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cAMP and cGMP Play an Essential Role in Galvanotaxis of Cell Fragments
Author(s) -
Zhu Kan,
Sun Yaohui,
Miu Anh,
Yen Michael,
Liu Bowei,
Zeng Qunli,
Mogilner Alex,
Zhao Min
Publication year - 2016
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.25229
Subject(s) - microbiology and biotechnology , chemotaxis , signal transduction , ly294002 , second messenger system , biology , cell migration , cell , cell signaling , cell type , chemistry , pi3k/akt/mtor pathway , receptor , biochemistry
Cell fragments devoid of the nucleus and major organelles are found in physiology and pathology, for example platelets derived from megakaryocytes, and cell fragments from white blood cells and glioma cells. Platelets exhibit active chemotaxis. Fragments from white blood cells display chemotaxis, phagocytosis, and bactericidal functions. Signaling mechanisms underlying migration of cell fragments are poorly understood. Here we used fish keratocyte fragments and demonstrated striking differences in signal transduction in migration of cell fragments and parental cells in a weak electric field. cAMP or cGMP agonists completely abolished directional migration of fragments, but had no effect on parental cells. The inhibition effects were prevented by pre‐incubating with cAMP and cGMP antagonists. Blocking cAMP and cGMP downstream signaling by inhibition of PKA and PKG also recovered fragment galvanotaxis. Both perturbations confirmed that the inhibitory effect was mediated by cAMP or cGMP signaling. Inhibition of cathode signaling with PI3K inhibitor LY294002 also prevented the effects of cAMP or cGMP agonists. Our results suggest that cAMP and cGMP are essential for galvanotaxis of cell fragments, in contrast to the signaling mechanisms in parental cells. J. Cell. Physiol. 231: 1291–1300, 2016. © 2015 Wiley Periodicals, Inc.