Paxillin in mechanosensitive spatial control of lung endothelial cell regeneration. NPJ Regen Med 2026 May 18;11(1)
Date
05/19/2026Pubmed ID
42151171Pubmed Central ID
PMC13627700DOI
10.1038/s41536-026-00476-9Scopus ID
2-s2.0-105052443766 (requires institutional sign-in at Scopus site) 1 CitationAbstract
Mechanical forces altered after unilateral pneumonectomy (PNX) control post-PNX lung growth. Here, we demonstrate that post-PNX endothelial regeneration is stimulated at the peripheral region of the mouse lung, requiring the focal adhesion (FA) protein, paxillin, while inhibition of mechanical tension attenuates the effects. Paxillin mediates stretching-induced YAP1-TEAD1 signaling, which stimulates GATA2 activity on angiogenic factor angiopoietin-2 (ANGPT2) transcription in endothelial cells (ECs), dictating post-PNX endothelial regeneration at the peripheral region. Deleting endothelial paxillin suppresses expression of GATA2 in the specific EC subtype, capillary type 1 ECs (CAP1s) following PNX. Extracellular matrix protein, collagen VI that impacts cell mechanical responses is expressed more at the peripheral region in the post-PNX mouse lungs, which drives paxillin expression, leading to EC regeneration. Mechanosensitive paxillin signaling in ECs mediates spatial control of post-PNX endothelial regeneration.
Author List
Mammoto T, Kyi P, Scheer M, Hunyenyiwa T, Hashemi E, Ma X, Turner CE, Lin CW, Malarkannan S, Mammoto AAuthors
Priscilla Kyi Postdoctoral Researcher in the Pediatrics department at Medical College of WisconsinChien-Wei Lin PhD Associate Professor in the Data Science Institute department at Medical College of Wisconsin
Subramaniam Malarkannan PhD Professor in the Medicine department at Medical College of Wisconsin
Akiko Mammoto MD, PhD Professor in the Pediatrics department at Medical College of Wisconsin
