ArticleStem cell research & therapy2026
Activation of the G-protein coupled estrogen receptor 1 (GPER1) reduces transient receptor potential vanilloid 1 (TRPV1) activity and human iPSC-derived nociceptive neuron firing.
Article in Stem cell research & therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Chronic pain affects approximately one fifth of people worldwide and displays a huge burden for health care institutions. Some chronic pain conditions have a higher prevalence in women than men. Previous studies related these sex-specific differences to sex-hormone receptor activation and interaction with pain-related receptors like the transient receptor potential vanilloid 1 (TRPV1). Here, especially estrogen seems to play a crucial role. While the role of estrogen receptor alpha and beta in modulating TRPV1 has already been studied, the interplay of the membrane-bound and G-protein -coupled estrogen receptor (GPER1) with nociceptor-associated ion channels is still unknown. The study at hand focuses on the establishment of a human induced pluripotent stem cell (iPSC) -based nociceptor model to unravel the effect of GPER1 activation on nociceptor excitability. Therefore, a human dermal fibroblast cell line was successfully reprogrammed into the iPSC line BO-VC1 and subsequently differentiated into nociceptors expressing GPER1 besides TRPV1 and the Twik-related spinal cord potassium channel (TRESK). The activation of GPER1 by its specific agonist G-1 led to significantly reduced action potential firing rates and TRPV1-mediated calcium influx. In addition, GPER1 was found to downregulate TRPV1-mediated ion currents upon G-1 treatment in a human embryonic kidney cell -based model. Our findings support the hypothesis that GPER1 activation silences neuronal excitability in nociceptors, probably being a candidate for future research focusing on targeted pain modulation.
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