PMID- 22989752
OWN - NLM
STAT- MEDLINE
DCOM- 20130227
LR  - 20211021
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Print)
IS  - 0006-291X (Linking)
VI  - 427
IP  - 1
DP  - 2012 Oct 12
TI  - Involvement of calmodulin and calmodulin kinase II in tumor necrosis factor 
      alpha-induced survival of bone marrow derived macrophages.
PG  - 178-84
LID - S0006-291X(12)01778-0 [pii]
LID - 10.1016/j.bbrc.2012.09.038 [doi]
AB  - We previously showed that survival signaling in TNFalpha-treated, human THP1-derived 
      macrophages (TDMs) has an obligatory requirement for constitutive Ca(2+) influx 
      through a mechanism involving calmodulin/calmodulin kinase II (CAM/CAMKII). We 
      also demonstrated that such requirement also applies to the protective actions of 
      TNFalpha in murine bone marrow-derived macrophages (BMDMs) and that TRPC3 channels 
      mediate constitutive Ca(2+) influx. Using a pharmacological approach we here 
      examined if in BMDMs, similarly to TDMs, TNFalpha-induced survival signaling also 
      involves CAM/CAMKII. In BMDMs, TNFalpha induced rapid activation of the survival 
      pathways NFkappaB, AKT and p38MAPK. All these routes were activated in a 
      PI3K-dependent fashion. Activation of AKT and NFkappaB, but not that of p38MAPK, was 
      abrogated by the CAM inhibitor W7, while KN-62, a CAMKII inhibitor, prevented 
      activation of AKT and p38MAPK but not that of NFkappaB. Inhibition of CAM or CAMKII 
      completely prevented the protective actions of TNFalpha. Our observations indicate 
      that in BMDMs CAM and CAMKII have differential contributions to the components of 
      TNFalpha-dependent survival signaling and underscore a complex interplay among 
      canonical survival routes. These findings set a signaling framework to understand 
      how constitutive Ca(2+) influx couples to macrophage survival in BMDMs.
CI  - Copyright (c) 2012 Elsevier Inc. All rights reserved.
FAU - Tano, Jean-Yves
AU  - Tano JY
AD  - Department of Physiology and Pharmacology, University of Toledo College of 
      Medicine, Health Science Campus, 3000 Arlington Av., Toledo, OH 43614, USA.
FAU - Lee, Robert H
AU  - Lee RH
FAU - Vazquez, Guillermo
AU  - Vazquez G
LA  - eng
GR  - R01 HL111877/HL/NHLBI NIH HHS/United States
GR  - 1R01HL111877-01/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20120916
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Calmodulin)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Type 2)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Bone Marrow Cells/cytology/physiology
MH  - Calcium/*metabolism
MH  - Calcium-Calmodulin-Dependent Protein Kinase Type 2/*metabolism
MH  - Calmodulin/*metabolism
MH  - Cell Survival
MH  - Cells, Cultured
MH  - Humans
MH  - Macrophages/drug effects/metabolism/*physiology
MH  - Mice
MH  - Tumor Necrosis Factor-alpha/pharmacology/*physiology
PMC - PMC3485643
MID - NIHMS410605
EDAT- 2012/09/20 06:00
MHDA- 2013/02/28 06:00
PMCR- 2012/11/01
CRDT- 2012/09/20 06:00
PHST- 2012/08/30 00:00 [received]
PHST- 2012/09/07 00:00 [accepted]
PHST- 2012/09/20 06:00 [entrez]
PHST- 2012/09/20 06:00 [pubmed]
PHST- 2013/02/28 06:00 [medline]
PHST- 2012/11/01 00:00 [pmc-release]
AID - S0006-291X(12)01778-0 [pii]
AID - 10.1016/j.bbrc.2012.09.038 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2012 Oct 12;427(1):178-84. doi: 
      10.1016/j.bbrc.2012.09.038. Epub 2012 Sep 16.