scholarly journals Sensitization of glutamate receptor ‐mediated pain behaviour via nerve growth factor‐dependent phosphorylation of transient receptor potential V1 under inflammatory conditions

2020 ◽  
Vol 177 (18) ◽  
pp. 4223-4241
Author(s):  
Takayoshi Masuoka ◽  
Yuka Yamashita ◽  
Junko Yoshida ◽  
Katsuya Nakano ◽  
Masashi Tawa ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Glutamate Receptor ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Pain Behaviour ◽  
Nerve Growth ◽  
Inflammatory Conditions ◽  
Transient Receptor

Signaling Pathways Relevant to Nerve Growth Factor-induced Upregulation of Transient Receptor Potential M8 Expression

Neuroscience ◽  
2017 ◽  
Vol 367 ◽  
pp. 178-188 ◽  
Author(s):  
Yohei Kayama ◽  
Mamoru Shibata ◽  
Tsubasa Takizawa ◽  
Keiji Ibata ◽  
Jin Nakahara ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Signaling Pathways ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Nerve Growth ◽  
Transient Receptor

Transient receptor potential vanilloid 1 mediates nerve growth factor-induced bladder hyperactivity and noxious input

2012 ◽  
Vol 110 (8b) ◽  
pp. E422-E428 ◽  
Author(s):  
Barbara Frias ◽  
Ana Charrua ◽  
Antonio Avelino ◽  
Martin C. Michel ◽  
Francisco Cruz ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
Nerve Growth ◽  
Transient Receptor

scholarly journals Nerve Growth Factor Regulates Transient Receptor Potential Vanilloid 2 via Extracellular Signal-Regulated Kinase Signaling To Enhance Neurite Outgrowth in Developing Neurons

2015 ◽  
Vol 35 (24) ◽  
pp. 4238-4252 ◽  
Author(s):  
Matthew R. Cohen ◽  
William M. Johnson ◽  
Jennifer M. Pilat ◽  
Janna Kiselar ◽  
Alicia DeFrancesco-Lisowitz ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Neurite Outgrowth ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Transient Receptor ◽  
Developing Neurons

Neurite outgrowth is key to the formation of functional circuits during neuronal development. Neurotrophins, including nerve growth factor (NGF), increase neurite outgrowth in part by altering the function and expression of Ca2+-permeable cation channels. Here we report that transient receptor potential vanilloid 2 (TRPV2) is an intracellular Ca2+-permeable TRPV channel upregulated by NGF via the mitogen-activated protein kinase (MAPK) signaling pathway to augment neurite outgrowth. TRPV2 colocalized with Rab7, a late endosome protein, in addition to TrkA and activated extracellular signal-regulated kinase (ERK) in neurites, indicating that the channel is closely associated with signaling endosomes. In line with these results, we showed that TRPV2 acts as an ERK substrate and identified the motifs necessary for phosphorylation of TRPV2 by ERK. Furthermore, neurite length, TRPV2 expression, and TRPV2-mediated Ca2+signals were reduced by mutagenesis of these key ERK phosphorylation sites. Based on these findings, we identified a previously uncharacterized mechanism by which ERK controls TRPV2-mediated Ca2+signals in developing neurons and further establish TRPV2 as a critical intracellular ion channel in neuronal function.

Importance of melastatin-like transient receptor potential 7 and magnesium in the stimulation of osteoblast proliferation and migration by platelet-derived growth factor

2009 ◽  
Vol 297 (2) ◽  
pp. C360-C368 ◽  
Author(s):  
Elie Abed ◽  
Robert Moreau
Keyword(s):  
Growth Factor ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Platelet Derived Growth Factor ◽  
Human Osteoblast ◽  
Osteoblast Proliferation ◽  
Transient Receptor ◽  
And Migration ◽  
Stimulation Of ◽  
Proliferation And Migration

Bone is a dynamic tissue that is continuously being remodeled throughout life. Specialized cells called osteoclasts transiently break down old bone (resorption process) at multiple sites as other cells known as osteoblasts are replacing it with new tissue (bone formation). Usually, both resorption and formation processes are in balance and thereby maintain skeletal strength and integrity. This equilibrium is assured by the coordination of proliferation, migration, differentiation, and secretory functions of the osteoblasts, which are essential for adequate formation and resorption processes. Disturbances of this equilibrium may lead to decreased bone mass (osteoporosis), increased bone fragility, and susceptibility to fractures. Epidemiological studies have linked insufficient dietary magnesium (Mg2+) intake in humans with low bone mass and osteoporosis. Here, we investigated the roles of Mg2+ and melastatin-like transient receptor potential 7 (TRPM7), known as Mg2+ channels, in human osteoblast cell proliferation and migration induced by platelet-derived growth factor (PDGF), which has been involved in the bone remodeling process. PDGF promoted an influx of Mg2+, enhanced cell migration, and stimulated the gene expression of TRPM7 channels in human osteoblast MG-63 cells. The stimulation of osteoblast proliferation and migration by PDGF was significantly reduced under culture conditions of low extracellular Mg2+ concentrations. Silencing TRPM7 expression in osteoblasts by specific small interfering RNA prevented the induction by PDGF of Mg2+ influx, proliferation, and migration. Our results indicate that extracellular Mg2+ and TRPM7 are important for PDGF-induced proliferation and migration of human osteoblasts. Thus Mg2+ deficiency, a common condition among the general population, may be associated with altered osteoblast functions leading to inadequate bone formation and the development of osteoporosis.

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