Polarization and migration of hematopoietic stem and progenitor cells rely on the RhoA/ROCK I pathway and an active reorganization of the microtubule network

Research output: Contribution to journalResearch articleContributedpeer-review

Abstract

Understanding the physiological migration of hematopoietic progenitors is important, not only for basic stem cell research, but also in view of their therapeutic relevance. Here, we investigated the role of the Rho kinase pathway in the morphology and migration of hematopoietic progenitors using an ex vivo co-culture consisting of human primary CD34(+) progenitors and mesenchymal stromal cells. The addition of the Rho kinase inhibitor Y-27632 led to the abolishment of the uropod and microvillar-like structures of hematopoietic progenitors, concomitant with a redistribution of proteins found therein (prominin-1 and ezrin). Y-27632-treated cells displayed a deficiency in migration. Time-lapse video microscopy revealed impairment of the rear pole retraction. Interestingly, the knockdown of ROCK I, but not ROCK II, using RNA interference (RNAi) was sufficient to cause the referred morphological and migrational changes. Unexpectedly, the addition of nocodazole to either Y-27632- or ROCK I RNAi-treated cells could restore their polarized morphology and migration suggesting an active role for the microtubule network in tail retraction. Finally, we could demonstrate using RNAi that RhoA, the upstream regulator of ROCK, is involved in these processes. Collectively, our data provide new insights regarding the role of RhoA/ROCK I and the microtubules in the migration of stem cells.

Details

Original languageEnglish
Pages (from-to)31661-31671
Number of pages11
JournalJournal of Biological Chemistry
Volume285
Issue number41
Publication statusPublished - Oct 2010
Peer-reviewedYes

External IDs

Scopus 77957812911
researchoutputwizard legacy.publication#35622
researchoutputwizard legacy.publication#36193
PubMed 20682776
PubMed PMC2951238
researchoutputwizard legacy.publication#36377
ORCID /0000-0003-1181-3659/work/142252214

Keywords