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CCL2 — JUN
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Desai et al., Lab Invest 1999
(Disease Models, Animal...) :
Because in vitro expression of
MCP-1 is in part
mediated by the redox-sensitive transcription factors nuclear factor-kappa B (NF-kappaB) and
activator protein-1 (AP-1) , we studied their activation as a function of varying intracellular GSH redox status in the pathogenesis of glucan induced pulmonary granulomatosis
Wang et al., Arterioscler Thromb Vasc Biol 1999
:
Adenovirus mediated overexpression of
c-Jun and c-Fos
induces intercellular adhesion molecule-1 and
monocyte chemoattractant protein-1 in human endothelial cells
Wang et al., Kidney Int 2000
:
These studies prove that NF-kappaB is critical for LPS induced MCP-1 transcription, and
AP-1 and Sp1 are
essential for basal expression of
MCP-1 in rat tubule cells
Lucio-Cazana et al., J Am Soc Nephrol 2001
:
Experiments that used pharmacologic and genetic inhibitors showed that the IL-1beta-inducible
MCP-1 expression was dependent on nuclear factor-kappaB (NF-kappaB) and
independent of
activator protein 1 (AP-1) ... In contrast, the constitutive expression of
MCP-1 was
dependent on both NF-kappaB and
AP-1 ... These data suggested that ( 1 ) constitutive and IL-1beta-inducible expression of MCP-1 was differently regulated by
AP-1 and NF-kappaB and ( 2 ) t-RA
inhibited selectively the constitutive expression of
MCP-1 via intervention in the AP-1 pathway
Galindo et al., Arthritis Rheum 2001
(Scleroderma, Systemic) :
Increased NF-kappaB or
AP-1 activation was not
responsible for the constitutive overexpression of
MCP-1 by SSc fibroblasts
Chang et al., Mol Pharmacol 2001
:
Furthermore, the PMA induced extracellular signal regulated kinase 1/2 and c-Jun amino-terminal kinase activities that contributed to
AP-1 activity and
MCP-1 gene
induction were obviously attenuated after pretreating ECs with Wog
Lakshminarayanan et al., Am J Pathol 2001
(Ischemia) :
These results suggest that reactive oxygen intermediate generation, after a brief ischemic episode, is capable of
inducing MCP-1 expression in venular endothelium through
AP-1 and NF-kappaB
Viedt et al., J Am Soc Nephrol 2002
(Nephritis) :
Binding activity of the
activator protein-1 (AP-1) , which has been implicated to regulate induction of the IL-6 gene together with NF-kappaB, was also
stimulated by
MCP-1
Takeshita et al., J Oral Sci 2002
:
Furthermore, 1alpha25 ( OH ) 2D3 actually blocked the
AP-1 mediated gene expression of monocyte chemoattractant
JE/MCP-1 induced in the cytokine treated cells
Sodhi et al., J Interferon Cytokine Res 2002
:
Monocyte chemoattractant protein-1 induced activation of p42/44 MAPK and
c-Jun in murine peritoneal macrophages : a potential pathway for macrophage activation
Viedt et al., Arterioscler Thromb Vasc Biol 2002
(Inflammation) :
MCP-1 stimulated the binding activity of NF-kappaB and of
activator protein-1 (AP-1) ... The results clearly demonstrate that
MCP-1 induces differential activation of NF-kappaB and
AP-1 in VSMCs
Oda et al., J Immunol 2002
:
While
AP-1 is
involved in regulating the IL-1alpha induced expression of IL-8, but not
MCP-1 , alprazolam potentiated the binding of c-Jun/c-Fos to the AP-1 oligonucleotide probe
Lee et al., J Immunol 2003
:
These data suggest that BMP-7
inhibits constitutive and IL-1 beta induced
MCP-1 expression in human mesangial cells partly by inhibiting c-Jun N-terminal kinase activity and subsequent
AP-1 activity, and provide new insight into the therapeutic potential of BMP-7 in the inflammatory renal diseases
Kanda et al., J Invest Dermatol 2003
:
These results suggest that E2-bound ERbeta may
inhibit MCP-1 gene expression by inhibiting Sp1 and
AP-1 transcriptional activities in keratinocytes
Yamada et al., Arterioscler Thromb Vasc Biol 2003
:
Ad-DN-c-Jun inhibited VEGF induced endothelial
MCP-1 mRNA expression and promoter activity in vitro
Park et al., Nephrol Dial Transplant 2004
:
Dexamethasone regulates
AP-1 to
repress TNF-alpha induced
MCP-1 production in human glomerular endothelial cells
Chen et al., J Pharmacol Exp Ther 2004
:
Dual
regulation of tumor necrosis factor-alpha induced
CCL2/monocyte chemoattractant protein-1 expression in vascular smooth muscle cells by nuclear factor-kappaB and
activator protein-1 : modulation by type III phosphodiesterase inhibition ... The NF-kappaB inhibitor carbobenzoxy-l-leucyl-l-leucyl-l-leucinal ( MG132 ) attenuated TNF-alpha induced
CCL2/MCP-1 production in the
presence of increased phospho-JNK and
phospho-c-Jun levels
Bian et al., Invest Ophthalmol Vis Sci 2004
:
To investigate the
role of the phosphatidylinositol 3-kinase (PI3K) pathway and the signal mediator
AP-1 in monocyte chemotactic protein
(MCP)-1 and interleukin (IL)-8 gene expression in human retinal pigment epithelial ( hRPE ) cells
Zhang et al., Zhonghua Bing Li Xue Za Zhi 2004
(Glomerulonephritis) :
Angiotensin II enhanced the expression of
MCP-1 and
activation of JNK and
AP-1 in cultured human mesangial cells in a dose dependent manner, with maximal stimulation seen at 100 nmol/L ( 20.99 +/- 4.71 ) folds, ( 6.91 +/- 1.65 ) folds and ( 7.82 +/- 1.32 ) folds respectively
Takeshita et al., J Oral Sci 2005
(Second Messenger Systems) :
Although TNF-alpha stimulated the
AP-1 mediated expression of the monocyte chemoattractant
JE/MCP-1 , this stimulation was inhibited by DHS
Kim-Mitsuyama et al., Gene Ther 2006
(Cardiomegaly...) :
Ad.DN-c-Jun , which was transferred to the heart 2 days before AngII infusion, prevented cardiac hypertrophy ( P < 0.01 ), decreased p70S6 kinase phosphorylation ( P < 0.05 ), and
suppressed cardiac gene expression of brain natriuretic peptide, collagen I, III, and IV,
monocyte chemoattractant protein-1 ( MCP-1 ) and plasminogen activator inhibitor-1 ( PAI-1 ) ( P < 0.01 )
Butler et al., J Biol Chem 2006
:
In this report we have shown that elafin
inhibits the lipopolysaccharide induced production of
monocyte chemoattractant protein-1 in monocytes by inhibiting
AP-1 and NF-kappaB activation
Marini et al., Cell Microbiol 2008
:
The effect of p17 on
MCP-1 expression was observed at the transcriptional level and was primarily
dependent on the activation of the transcription factor
AP-1
Demicheva et al., Circ Res 2008
:
Stretch induced activation of the transcription factor
activator protein-1 controls
monocyte chemoattractant protein-1 expression during arteriogenesis ... Collectively, these findings point toward a stretch induced
activator protein-1 mediated rise in
MCP-1 expression in vascular smooth muscle cells as a critical determinant for the initiation of arteriogenesis
Lee et al., J Immunol 2008
(Encephalitis) :
Of interest, the negative effects of 15d-PGJ ( 2 ) on
AP-1/specificity protein-1 signaling and the resulting
inhibition of
MCP-1 expression were mediated by MAPK phosphatase (MKP)-1 activity, which was induced by 15d-PGJ ( 2 ) in a peroxisome proliferator activated receptor independent manner
Vukic et al., Neurobiol Dis 2009
(Alzheimer Disease) :
Western blot analyses showed that c-Jun was activated via JNK mediated phosphorylation, suggesting that as a
result of
c-Jun phosphorylation, AP-1 was activated and thus up-regulated
MCP-1 expression
Majkova et al., Toxicol Appl Pharmacol 2009
(Atherosclerosis...) :
Also,
MCP-1 up-regulation by PCB77 was
prevented by inhibiting p38 and
c-Jun N-terminal kinase (JNK) , but not ERK1/2, suggesting regulatory functions via p38 and JNK MAPK pathways
Sutcliffe et al., Br J Pharmacol 2009
:
Transcriptional regulation of
monocyte chemotactic protein-1 release by endothelin-1 in human airway smooth muscle cells
involves NF-kappaB and
AP-1
Chen et al., Am J Physiol Cell Physiol 2010
:
Besides the suppression of intracellular ROS generation, the inhibition of nuclear translocation of
AP-1 and Ref-1 are mainly
responsible for the downregulation of
MCP-1 by Trx1
Chen et al., J Virol 2010
:
The upregulation of
CCL2 by SARS-CoV spike protein was mainly
mediated by extracellular signal regulated kinase 1 and 2 ( ERK1/2 ) and
AP-1 but not the IkappaBalpha-NF-kappaB signaling pathway
Ding et al., World journal of pediatrics : WJP 2010
:
We investigated the
role of
c-Jun NH2-terminal kinase (JNK) , a member of the mitogen activated protein kinase family, in the expression of angiotensin II (Ang II) induced
monocyte chemoattractant protein-1 ( MCP-1 ) and transforming growth factor-1 ( TGF-1 ), and in the production of fibronectin ( FN ), by human mesangial cells ( HMCs )
Cai et al., PloS one 2011
:
EMSA showed that JNK and ERK1/2 were involved in
MCP-1 induced
AP1 activation
Li et al., J Clin Endocrinol Metab 2011
(Inflammation...) :
In IL-1ß- or TNF-a stimulated first trimester decidual cells, NF?B inhibitor suppressed production of all six chemokines ;
JUN NH2-terminal kinase inhibitor
inhibited secretion of
CCL2 , CCL4, and CCL5 ; and MAPK kinase and p38 inhibitor decreased production of CXCL8
Huang et al., Arthritis Rheum 2012
:
Thrombin mediated
CCL2 production was
attenuated by the thrombin inhibitor PPACK, the protein kinase Cd ( PKCd ) inhibitor rottlerin, the c-Src inhibitor PP2, epidermal growth factor receptor (EGFR) inhibitor AG-1478, MEK inhibitors PD98059 and U0126, or
AP-1 inhibitors curcumin and tanshinone IIA
Higa et al., PloS one 2012
:
Adding bamboo extract ( BEX ) inhibited the effects of PA, reduced
MCP-1 production, and
inhibited nuclear translocation of NF-?B and
AP-1 subunits
Bethel-Brown et al., Journal of neuroinflammation 2012
(HIV Infections) :
MCP-1 induction was
regulated by activation of extracellular-signal regulated kinase ( ERK ) 1/2,
c-Jun N-terminal kinase (JNK) and p38 mitogen activated protein ( MAP ) kinases and phosphatidylinositol 3-kinase (PI3K)/Akt pathways and the downstream transcription factor, nuclear factor ?B ( NF?B )
Deng et al., Int J Biochem Cell Biol 2013
(Pulmonary Fibrosis) :
Transcriptional regulation of increased
CCL2 expression in pulmonary fibrosis
involves nuclear factor-?B and
activator protein-1 ... Collectively, these findings strongly suggest that the increased binding of transcription factors to NF-?B and
AP-1 elements in the CCL2 promoter is
responsible for the active transcription expression of
CCL2 in pulmonary fibrosis