Display Settings:

Items per page
We are sorry, but NCBI web applications do not support your browser and may not function properly. More information

Results: 7

1.
FIG. 3.

FIG. 3. From: Mitogen-Activated Protein Kinase Phosphatase 2 Regulates the Inflammatory Response in Sepsis .

MKP-2 regulates cytokine production in BMDMs. ELISAs for immunoreactive TNF-α (A) and IL-10 (B) performed on MKP-2−/− and WT BMDM media following stimulation with LPS (100 ng/ml) for the times indicated. Data are shown as mean ± SEM (**, P < 0.01). These data are representative of three independent bone marrow harvests.

Timothy T. Cornell, et al. Infect Immun. 2010 June;78(6):2868-2876.
2.
FIG. 2.

FIG. 2. From: Mitogen-Activated Protein Kinase Phosphatase 2 Regulates the Inflammatory Response in Sepsis .

Attenuated serum cytokine levels in the absence of MKP-2. Multiplex cytokine array on serum samples from mice following i.p. injections of LPS (30 mg/kg) at the times indicated (at 8 h, n = 10 for WT and n = 10 for MKP-2−/−; at 24 h, n = 11 for WT and n = 11 for MKP-2−/−). Data are shown as mean ± SEM. *, P < 0.05; **, P < 0.01.

Timothy T. Cornell, et al. Infect Immun. 2010 June;78(6):2868-2876.
3.
FIG. 4.

FIG. 4. From: Mitogen-Activated Protein Kinase Phosphatase 2 Regulates the Inflammatory Response in Sepsis .

MKP-2 is induced by TLR ligands. qRT-PCR (A) and Western blot analysis (B) results showing mRNA and protein induction of MKP-2 in WT BMDMs following stimulation with LPS (100 ng/ml) for the times indicated. (C and D) qRT-PCR data indicating an increase in MKP-2 mRNA following stimulation of WT BMDMs with LTA (10 μg/ml) (C) and poly(I:C) (1 μg/ml) (D). qRT-PCR data are shown as mean ± SEM. These data are representative of three independent BMDM preparations.

Timothy T. Cornell, et al. Infect Immun. 2010 June;78(6):2868-2876.
4.
FIG. 1.

FIG. 1. From: Mitogen-Activated Protein Kinase Phosphatase 2 Regulates the Inflammatory Response in Sepsis .

Improved survival in MKP-2−/− mice following LPS and CLP models of sepsis. (A) Age- and sex-matched WT (n = 29) and MKP-2−/− (n = 29) mice received i.p. injections of LPS (30 mg/kg). The percentage of alive mice was documented every 12 h for 5 days following injection. (B) Age- and sex-matched WT (n = 20) and MKP-2−/− (n = 20) mice underwent CLP (two punctures with a 21-gauge needle). Survival was documented every 12 h for 7 days following injection. **, P < 0.01.

Timothy T. Cornell, et al. Infect Immun. 2010 June;78(6):2868-2876.
5.
FIG. 7.

FIG. 7. From: Mitogen-Activated Protein Kinase Phosphatase 2 Regulates the Inflammatory Response in Sepsis .

Proposed regulatory mechanism of MKP-2 impacting MKP-1 levels via ERK deactivation. Following LPS binding to TLR4, the three MAPK pathways are activated. Activation of ERK results in the induction and stabilization of MKP-1. The activation of JNK and p38 results in cytokine production for a period prior to MKP-1 induction. Once induced and stabilized by ERK, MKP-1 negatively regulates early cytokine production. Ongoing TLR4 activation results in the induction of MKP-2, which in turn deactivates ERK, decreasing the stabilization of MKP-1, which removes the cytokine inhibition, allowing for late cytokine production.

Timothy T. Cornell, et al. Infect Immun. 2010 June;78(6):2868-2876.
6.
FIG. 5.

FIG. 5. From: Mitogen-Activated Protein Kinase Phosphatase 2 Regulates the Inflammatory Response in Sepsis .

MKP-2 regulates activation of ERK, JNK, and p38. BMDMs from WT and MKP-2−/− mice were stimulated with LPS (100 ng/ml) for the times indicated. (A) Western blots of cell lysates probed with antibodies to the phosphorylated forms of JNK, p38, and ERK indicating increased phosphorylation of ERK and decreased phosphorylation of JNK and p38. (B) Graphs showing the percentages of phosphorylated MAPK generated by normalizing densitometry of phosphorylated MAPK to the densitometry of the signal for the corresponding nonphosphorylated MAPK obtained after stripping and reprobing Western blots. These data are reported as the percentages of phosphorylated MAPK, and they are representative of three experiments employing independent BMDM preparations.

Timothy T. Cornell, et al. Infect Immun. 2010 June;78(6):2868-2876.
7.
FIG. 6.

FIG. 6. From: Mitogen-Activated Protein Kinase Phosphatase 2 Regulates the Inflammatory Response in Sepsis .

Increased levels of MKP-1 in MKP-2−/− BMDMs attenuate cytokine production. (A) Western blots of WT and MKP-2−/− BMDM whole-cell lysates probed with antibodies to MKP-1 indicate increased levels of MKP-1 in MKP-2−/− BMDMs compared to that in WT BMDMs. (B) ELISA for immunoreactive TNF-α in cell media after transfection of MKP-2−/− BMDMs with control siRNA or siMKP-1 and subsequent LPS stimulation (100 ng/ml) for 2 h shows that cytokine production is restored in MKP-2−/− BMDMs following MKP-1 knockdown (as indicated by decreased protein levels detected by Western blotting). (C) ELISA for immunoreactive TNF-α in cell media after transfection of BMDMs with control siRNA or siMKP-1 and subsequent LPS stimulation (100 ng/ml) for 2 h shows similar fold increases in WT and MKP-2−/− BMDMs following MKP-1 knockdown. Data are representative of three independent BMDM isolations and are shown as mean ± SEM (*, P < 0.01).

Timothy T. Cornell, et al. Infect Immun. 2010 June;78(6):2868-2876.

Display Settings:

Items per page

Supplemental Content

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...
Write to the Help Desk