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Direct Regulation of TLR5 Expression by Caveolin-1.

Lim JS, Nguyen KC, Han JM, Jang IS, Fabian C, Cho KA - Mol. Cells (2015)

Bottom Line: To assess the effect of caveolin-1 on TLR5, we analyzed TLR5 expression in senescent fibroblasts and aged tissues expressing high levels of caveolin-1.Moreover, overexpressed caveolin-1 in vitro enhanced TLR5 mRNA through the MAPK pathway and prolonged TLR5 protein half-life through direct interaction.These results suggest that caveolin-1 may play a crucial role in maintaining of TLR5 by regulating transcription systems and increasing protein half-life.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry, Chonnam National University Medical School, Gwangju 501-746, Korea.

ABSTRACT
Toll-like receptor 5 (TLR5) is a specific receptor for microbial flagellin and is one of the most well-known receptors in the TLR family. We reported previously that TLR5 signaling is well maintained during aging and that caveolin-1 may be involved in TLR5 signaling in aged macrophages through direct interactions. Therefore, it is important to clarify whether caveolin-1/TLR5 interactions affect TLR5 expression during aging. To assess the effect of caveolin-1 on TLR5, we analyzed TLR5 expression in senescent fibroblasts and aged tissues expressing high levels of caveolin-1. As expected, TLR5 mRNA and protein expression was well maintained in senescent fibroblasts and aged tissues, whereas TLR4 mRNA and protein were diminished in those cells and tissues. To determine the mechanism of caveolin-1-dependent TLR5 expression, we examined TLR5 expression in caveolin-1 deficient mice. Interestingly, TLR5 mRNA and protein levels were decreased dramatically in tissues from caveolin-1 knockout mice. Moreover, overexpressed caveolin-1 in vitro enhanced TLR5 mRNA through the MAPK pathway and prolonged TLR5 protein half-life through direct interaction. These results suggest that caveolin-1 may play a crucial role in maintaining of TLR5 by regulating transcription systems and increasing protein half-life.

No MeSH data available.


Related in: MedlinePlus

TLR5 expression decreases in caveolin-1 knockout mice. RNA and protein were isolated from small intestine (S.I.), skin, and spleen of wild type (WT) and caveolin-1 knockout (Cav1−/−) mice. (A) Caveolin-1, TLR4, and TLR5 mRNA levels were analyzed by RT-PCR with specific primers. (B) Caveolin-1, TLR4, and TLR5 protein expression was detected by Western blotting with specific antibodies. The β-actin was used as the loading control for both RT-PCR and Western blotting. Relative density of protein expression and mRNA levels were normalized to β-actin and represented by quantitative graphs. Data are presented as mean ± SD from five independent experiments (n = 3 mice/group); *p < 0.05; ns, not significant.
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f3-molce-38-12-1111: TLR5 expression decreases in caveolin-1 knockout mice. RNA and protein were isolated from small intestine (S.I.), skin, and spleen of wild type (WT) and caveolin-1 knockout (Cav1−/−) mice. (A) Caveolin-1, TLR4, and TLR5 mRNA levels were analyzed by RT-PCR with specific primers. (B) Caveolin-1, TLR4, and TLR5 protein expression was detected by Western blotting with specific antibodies. The β-actin was used as the loading control for both RT-PCR and Western blotting. Relative density of protein expression and mRNA levels were normalized to β-actin and represented by quantitative graphs. Data are presented as mean ± SD from five independent experiments (n = 3 mice/group); *p < 0.05; ns, not significant.

Mentions: To clarify the role of caveolin-1 in the preservation of TLR5, we examined TLR5 expression in several tissues from caveolin-1 knockout (Cav1−/−) mice. Interestingly, TLR5 mRNA was decreased significantly in tissues from Cav1−/− mice compared with those from normal mice, whereas TLR4 mRNA level was not affected by the caveolin-1 genetic deletion (Fig. 3A). Moreover, mRNA level was correlated with protein expression, demonstrating that TLR5 but not TLR4 was decreased in Cav1 −/− tissues (Fig. 3B). This result indicates that caveolin-1 may regulate TLR5 through both transcriptional and translational processes.


Direct Regulation of TLR5 Expression by Caveolin-1.

Lim JS, Nguyen KC, Han JM, Jang IS, Fabian C, Cho KA - Mol. Cells (2015)

TLR5 expression decreases in caveolin-1 knockout mice. RNA and protein were isolated from small intestine (S.I.), skin, and spleen of wild type (WT) and caveolin-1 knockout (Cav1−/−) mice. (A) Caveolin-1, TLR4, and TLR5 mRNA levels were analyzed by RT-PCR with specific primers. (B) Caveolin-1, TLR4, and TLR5 protein expression was detected by Western blotting with specific antibodies. The β-actin was used as the loading control for both RT-PCR and Western blotting. Relative density of protein expression and mRNA levels were normalized to β-actin and represented by quantitative graphs. Data are presented as mean ± SD from five independent experiments (n = 3 mice/group); *p < 0.05; ns, not significant.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4697003&req=5

f3-molce-38-12-1111: TLR5 expression decreases in caveolin-1 knockout mice. RNA and protein were isolated from small intestine (S.I.), skin, and spleen of wild type (WT) and caveolin-1 knockout (Cav1−/−) mice. (A) Caveolin-1, TLR4, and TLR5 mRNA levels were analyzed by RT-PCR with specific primers. (B) Caveolin-1, TLR4, and TLR5 protein expression was detected by Western blotting with specific antibodies. The β-actin was used as the loading control for both RT-PCR and Western blotting. Relative density of protein expression and mRNA levels were normalized to β-actin and represented by quantitative graphs. Data are presented as mean ± SD from five independent experiments (n = 3 mice/group); *p < 0.05; ns, not significant.
Mentions: To clarify the role of caveolin-1 in the preservation of TLR5, we examined TLR5 expression in several tissues from caveolin-1 knockout (Cav1−/−) mice. Interestingly, TLR5 mRNA was decreased significantly in tissues from Cav1−/− mice compared with those from normal mice, whereas TLR4 mRNA level was not affected by the caveolin-1 genetic deletion (Fig. 3A). Moreover, mRNA level was correlated with protein expression, demonstrating that TLR5 but not TLR4 was decreased in Cav1 −/− tissues (Fig. 3B). This result indicates that caveolin-1 may regulate TLR5 through both transcriptional and translational processes.

Bottom Line: To assess the effect of caveolin-1 on TLR5, we analyzed TLR5 expression in senescent fibroblasts and aged tissues expressing high levels of caveolin-1.Moreover, overexpressed caveolin-1 in vitro enhanced TLR5 mRNA through the MAPK pathway and prolonged TLR5 protein half-life through direct interaction.These results suggest that caveolin-1 may play a crucial role in maintaining of TLR5 by regulating transcription systems and increasing protein half-life.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry, Chonnam National University Medical School, Gwangju 501-746, Korea.

ABSTRACT
Toll-like receptor 5 (TLR5) is a specific receptor for microbial flagellin and is one of the most well-known receptors in the TLR family. We reported previously that TLR5 signaling is well maintained during aging and that caveolin-1 may be involved in TLR5 signaling in aged macrophages through direct interactions. Therefore, it is important to clarify whether caveolin-1/TLR5 interactions affect TLR5 expression during aging. To assess the effect of caveolin-1 on TLR5, we analyzed TLR5 expression in senescent fibroblasts and aged tissues expressing high levels of caveolin-1. As expected, TLR5 mRNA and protein expression was well maintained in senescent fibroblasts and aged tissues, whereas TLR4 mRNA and protein were diminished in those cells and tissues. To determine the mechanism of caveolin-1-dependent TLR5 expression, we examined TLR5 expression in caveolin-1 deficient mice. Interestingly, TLR5 mRNA and protein levels were decreased dramatically in tissues from caveolin-1 knockout mice. Moreover, overexpressed caveolin-1 in vitro enhanced TLR5 mRNA through the MAPK pathway and prolonged TLR5 protein half-life through direct interaction. These results suggest that caveolin-1 may play a crucial role in maintaining of TLR5 by regulating transcription systems and increasing protein half-life.

No MeSH data available.


Related in: MedlinePlus