Biophysical forces mediated by respiration maintain lung alveolar epithelial cell fate

被引：66

作者：

Shiraishi, Kazushige ^{[1
,2
]}

Shah, Parisha P. ^{[1
,2
,3
,4
]}

Morley, Michael P. ^{[1
,2
,4
]}

Loebel, Claudia ^{[6
,7
]}

Santini, Garrett T. ^{[1
,2
,3
,4
,5
]}

Katzen, Jeremy ^{[1
,2
]}

Basil, Maria C. ^{[1
,2
]}

Lin, Susan M. ^{[1
,2
]}

Planer, Joseph D. ^{[1
,2
]}

Cantu, Edward ^{[2
,8
]}

Jones, Dakota L. ^{[1
,2
]}

Nottingham, Ana N. ^{[1
,2
]}

Li, Shanru ^{[1
,2
]}

Crdenas-Diaz, Fabian L. ^{[1
,2
]}

Zhou, Su ^{[1
,2
,3
]}

Burdick, Jason A. ^{[6
,9
,10
]}

Jain, Rajan ^{[1
,2
,3
,4
]}

Morrisey, Edward E. ^{[1
,2
,3
,4
]}

机构：

[1] Univ Penn, Perelman Sch Med, Dept Med, Philadelphia, PA 19104 USA

[2] Univ Penn, Penn CHOP Lung Biol Inst, Perelman Sch Med, Philadelphia, PA 19104 USA

[3] Univ Penn, Perelman Sch Med, Dept Cell & Dev Biol, Philadelphia, PA 19104 USA

[4] Univ Penn, Penn Cardiovasc Inst, Philadelphia, PA 19104 USA

[5] Univ Penn, Penn Epigenet Inst, Perelman Sch Med, Philadelphia, PA USA

[6] Univ Penn, Dept Bioengn, Philadelphia, PA USA

[7] Univ Michigan, Dept Mat Sci & Engn, Ann Arbor, MI USA

[8] Univ Penn, Perelman Sch Med, Dept Surg, Div Cardiovasc Surg, Philadelphia, PA USA

[9] Univ Colorado Boulder, BioFrontiers Inst, Boulder, CO USA

[10] Univ Colorado Boulder, Dept Chem & Biol Engn, Boulder, CO USA

来源：

CELL | 2023年 / 186卷 / 07期

基金：

美国国家卫生研究院; 美国国家科学基金会;

关键词：

NUCLEAR LAMINA INTERACTIONS; FOCAL ADHESION KINASE; PLASTICITY; TENSION; YAP;

D O I：

10.1016/j.cell.2023.02.010

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Lungs undergo mechanical strain during breathing, but how these biophysical forces affect cell fate and tis-sue homeostasis are unclear. We show that biophysical forces through normal respiratory motion actively maintain alveolar type 1 (AT1) cell identity and restrict these cells from reprogramming into AT2 cells in the adult lung. AT1 cell fate is maintained at homeostasis by Cdc42-and Ptk2-mediated actin remodeling and cytoskeletal strain, and inactivation of these pathways causes a rapid reprogramming into the AT2 cell fate. This plasticity induces chromatin reorganization and changes in nuclear lamina-chromatin interactions, which can discriminate AT1 and AT2 cell identity. Unloading the biophysical forces of breathing movements leads to AT1-AT2 cell reprogramming, revealing that normal respiration is essential to maintain alveolar epithelial cell fate. These data demonstrate the integral function of mechanotransduction in maintaining lung cell fate and identifies the AT1 cell as an important mechanosensor in the alveolar niche.

引用

页码：1478 / +

页数：31

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