meissner corpuscles
TRPV4 is essential for human retinal capillary endothelial cell migration and tube formation, and maybe a potential therapeutic target for retinal vascular diseases.
TRPV4 is believed to be a mechanoreceptor in the bladder and is also involved in intercellular connectivity and structural integrity of the epithelium
this study, demonstrates for the first time that calcium exerts an oncogenic action in the stomach through activation of CaSR and TRPV4 channels. Both CaSR and TRPV4 were involved in Ca2+-induced proliferation, migration, and invasion of gastric cancer cells through a Ca2+/AKT/beta-catenin relay, which occurred only in gastric cancer cells or normal cells overexpressing CaSR.
TRPV4 involvement in RVD depends on the type of stimuli and/or degree of channel activation, leading to a maximum RVD response when Ca(2+) influx overcomes a threshold and activates further signaling pathways in cell volume regulation.
Studies demonstrate that TRPV4 play a leading function in many fibrotic disease. Increasing evidence shows that TRPV4 modulated fibroblasts proliferation and differentiation to myofibroblasts. While in cystic fibrosis, the defective regulatory volume decrease might be caused by the absence TRPV4 and in pancreatic fibrosis, TRPV4 serves as a sensor responsive to inflammation, hypotonic saline and pain. [review]
Arg594His substitution in TRPV4 causes SMD Kozlowski type.
Data show that transient receptor potential vanilloid 4 (TRPV4)expression is enhanced in a subset of basal breast cancers.
studies identified TRPV4 as a channel that contributes to both histamine- and chloroquine-induced itch and indicated that the function of TRPV4 in itch signaling involves TRPV1-mediated facilitation.
the results of this study suggest that clinical evaluation of patients with musculoskeletal disorders similar to the peripheral neuropathies or skeletal dysplasias with scoliosis that have been ascribed to the TRPV4 spectrum could consider whether the phenotypes might result from somatic mosaicism in the target tissues affected in these phenotypes.
Smooth muscle cell Gq protein-coupled receptor stimulation triggers inositol 1,4,5-trisphosphate-dependent activation of endothelial TRPV4 channels to limit vasoconstriction.
Muscarinic stimulation of saliva and tear secretion was down-regulated in TRPV4-deficient mice. Temperature dependence of muscarinic salivation was depended mainly on TRPV4.
STIM1 and TRPV4 act as mechanical transduction channels for osteoclasts during the early and late differentiation stages, respectively.
mediates immediate LPS-induced increases in ciliary beat frequency and the production of bactericidal nitric oxide
that TRPV4 activation results in the proliferation of stem cells in the adult hippocampal dentate gyrus
a role of TRPV4 in skin diseases such as systemic scleroderma.
TRPV4 plays a key role in LL37- driven mast cell activation in rosacea.
High TRPV4 expression is associated with maternal fever-associated birth defects.
Cartilage-specific knockout of TRPV4 decreases age-related osteoarthritis.
TRPV4 was shown to be required for breast cancer cell invasion and transendothelial migration but not growth/proliferation. Knockdown of Trpv4 significantly reduced the number of metastatic nodules in mouse xenografts leaving the size unaffected.
Study found that TRPV4, but not AQP4, contributes to the calcium influx into astrocytes and neurons as well as glutamate accumulation during middle cerebral artery occlusion stroke model-associated peri-infarct depolarizations (PIDs), but that neither channel influences the threshold for PID in the first hours after stroke.
The findings identify a novel role for TRPV4 in regulating macrophage foam cell formation by modulating uptake of oxLDL.
Fluorescence resonance energy transfer experiments showed that FliI-NMMIIA interactions require Ca(2+) influx. We conclude that Ca(2+) influx through the TRPV4 channel regulates FliI-NMMIIA interaction, which in turn enables generation of the cell extensions essential for collagen remodeling
Regulation of TRPV4 activity in the distal nephron by dietary potassium is an indispensable component of whole body potassium balance.
Both TRPV4 and PIEZO1 channels contribute to currents activated by stimuli applied at cell-substrate contacts but only PIEZO1 mediates stretch-activated currents. These data demonstrate that there are separate, but overlapping, mechanoelectrical transduction pathways in chondrocytes.
These results suggest that TRPV4, TRPV3 and TRPM8 proteins, but not their ion channel activities are necessary for the induction of CIPs at 32 degrees C. Identification of proteins that differentially interact with these TRP channels at 37 degrees C and 32 degrees C would help elucidate the underlying mechanisms of CIP induction by hypothermia.
we show that TRPV4 is activated both by damage associated molecular pattern HMGB1 and collagen in diseased Kupffer cells that in turn activate the endothelial NOS (NOS3) to release nitric oxide (NO). The diffusible NO acts in a paracrine fashion in neighboring hepatocytes to deactivate the redox toxicity induced by CYP2E1
these data suggest that TRPV4 regulates angiogenesis endogenously via modulation of endothelial cells mechanosensitivity
findings also indicate that TRPV4 channels are mechanosensors in neonatal pig preglomerular vascular SMCs and contribute to renal myogenic autoregulation
Data indicate a physiologic function of transient receptor potential vanilloid 4 (TRPV4) in the regulation of blood-cerebrospinal fluid barrier (BCSFB) permeability.
Hyposmotic shock-induced TRPV4 channel activation regulates hemichannel-mediated ATP release and Na-K-ATPase activity in lens epithelium.
The large amounts of transported calcium and the short signaling ways suggest a potentially important role of TRPV4 in many physiological processes.
TRPV4 is present in articular chondrocytes in swine, and chondrocyte response to hypo-osmotic stress is mediated by this channel, which involves both an extracellular Ca(2+) and intracellular Ca(2+) release.
reduced tissue osmolarity, likely following proteoglycan degradation, can increase TRPV4 signalling and enhance pro-inflammatory cytokine production.
TRPV4 channels activity in bovine articular chondrocytes are regulated by obesity-associated mediators.
TRPV4 channels mediate cyclic strain-induced endothelial cell reorientation through integrin-to-integrin signaling.
This gene encodes a member of the OSM9-like transient receptor potential channel (OTRPC) subfamily in the transient receptor potential (TRP) superfamily of ion channels. The encoded protein is a Ca2+-permeable, nonselective cation channel that is thought to be involved in the regulation of systemic osmotic pressure. Mutations in this gene are the cause of spondylometaphyseal and metatropic dysplasia and hereditary motor and sensory neuropathy type IIC. Multiple transcript variants encoding different isoforms have been found for this gene.
transient receptor potential cation channel subfamily V member 4
, transient receptor potential cation channel, subfamily V, member 4
, transient receptor potential cation channel subfamily V member 4-like
, OSM9-like transient receptor potential channel 4
, osm-9-like TRP channel 4
, osmosensitive transient receptor potential channel 4
, transient receptor potential protein 12
, vanilloid receptor-like channel 2
, vanilloid receptor-related osmotically activated channel
, vanilloid receptor-like protein 2
, vanilloid receptor-related osmotically-activated channel
, transient receptor potential cation channel, subfamily 5, member 4
, vanilloid receptor-related osmotically activated channel (Vroac)
, vanilloid receptor-related osmotically activated channel protein