Abstract
Leukotactin(Lkn)-1 is a CC chemokine and is upregulated in macrophages in response to Mycobacterium tuberculosis (MTB) infection. We investigated whether mitogen-activated protein kinases (MAPKs) are involved in MTB-induced expression of Lkn-1. The up-regulation of Lkn-1 by infection with MTB was inhibited in cells treated with inhibitors specific for JNK (SP600125) or p38 MAPK (SB202190). Since the up-regulation of Lkn-1 by MTB has been reported to be mediated by the PI3-K/PDK1/Akt signaling, we examined whether JNK and/or p38 MAPK are also involved in this signal pathway. MTB-induced Akt phosphorylation was blocked by treatment with JNK- or p38 MAPK-specific inhibitors implying that p38 and JNK are upstream of Akt. In addition, treatment with the PI3-K-specific inhibitor inhibited MTB-stimulated activation of JNK or p38 MAPK implying that PI3-K is upstream of JNK and p38 MAPK. These results collectively suggest that JNK and p38 MAPK are involved in the signal pathway responsible for MTB-induced up-regulation of Lkn-1.
| Original language | English |
|---|---|
| Pages (from-to) | 583-588 |
| Number of pages | 6 |
| Journal | BMB reports |
| Volume | 45 |
| Issue number | 10 |
| DOIs | |
| Publication status | Published - 2012 Dec 27 |
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All Science Journal Classification (ASJC) codes
- Biochemistry
- Molecular Biology
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C-Jun n-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK) are involved in mycobacterium tuberculosis-induced expression of leukotactin-1. / Cho, Jang Eun; Park, Sangjung; Cho, Sang Nae; Lee, Hyeyoung; Kim, Yoon Suk.
In: BMB reports, Vol. 45, No. 10, 27.12.2012, p. 583-588.Research output: Contribution to journal › Article
TY - JOUR
T1 - C-Jun n-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK) are involved in mycobacterium tuberculosis-induced expression of leukotactin-1
AU - Cho, Jang Eun
AU - Park, Sangjung
AU - Cho, Sang Nae
AU - Lee, Hyeyoung
AU - Kim, Yoon Suk
PY - 2012/12/27
Y1 - 2012/12/27
N2 - Leukotactin(Lkn)-1 is a CC chemokine and is upregulated in macrophages in response to Mycobacterium tuberculosis (MTB) infection. We investigated whether mitogen-activated protein kinases (MAPKs) are involved in MTB-induced expression of Lkn-1. The up-regulation of Lkn-1 by infection with MTB was inhibited in cells treated with inhibitors specific for JNK (SP600125) or p38 MAPK (SB202190). Since the up-regulation of Lkn-1 by MTB has been reported to be mediated by the PI3-K/PDK1/Akt signaling, we examined whether JNK and/or p38 MAPK are also involved in this signal pathway. MTB-induced Akt phosphorylation was blocked by treatment with JNK- or p38 MAPK-specific inhibitors implying that p38 and JNK are upstream of Akt. In addition, treatment with the PI3-K-specific inhibitor inhibited MTB-stimulated activation of JNK or p38 MAPK implying that PI3-K is upstream of JNK and p38 MAPK. These results collectively suggest that JNK and p38 MAPK are involved in the signal pathway responsible for MTB-induced up-regulation of Lkn-1.
AB - Leukotactin(Lkn)-1 is a CC chemokine and is upregulated in macrophages in response to Mycobacterium tuberculosis (MTB) infection. We investigated whether mitogen-activated protein kinases (MAPKs) are involved in MTB-induced expression of Lkn-1. The up-regulation of Lkn-1 by infection with MTB was inhibited in cells treated with inhibitors specific for JNK (SP600125) or p38 MAPK (SB202190). Since the up-regulation of Lkn-1 by MTB has been reported to be mediated by the PI3-K/PDK1/Akt signaling, we examined whether JNK and/or p38 MAPK are also involved in this signal pathway. MTB-induced Akt phosphorylation was blocked by treatment with JNK- or p38 MAPK-specific inhibitors implying that p38 and JNK are upstream of Akt. In addition, treatment with the PI3-K-specific inhibitor inhibited MTB-stimulated activation of JNK or p38 MAPK implying that PI3-K is upstream of JNK and p38 MAPK. These results collectively suggest that JNK and p38 MAPK are involved in the signal pathway responsible for MTB-induced up-regulation of Lkn-1.
UR - http://www.scopus.com/inward/record.url?scp=84871403015&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84871403015&partnerID=8YFLogxK
U2 - 10.5483/BMBRep.2012.45.10.120
DO - 10.5483/BMBRep.2012.45.10.120
M3 - Article
C2 - 23101513
AN - SCOPUS:84871403015
VL - 45
SP - 583
EP - 588
JO - BMB Reports
JF - BMB Reports
SN - 1976-6696
IS - 10
ER -