Disease relevance of Trpv2

• Dual expression of mouse and rat VRL-1 in the dorsal root ganglion derived cell line F-11 and biochemical analysis of VRL-1 after heterologous expression [1].
• Consistent with these findings, cardiac-specific expression of GRC in a transgenic mouse model produced cardiomyopathy due to Ca2+ overloading, with disease expression roughly parallel to sarcolemmal GRC levels [2].
• Regulation of GRC, the murine homolog of TRPV2 has been studied in insulinoma cells and myocytes [3].

High impact information on Trpv2

• Upon stimulation of cells by IGF-I, GRC translocates to the plasma membrane [4].
• Analysis of the properties of myotubes prepared from delta-sarcoglycan-deficient BIO14.6 hamsters revealed that GRC is activated in response to myocyte stretch and is responsible for enhanced Ca2+ influx and resultant cell damage as measured by creatine phosphokinase efflux [2].
• We found that cell stretch increases GRC translocation to the sarcolemma, which requires entry of external Ca2+ [2].
• These data indicate that in whole splenic cell populations, GRC is derived from IgG-bearing B cells that are stimulated by antigen and a component in TRF [5].
• GRC has been shown to be unrestricted by histocompatibility barriers since it enhanced IgG antibody production in mice of diverse genetic backgrounds [5].

Biological context of Trpv2

• Head activator functions as an inducer of GRC translocation in neuronal and neuroendocrine cells, which express GRC endogenously, and also in COS-7 cells after transfection with GRC [6].
• Furthermore we cloned VRL-1 from rat brain and analyzed its glycosylation and localization in comparison to the endogenously expressed protein in F-11 cells [1].
• Cell size of primary sensory neurons and distribution patterns of neurons that are immunopositive (ip) for VRL-1, a newly cloned capsaicin-receptor homologue, were examined in trigeminal ganglia (TGs) of knockout mice for trkA, trkB or trkC to determine the developmental dependency of myelinated nociceptors on expression of the genes [7].
• Another set of genes, which influences growth and development, is linked to the MHC in the mouse (T/t complex) and in the rat (Grc): this entire chromosomal region may function as a "supergene" with broad effects on tissue organization and compatibility [8].
• Cytogenetic localization of the growth and reproduction complex (Grc) in the rat and in the mouse and its position in relation to RT1.EC and other loci in the rat MHC [9].

Anatomical context of Trpv2

• A high expression level of the VR-1 like protein (VRL-1) was observed in peritoneal macrophages, while the expression of VR-1 was not detected [10].
• The F-11 parental cell line N18TG2 also expressed murine VRL-1 [1].
• Here we describe the expression of VRL-1 in the rat dorsal root ganglion-derived cell line F-11, a hybridoma of mouse neuroblastoma (N18TG2) and rat dorsal root ganglion cells [1].
• The results suggest that GRC is a key player in the pathogenesis of myocyte degeneration caused by dystrophin-glycoprotein complex disruption [2].
• Hence, B cells lacking IgG but possessing IgM surface immunoglobulins appear to be those that are acted upon by GRC [5].

Associations of Trpv2 with chemical compounds

• In contrast to VR1, VRL-1 is activated at a higher temperature threshold and it does not respond to capsaicin or protons [1].

Other interactions of Trpv2

• Immunohistochemistry for protein gene product 9.5 (PGP 9.5, a neuron specific protein) and vanilloid receptor 1-like receptor (VRL-1, a marker for medium-sized to large primary nociceptors) were used to assess the effects of Brn-3a deficiency on neuronal innervation of oral tissues and neurons of the trigeminal ganglion (TG) [11].

Analytical, diagnostic and therapeutic context of Trpv2

• We found by RT-PCR that F-11 cells express not only the rat VRL-1, but also its mouse orthologue in a single cell [1].
• Immunofluorescence analysis of the endogenous VRL-1 in F-11 cells gives only weak signals in the cytoplasm whereas the overexpressed rat VRL-1 appears mainly at the plasma membrane [1].

References