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Published ahead of print on January 24, 2005, doi:10.1165/rcmb.2004-0118OC

Am. J. Respir. Cell Mol. Biol., Volume 32, Number 4, April 2005, 301-310

A more recent version of this article appeared on April 1, 2005
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Submitted on April 14, 2004
Revised on January 20, 2005

Stress Activated Protein Kinases Mediate Cell Migration in Human Airway Epithelial Cells

Steven R White1*, Roberta Tse1, and Bertha A Marroquin1

1 University of Chicago, Chicago, IL, United States

* To whom correspondence should be addressed. E-mail: swhite{at}medicine.bsd.uchicago.edu.

Airway epithelial cell (AEC) repair immediately after injury requires coordinated cell spreading and migration at the site of injury. Stress activated protein kinases such as p38 MAPK and c-Jun N-terminal Protein Kinase (JNK) modulate several responses to cell stress and injury, but their role in AEC migration is not clear. We examined migration in confluent 16HBE14o - human AEC lines and in primary AEC grown on collagen-IV. Wounds were created by mechanical abrasion and followed to closure using digital microscopy. Inhibitors of either p38 ERK1/2 (PD98059), MAPK (SB203580) or JNK (SP600125) could block cell migration sub-stantially. Inhibiting JNK but not p38 MAPK or ERK1/2 blocked extension of cells into the wound region from the original line of injury. Initial migration was associated with phosphorylation of ERK, p38 MAPK and JNK within 5 - 15 min. The downstream effector of p38, heat shock protein 27 (hsp-27), also was phosphorylated rapidly after injury; phosphorylation could be blocked by prior treatment with SB203580 but not SP600125. The downstream effector of JNK, c-Jun, likewise was phosphorylated rapidly after injury and could be blocked by inhibiting JNK. Our data demonstrate that p38 MAPK, JNK, and ERK1/2 participate in the early stages of airway epithelial cell migration.




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