TITLE:
Dephosphorylation of myristoylated alanine-rich C kinase substrate accelerates wound-induced migration of SH-SY5Y cells
AUTHORS:
Atsuhiro Tanabe, Mitsuya Shiraishi, Yasuharu Sasaki
KEYWORDS:
Wound Healing; MARCKS; Phosphorylation/Dephosphorylation; Cell Migration; Inflammation; ROCK
JOURNAL NAME:
Advances in Bioscience and Biotechnology,
Vol.4 No.8B,
August
8,
2013
ABSTRACT: Inflammation, which is induced after infection of
bacteria and tissue injury, is one of the important early stages of wound
healing. Bradykinin is increased during acute and chronic inflammation. We previously reported that bradykinin stimulation induces dephosphorylation of
myristoylated alanine-rich C kinase substrate (MARCKS) after phosphorylation by
ROCK leading neurite outgrowth in neuroblastoma SH-SY5Y cells. In this report
we showed that knock-down of MARCKS by RNAi reduced cell migration. Wild-type MARCKS-overexpressed SH-SY5Y
cells migrated faster than the control cells. Unphosphorylatable
MARCKS-overexpressed cells notably migrated fast. Moreover, chronic MARCKS dephosphorylation
by a ROCK inhibitor HA-1077 promoted the cell migration, on the other hand a
PKC inhibitor Ro-31-8220 did not. After wounding, MARCKS was transiently
phosphorylated and dephospho-rylated by 20 min. Immunocytochemistry showed
that the dephosphorylated MARCKS was localized at neurite tips. These findings
suggest that MARCKS dephosphorylation is important in wound-induced migration
of SH-SY5Y cells. It indicates the possibility that MARCKS is associated with
wound repair after inflammation.