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Mechanism of Macrophage-Derived Chemokine/CCL22 Production by HaCaT Keratinocytes.

Yano C, Saeki H, Komine M, Kagami S, Tsunemi Y, Ohtsuki M, Nakagawa H - Ann Dermatol (2015)

Bottom Line: TNF-α- and IFN-γ-induced CCL22 production was inhibited by PD98059, PD153035, Bay 11-7085, SB202190, c-Jun N-terminal kinase (JNK) inhibitor II, and Janus kinase (JAK) inhibitor 1.Our results indicate that CCL22 production in HaCaT cells is dependent on ERK, EGFR, p38 MAPK, JNK, and JAK and is mediated by different signal pathways from those regulating CCL17 production.Altogether, our previous and present results suggest that EGFR activation represses CCL17 but enhances CCL22 production by these cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Dermatology, The Jikei University School of Medicine, Tokyo, Japan.

ABSTRACT

Background: CC chemokine ligand 17 (CCL17) and CCL22 are the functional ligands for CCR4. We previously reported that inhibitors of nuclear factor-kappa B and p38 mitogen-activated protein kinase (p38 MAPK), but not of extracellular signal-related kinase (ERK), inhibited tumor necrosis factor (TNF)-α- and interferon (IFN)-γ-induced production of CCL17 by the human keratinocyte cell line, HaCaT. Further, an inhibitor of epidermal growth factor receptor (EGFR) enhanced the CCL17 production by these keratinocytes.

Objective: To identify the mechanism underlying CCL22 production by HaCaT cells.

Methods: We investigated the signal transduction pathways by which TNF-α and IFN-γ stimulate HaCaT cells to produce CCL22 by adding various inhibitors.

Results: TNF-α- and IFN-γ-induced CCL22 production was inhibited by PD98059, PD153035, Bay 11-7085, SB202190, c-Jun N-terminal kinase (JNK) inhibitor II, and Janus kinase (JAK) inhibitor 1.

Conclusion: Our results indicate that CCL22 production in HaCaT cells is dependent on ERK, EGFR, p38 MAPK, JNK, and JAK and is mediated by different signal pathways from those regulating CCL17 production. Altogether, our previous and present results suggest that EGFR activation represses CCL17 but enhances CCL22 production by these cells.

No MeSH data available.


Related in: MedlinePlus

Enzyme-linked immunosorbent assay of CC chemokine ligand 22 (CCL22) using culture supernatants of HaCaT cells. Each culture condition was tested in triplicate. The error bars indicate standard deviation. *p<0.05, **p<0.01. (A) 24-hour culture. These are representative data from three experiments. Tumor necrosis factor (TNF)-α- and interferon (IFN)-γ-induced CCL22 production was inhibited by PD98059, PD153035, Parthenolide, Bay 11-7085, SB202190, c-Jun N-terminal kinase (JNK) inhibitor II, and Janus kinase (JAK) inhibitor 1 by 90%, 90%, 35%, 70%, 80%, 70%, and 75%, respectively. (B) 48-hour culture. These are representative data from two experiments. TNF-α- and IFN-γ-induced CCL22 production was inhibited by PD98059, PD153035, Bay 11-7085, SB202190, JNK inhibitor II, and JAK inhibitor 1 by 85%, 80%, 55%, 70%, 40%, and 30%, respectively.
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Figure 1: Enzyme-linked immunosorbent assay of CC chemokine ligand 22 (CCL22) using culture supernatants of HaCaT cells. Each culture condition was tested in triplicate. The error bars indicate standard deviation. *p<0.05, **p<0.01. (A) 24-hour culture. These are representative data from three experiments. Tumor necrosis factor (TNF)-α- and interferon (IFN)-γ-induced CCL22 production was inhibited by PD98059, PD153035, Parthenolide, Bay 11-7085, SB202190, c-Jun N-terminal kinase (JNK) inhibitor II, and Janus kinase (JAK) inhibitor 1 by 90%, 90%, 35%, 70%, 80%, 70%, and 75%, respectively. (B) 48-hour culture. These are representative data from two experiments. TNF-α- and IFN-γ-induced CCL22 production was inhibited by PD98059, PD153035, Bay 11-7085, SB202190, JNK inhibitor II, and JAK inhibitor 1 by 85%, 80%, 55%, 70%, 40%, and 30%, respectively.

Mentions: As shown in Fig. 1A, TNF-α- and IFN-γ-induced CCL22 production in HaCaT cells was inhibited by inhibitors PD98059 (ERK inhibitor), PD153035 (EGFR inhibitor), Parthenolide (NF-κB inhibitor), Bay 11-7085 (NF-κB inhibitor), SB202190 (p38 MAPK inhibitor), JNK inhibitor II, and JAK inhibitor 1 by 90%, 90%, 35%, 70%, 80%, 70%, and 75%, respectively, in 24-hour culture.


Mechanism of Macrophage-Derived Chemokine/CCL22 Production by HaCaT Keratinocytes.

Yano C, Saeki H, Komine M, Kagami S, Tsunemi Y, Ohtsuki M, Nakagawa H - Ann Dermatol (2015)

Enzyme-linked immunosorbent assay of CC chemokine ligand 22 (CCL22) using culture supernatants of HaCaT cells. Each culture condition was tested in triplicate. The error bars indicate standard deviation. *p<0.05, **p<0.01. (A) 24-hour culture. These are representative data from three experiments. Tumor necrosis factor (TNF)-α- and interferon (IFN)-γ-induced CCL22 production was inhibited by PD98059, PD153035, Parthenolide, Bay 11-7085, SB202190, c-Jun N-terminal kinase (JNK) inhibitor II, and Janus kinase (JAK) inhibitor 1 by 90%, 90%, 35%, 70%, 80%, 70%, and 75%, respectively. (B) 48-hour culture. These are representative data from two experiments. TNF-α- and IFN-γ-induced CCL22 production was inhibited by PD98059, PD153035, Bay 11-7085, SB202190, JNK inhibitor II, and JAK inhibitor 1 by 85%, 80%, 55%, 70%, 40%, and 30%, respectively.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4377403&req=5

Figure 1: Enzyme-linked immunosorbent assay of CC chemokine ligand 22 (CCL22) using culture supernatants of HaCaT cells. Each culture condition was tested in triplicate. The error bars indicate standard deviation. *p<0.05, **p<0.01. (A) 24-hour culture. These are representative data from three experiments. Tumor necrosis factor (TNF)-α- and interferon (IFN)-γ-induced CCL22 production was inhibited by PD98059, PD153035, Parthenolide, Bay 11-7085, SB202190, c-Jun N-terminal kinase (JNK) inhibitor II, and Janus kinase (JAK) inhibitor 1 by 90%, 90%, 35%, 70%, 80%, 70%, and 75%, respectively. (B) 48-hour culture. These are representative data from two experiments. TNF-α- and IFN-γ-induced CCL22 production was inhibited by PD98059, PD153035, Bay 11-7085, SB202190, JNK inhibitor II, and JAK inhibitor 1 by 85%, 80%, 55%, 70%, 40%, and 30%, respectively.
Mentions: As shown in Fig. 1A, TNF-α- and IFN-γ-induced CCL22 production in HaCaT cells was inhibited by inhibitors PD98059 (ERK inhibitor), PD153035 (EGFR inhibitor), Parthenolide (NF-κB inhibitor), Bay 11-7085 (NF-κB inhibitor), SB202190 (p38 MAPK inhibitor), JNK inhibitor II, and JAK inhibitor 1 by 90%, 90%, 35%, 70%, 80%, 70%, and 75%, respectively, in 24-hour culture.

Bottom Line: TNF-α- and IFN-γ-induced CCL22 production was inhibited by PD98059, PD153035, Bay 11-7085, SB202190, c-Jun N-terminal kinase (JNK) inhibitor II, and Janus kinase (JAK) inhibitor 1.Our results indicate that CCL22 production in HaCaT cells is dependent on ERK, EGFR, p38 MAPK, JNK, and JAK and is mediated by different signal pathways from those regulating CCL17 production.Altogether, our previous and present results suggest that EGFR activation represses CCL17 but enhances CCL22 production by these cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Dermatology, The Jikei University School of Medicine, Tokyo, Japan.

ABSTRACT

Background: CC chemokine ligand 17 (CCL17) and CCL22 are the functional ligands for CCR4. We previously reported that inhibitors of nuclear factor-kappa B and p38 mitogen-activated protein kinase (p38 MAPK), but not of extracellular signal-related kinase (ERK), inhibited tumor necrosis factor (TNF)-α- and interferon (IFN)-γ-induced production of CCL17 by the human keratinocyte cell line, HaCaT. Further, an inhibitor of epidermal growth factor receptor (EGFR) enhanced the CCL17 production by these keratinocytes.

Objective: To identify the mechanism underlying CCL22 production by HaCaT cells.

Methods: We investigated the signal transduction pathways by which TNF-α and IFN-γ stimulate HaCaT cells to produce CCL22 by adding various inhibitors.

Results: TNF-α- and IFN-γ-induced CCL22 production was inhibited by PD98059, PD153035, Bay 11-7085, SB202190, c-Jun N-terminal kinase (JNK) inhibitor II, and Janus kinase (JAK) inhibitor 1.

Conclusion: Our results indicate that CCL22 production in HaCaT cells is dependent on ERK, EGFR, p38 MAPK, JNK, and JAK and is mediated by different signal pathways from those regulating CCL17 production. Altogether, our previous and present results suggest that EGFR activation represses CCL17 but enhances CCL22 production by these cells.

No MeSH data available.


Related in: MedlinePlus