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TRPV3 regulates nitric oxide synthase-independent nitric oxide synthesis in the skin
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Journal Article
TRPV3 regulates nitric oxide synthase-independent nitric oxide synthesis in the skin
2011
Overview
Nitric oxide (NO) is an unstable signalling molecule synthesized
de novo
mainly from
L
-arginine by NO synthase (NOS) enzymes. Nitrite reduction can also produce NO, predominantly within body fluids (for example, saliva, sweat and blood plasma) and under extreme hypoxic and acidic conditions. It remains unknown if intracellular canonical signalling pathways regulate nitrite-dependent NO production. Here we examine NO production in the skin, a hypoxic tissue enriched in nitrites wherein NO has important roles in wound healing and other biological processes. We show that activation of TRPV3, a heat-activated transient receptor potential ion channel expressed in keratinocytes, induces NO production via a nitrite-dependent pathway. TRPV3 and nitrite are involved in keratinocyte migration
in vitro
and in wound healing and thermosensory behaviours
in vivo
. Our study demonstrates that activation of an ion channel can induce NOS-independent NO production in keratinocytes.
Nitric oxide can be produced by nitric oxide synthase or by nitrite reduction, but whether the latter occurs inside cells is unknown. Here, the TRPV3 ion channel is shown to induce nitrite-dependent nitric oxide production in keratinocytes, where it has a role in thermosensory behaviour and wound healing.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
