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Involvement of Rac GTPase activation in phosphatidylcholine hydroperoxide-induced THP-1 cell adhesion to ICAM-1

Asai, Akira; Okajima, Fumitaka; Nakajima, Yasushi; Nagao, Mototsugu LU ; Nakagawa, Kiyotaka; Miyazawa, Teruo and Oikawa, Shinichi (2011) In Biochemical and Biophysical Research Communications 406(2). p.273-277
Abstract

Increasing evidence indicates that phospholipid oxidation plays important roles in atherosclerosis. Here, we investigated the involvement of Rho-family GTPases inphosphatidylcholine hydroperoxide (PCOOH)-induced THP-1 cell adhesion to ICAM-1. Isoprenoid depletion by fluvastatin and geranylgeranyltransferase inhibition by GGTI-286 suppressed PCOOH-induced cell adhesion to ICAM-1 and F-actin-rich membrane protrusion formation. Pull-down assays demonstrated the activation of Rac1 and Rac2 in PCOOH-treated cells. Pan-Rho-family GTPase inhibitor Clostridium difficile toxin B, Rac-specific inhibitor NSC23776, and RNA interference of the Rac isoforms suppressed the cell adhesion. These findings indicate the involvement of Rac GTPase activation... (More)

Increasing evidence indicates that phospholipid oxidation plays important roles in atherosclerosis. Here, we investigated the involvement of Rho-family GTPases inphosphatidylcholine hydroperoxide (PCOOH)-induced THP-1 cell adhesion to ICAM-1. Isoprenoid depletion by fluvastatin and geranylgeranyltransferase inhibition by GGTI-286 suppressed PCOOH-induced cell adhesion to ICAM-1 and F-actin-rich membrane protrusion formation. Pull-down assays demonstrated the activation of Rac1 and Rac2 in PCOOH-treated cells. Pan-Rho-family GTPase inhibitor Clostridium difficile toxin B, Rac-specific inhibitor NSC23776, and RNA interference of the Rac isoforms suppressed the cell adhesion. These findings indicate the involvement of Rac GTPase activation in PCOOH-induced cell adhesion to ICAM-1 via actin reorganization.

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author
publishing date
type
Contribution to journal
publication status
published
keywords
Actin, Cell adhesion, Monocyte, Phosphatidylcholine hydroperoxide, Phospholipid oxidation, Rac
in
Biochemical and Biophysical Research Communications
volume
406
issue
2
pages
5 pages
publisher
Elsevier
external identifiers
  • scopus:79952450625
ISSN
0006-291X
DOI
10.1016/j.bbrc.2011.02.032
language
English
LU publication?
no
id
db223ece-ddea-444f-86f0-9488449fcd09
date added to LUP
2017-08-23 20:05:39
date last changed
2017-08-27 06:46:37
@article{db223ece-ddea-444f-86f0-9488449fcd09,
  abstract     = {<p>Increasing evidence indicates that phospholipid oxidation plays important roles in atherosclerosis. Here, we investigated the involvement of Rho-family GTPases inphosphatidylcholine hydroperoxide (PCOOH)-induced THP-1 cell adhesion to ICAM-1. Isoprenoid depletion by fluvastatin and geranylgeranyltransferase inhibition by GGTI-286 suppressed PCOOH-induced cell adhesion to ICAM-1 and F-actin-rich membrane protrusion formation. Pull-down assays demonstrated the activation of Rac1 and Rac2 in PCOOH-treated cells. Pan-Rho-family GTPase inhibitor Clostridium difficile toxin B, Rac-specific inhibitor NSC23776, and RNA interference of the Rac isoforms suppressed the cell adhesion. These findings indicate the involvement of Rac GTPase activation in PCOOH-induced cell adhesion to ICAM-1 via actin reorganization.</p>},
  author       = {Asai, Akira and Okajima, Fumitaka and Nakajima, Yasushi and Nagao, Mototsugu and Nakagawa, Kiyotaka and Miyazawa, Teruo and Oikawa, Shinichi},
  issn         = {0006-291X},
  keyword      = {Actin,Cell adhesion,Monocyte,Phosphatidylcholine hydroperoxide,Phospholipid oxidation,Rac},
  language     = {eng},
  month        = {03},
  number       = {2},
  pages        = {273--277},
  publisher    = {Elsevier},
  series       = {Biochemical and Biophysical Research Communications},
  title        = {Involvement of Rac GTPase activation in phosphatidylcholine hydroperoxide-induced THP-1 cell adhesion to ICAM-1},
  url          = {http://dx.doi.org/10.1016/j.bbrc.2011.02.032},
  volume       = {406},
  year         = {2011},
}