2023-04-04 ワシントン州立大学(WSU)
C. elegans線虫を用いた研究で、神経系に存在するタンパク質が多くの動物の皮膚、骨、結合組織の主要な構成要素であるコラーゲンの発現を制御することが明らかになった。
このタンパク質は人間を含む他の種類の神経系受容体タンパク質と類似しており、コラーゲン発現を利用して、気温上昇に伴う人間の老化を遅らせ、寿命を延ばす方法を見つけることができる可能性がある。
<関連情報>
- https://news.wsu.edu/press-release/2023/04/04/discovery-could-hold-the-key-to-healthy-aging-during-global-warming/
- https://onlinelibrary.wiley.com/doi/10.1111/acel.13815
温熱による長寿反応は、コラーゲン遺伝子の制御を介して神経的にコントロールされている。 The longevity response to warm temperature is neurally controlled via the regulation of collagen genes
Sankara Naynar Palani, Durai Sellegounder, Phillip Wibisono, Yiyong Liu
Aging Cell Published: 09 March 2023
DOI:https://doi.org/10.1111/acel.13815
Abstract
Studies in diverse species have associated higher temperatures with shorter lifespan and lower temperatures with longer lifespan. These inverse effects of temperature on longevity are traditionally explained using the rate of living theory, which posits that higher temperatures increase chemical reaction rates, thus speeding up the aging process. Recent studies have identified specific molecules and cells that affect the longevity response to temperature, indicating that this response is regulated, not simply thermodynamic. Here, we demonstrate that in Caenorhabditis elegans, functional loss of NPR-8, a G protein-coupled receptor related to mammalian neuropeptide Y receptors, increases worm lifespan at 25°C but not at 20°C or 15°C, and that the lifespan extension at 25°C is regulated by the NPR-8-expressing AWB and AWC chemosensory neurons as well as AFD thermosensory neurons. Integrative transcriptomic analyses revealed that both warm temperature and old age profoundly alter gene expression and that genes involved in the metabolic and biosynthetic processes increase expression at 25°C relative to 20°C, indicating elevated metabolism at warm temperature. These data demonstrate that the temperature-induced longevity response is neurally regulated and also provide a partial molecular basis for the rate of living theory, suggesting that these two views are not mutually exclusive. Genetic manipulation and functional assays further uncovered that the NPR-8-dependent longevity response to warm temperature is achieved by regulating the expression of a subset of collagen genes. As increased collagen expression is a common feature of many lifespan-extending interventions and enhanced stress resistance, collagen expression could be critical for healthy aging.
