scholarly journals CB1 Cannabinoid Receptor Stimulation Modulates Transient Receptor Potential Vanilloid Receptor 1 Activities in Calcium Influx and Substance P Release in Cultured Rat Dorsal Root Ganglion Cells

2005 ◽  
Vol 97 (3) ◽  
pp. 377-385 ◽  
Author(s):  
Kyoko Oshita ◽  
Atsuko Inoue ◽  
He-Bin Tang ◽  
Yoshihiro Nakata ◽  
Masashi Kawamoto ◽  
...  
Keyword(s):  
Transient Receptor Potential ◽  
Cannabinoid Receptor ◽  
Ganglion Cells ◽  
Calcium Influx ◽  
Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
Cb1 Cannabinoid Receptor ◽  
Vanilloid Receptor 1 ◽  
Transient Receptor ◽  
Dorsal Root Ganglion Cells

scholarly journals Molecular mapping of transmembrane mechanotransduction through the β1 integrin–CD98hc–TRPV4 axis

2020 ◽  
Vol 133 (20) ◽  
pp. jcs248823 ◽  
Author(s):  
Ratnakar Potla ◽  
Mariko Hirano-Kobayashi ◽  
Hao Wu ◽  
Hong Chen ◽  
Akiko Mammoto ◽  
...  
Keyword(s):  
Transient Receptor Potential ◽  
Molecular Mapping ◽  
Calcium Influx ◽  
Focal Adhesions ◽  
Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
Β1 Integrin ◽  
Mechanical Forces ◽  
C Terminus ◽  
Transient Receptor

ABSTRACTOne of the most rapid (less than 4 ms) transmembrane cellular mechanotransduction events involves activation of transient receptor potential vanilloid 4 (TRPV4) ion channels by mechanical forces transmitted across cell surface β1 integrin receptors on endothelial cells, and the transmembrane solute carrier family 3 member 2 (herein denoted CD98hc, also known as SLC3A2) protein has been implicated in this response. Here, we show that β1 integrin, CD98hc and TRPV4 all tightly associate and colocalize in focal adhesions where mechanochemical conversion takes place. CD98hc knockdown inhibits TRPV4-mediated calcium influx induced by mechanical forces, but not by chemical activators, thus confirming the mechanospecificity of this signaling response. Molecular analysis reveals that forces applied to β1 integrin must be transmitted from its cytoplasmic C terminus via the CD98hc cytoplasmic tail to the ankyrin repeat domain of TRPV4 in order to produce ultrarapid, force-induced channel activation within the focal adhesion.

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