Research press release





今回Ardem Patapoutianの研究グループはマウスを使った研究で、Piezo2が肺の膨張を調節する役割について調べた。今回の研究では、成体マウスの特定のニューロンにおいてPiezo2を欠損させると、へーリング・ブロイウェル反射が損なわれ、肺の1回換気量が増加し、マウスが通常より大きく息を吸い込むようになった。また、Piezo2を欠損したマウスが、死産で生まれた。


The over-inflation of mouse lungs is prevented by the protein Piezo2, reports a study published online in Nature this week. The protein, previously implicated in the skin's sense of touch, regulates normal breathing and is also required for the initial lung inflation at birth. These findings may provide insights into respiratory disorders, such as sleep apnoea or chronic obstructive pulmonary disease.

Most mammals prevent their lungs from over-inflating through a response known as the Hering-Breuer reflex, which immediately stops further inhalation. The details of how this reflex works are, however, unclear. Piezo2 has previously been shown to help cells sense and respond to mechanical forces, and is abundant in sensory neurons.

Ardem Patapoutian and colleagues investigated the role of Piezo2 in regulating lung inflation in mice. They find that deleting Piezo2 in specific neurons in adult mice impairs the Hering-Breuer reflex, resulting in increased tidal lung volume (taking larger breaths than normal). Newborn mice that are deficient in Piezo2 die at birth.

These results indicate that Piezo2 senses when airways are stretching, establishing respiration in newborn mice and regulating normal breathing in adults. The authors propose that defects in the action of this stretch sensor may be implicated in respiratory disorders, such as chronic obstructive pulmonary disease, sudden infant death syndrome or adult sleep apnoea. However, the role of human PIEZO2 in respiration requires further investigation.

doi: 10.1038/nature20793

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