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诺奖文集 2021年诺贝尔医学奖 帕塔普蒂安

已有 805 次阅读 2022-9-20 06:07 |个人分类:诺贝尔奖|系统分类:论文交流



Ardem Patapoutian, male, born in Beirut, Lebanon in 1967, of Armenian origin, is a molecular biologist and neuroscientist at the Scripps Institute in La Jolla, California, USA. [2] [4]

On October 4, 2021, he won the 2021 Nobel Prize in Physiology or Medicine. [1]

雅顿·帕塔普蒂安(Ardem Patapoutian),男,1967年出生于黎巴嫩贝鲁特,亚美尼亚裔,分子生物学家和神经学家,在美国加利福尼亚州拉霍亚斯克里普斯研究所。 [2]  [4] 

2021年10月4日,获得2021年诺贝尔生理学或医学奖 [1]

https://baike.baidu.com/item/%E9%9B%85%E9%A1%BF%C2%B7%E5%B8%95%E5%A1%94%E6%99%AE%E8%92%82%E5%AE%89/58754597?fromModule=lemma_inlink



https://pubmed.ncbi.nlm.nih.gov/34569935/


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Elifev

2021 Sep 27;10:e65415.

 doi: 10.7554/eLife.65415.

Spatiotemporal dynamics of PIEZO1 localization controls keratinocyte migration during wound healing

Jesse R Holt 1 2 3Wei-Zheng Zeng # 4Elizabeth L Evans # 1 2Seung-Hyun Woo # 4Shang Ma 4Hamid Abuwarda 1 2Meaghan Loud 4Ardem Patapoutian 4Medha M Pathak 1 2 3 5

Affiliations expand

Free PMC article

Erratum in

Abstract

Keratinocytes, the predominant cell type of the epidermis, migrate to reinstate the epithelial barrier during wound healing. Mechanical cues are known to regulate keratinocyte re-epithelialization and wound healing; however, the underlying molecular transducers and biophysical mechanisms remain elusive. Here, we show through molecular, cellular, and organismal studies that the mechanically activated ion channel PIEZO1 regulates keratinocyte migration and wound healing. Epidermal-specific Piezo1 knockout mice exhibited faster wound closure while gain-of-function mice displayed slower wound closure compared to littermate controls. By imaging the spatiotemporal localization dynamics of endogenous PIEZO1 channels, we find that channel enrichment at some regions of the wound edge induces a localized cellular retraction that slows keratinocyte collective migration. In migrating single keratinocytes, PIEZO1 is enriched at the rear of the cell, where maximal retraction occurs, and we find that chemical activation of PIEZO1 enhances retraction during single as well as collective migration. Our findings uncover novel molecular mechanisms underlying single and collective keratinocyte migration that may suggest a potential pharmacological target for wound treatment. More broadly, we show that nanoscale spatiotemporal dynamics of Piezo1 channels can control tissue-scale events, a finding with implications beyond wound healing to processes as diverse as development, homeostasis, disease, and repair.

Keywords: cell biology; cell migration; cellular retraction; collective migration; ion channel dynamics; mechanically activated ion channels; mechanotransduction; molecular biophysics; mouse; structural biology.

Plain language summary

The skin is the largest organ of the body. It enables touch sensation and protects against external insults. Wounding of the skin exposes the body to an increased risk of infection, disease and scar formation. During wound healing, the cells in the topmost layer of the skin, called keratinocytes, move in from the edges of the wound to close the gap. This helps to restore the skin barrier. Previous research has shown that the mechanical forces experienced by keratinocytes play a role in wound closure. Several proteins, called mechanosensors, perceive these forces and instruct the cells what to do. Until now, it was unclear what kind of mechanosensors control wound healing. To find out more, Holt et al. studied a recently discovered mechanosensor (for which co-author Ardem Pataputian received the Nobel Prize in 2021), called Piezo1, using genetically engineered mice. The experiments revealed that skin wounds in mice without Piezo1 in their keratinocytes healed faster than mice with normal levels of Piezo1. In contrast, skin wounds of mice with increased levels of Piezo1 in their keratinocytes healed slower than mice with normal levels of Piezo1. The same pattern held true for keratinocytes grown in the laboratory that had been treated with chemicals to increase the activity of Piezo1. To better understand how Piezo1 slows wound healing, Holt et al. tracked its location inside the keratinocytes. This revealed that the position of Piezo1 changes over time. It builds up near the edge of the wound in some places, and at those regions makes the cells move backwards rather than forwards. In extreme cases, an increased activity of Piezo1 can cause an opening of the wound instead of closing it. These findings have the potential to guide research into new wound treatments. But first, scientists must confirm that blocking Piezo1 would not cause side effects, like reducing the sensation of touch. Moreover, it would be interesting to see if Piezo1 also plays a role in other important processes, such as development or certain diseases.

Conflict of interest statement

JH, WZ, EE, SW, SM, HA, ML, AP, MP No competing interests declared

Figures

Figure 1.

Figure 1.. PIEZO1 is expressed in keratinocytes,…

 Figure 1—figure supplement 1.

Figure 1—figure supplement 1.. Piezo1 -cKO mice…

 Figure 1—figure supplement 2.

Figure 1—figure supplement 2.. Piezo1 is the…

 Figure 1—figure supplement 3.

Figure 1—figure supplement 3.. Yoda1 inhibits scratch…

 Figure 2.

Figure 2.. PIEZO1 mediates speed and direction…

 Figure 2—figure supplement 1.

Figure 2—figure supplement 1.. Piezo1 -cKO keratinocytes…

All figures (16)

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References


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Show all 66 references

Publication types

  • Research Support, N.I.H., Extramural

  • Research Support, Non-U.S. Gov't

  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals

  • Cell Movement*

  • Female

  • Ion Channels / genetics*

  • Ion Channels / metabolism

  • Keratinocytes / physiology*

  • Male

  • Mice

  • Mice, Transgenic

  • Signal Transduction*

  • Wound Healing / genetics*

Substances

  • Ion Channels

  • Piezo1 protein, mouse

Associated data

Related information

Grant support

Show all 6 grants

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