Article Figures & Data
Figures
- Figure 1.
Suppression of constitutive but not interleukin-1β (IL-1β)-inducible expression of monocyte chemoattractant protein 1 (MCP-1) by all-trans-retinoic acid (t-RA). (A) Rat mesangial cells (SM43) were serum deprived (0.5% fetal calf serum [FCS] for 24 h), treated with t-RA (5 μM) for 6 and 24 h, and subjected to Northern blot analysis of MCP-1. Expression of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is shown as a loading control. (B) Mesangial cells were treated with various concentrations of t-RA (0.5 to 5 μM) for 24 h, and Northern blot analysis was performed. (C) Mesangial cells were pretreated with (+) or without (-) t-RA for 2 h and stimulated with IL-1β (10 ng/ml) for 24 h, and Northern blot analysis was performed.
- Figure 2.
Suppression of constitutive but not IL-1β—inducible expression of MCP-1 by 9-cis-RA. (A) Mesangial cells were serum deprived, treated with 9-cis-RA (5 μM) for 6 and 24 h, and subjected to Northern blot analysis of MCP-1. (B) Mesangial cells were pretreated with (+) or without (-) 9-cis-RA for 2 h and stimulated with IL-1β (10 ng/ml) for 24 h, and Northern blot analysis was performed.
- Figure 3.
Requirement of retinoic acid receptors (RAR) for the anti—MCP-1 effect of t-RA. Mesangial cells were treated with t-RA (2.5 μM) together with or without a selective pan-RAR antagonist, AGN193109 (5 μM), for 6 h, and Northern blot analysis was performed.
- Figure 4.
Effect of t-RA on the stability of MCP-1 mRNA. (A) Serum-deprived mesangial cells were treated with actinomycin D (ActD; 500 ng/ml) for 2 to 8 h, and the level of MCP-1 transcript was examined by Northern analysis. (B) Serum-deprived mesangial cells were exposed to actinomycin D for 6 h in the presence or absence of t-RA during the last 1.5 to 6 h and subjected to Northern blot analysis.
- Figure 5.
Roles of nuclear factor-κB (NF-κB) and activator protein 1 (AP-1) in the constitutive and cytokine-inducible expression of MCP-1. (A) Transfectants stably expressing a neomycin phosphotransferase gene (neo) alone (SM/Neo), neo and a dominant-negative mutant of c-jun (SM/JUNDN), and neo and a super-repressor mutant of IκBα (SM/IκBαM) were treated with (left) or without (right) IL-1β. Northern blot analysis was performed on the expression of MCP-1. (B) Mesangial cells were pretreated with (+) or without (-) the c-Jun/AP-1 inhibitor curcumin (20 μM) and treated with (left) or without (right) IL-1β for 8 h. Northern blot analysis was performed.
- Figure 6.
Effects of t-RA on the constitutive activity of AP-1 and NF-κB. Mesangial cells cultured in 24-well plates were transfected transiently with an AP-1 reporter plasmid pTRE-LacZ (A) or an NF-κB reporter plasmid pHIVLTRβ-gal (B). After the transfection, cells were incubated in 0.5% FCS in the presence (+) or absence (-) of t-RA (5 μM) for 48 h and subjected to 5-bromo-4-chloro-3-indolyl β-D-galactopyranoside (X-gal) assay. The activity of AP-1 and NF-κB was evaluated as described in the Materials and Methods section. Assays were performed in quadruplicate. Data are shown as means ± SEM. *, statistically significant difference (P < 0.05).
Tables
t-RA Exposure Time (h) 0 6 24 at-RA, all-trans-retinoic acid. Serum-deprived, confluent mesangial cells were treated with t-RA (5 μM) for 6 h and 24 h, and incidence of apoptosis and necrosis was examined by Hoechst staining and trypan blue exclusion, respectively. Both assays were performed in quadruplicate. Data are means ± SEM. Hoechst staining 98.0 ± 0.4 98.0 ± 0.4 98.9 ± 0.4 Trypan blue exclusion 97.9 ± 0.4 97.6 ± 0.3 97.9 ± 0.7
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