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Communications to the Editor |

Peroxisome Proliferator-Activated Receptor-γ Expression in Lung FREE TO VIEW

Ken-ichiro Inoue, MD; Yutaka Kawahito, MD, PhD; Hajime Sano, MD, PhD
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Naka Central Hospital, Ibaraki Prefecture, Japan

Correspondence to: Ken-ichiro Inoue, MD, Department of Internal Medicine, Naka Central Hospital, 1733-1, Iida, Naka-cho, Naka-gun, Ibaraki Prefecture, 311-0134, Japan; e-mail: keni@kk.iij4u.or.jp



Chest. 2002;122(1):386-387. doi:10.1378/chest.122.1.386-a
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To the Editor:

We are pleased to accept the hypothesis by Momoi et al,1 by adding our experimental results. Momoi et al1 have demonstrated that thiazolidinedione (TZD) inhibits monocyte chemoattractant protein (MCP)-1 protein and messenger RNA expression in cytokine-treated human lung epithelial cells (type II-like epithelial cells). Showing the gene expression of peroxisome proliferator-activated receptor (PPAR)-γ in the lung epithelial cells, they raised the possibility that the efficacy of TZD on the lung epithelial cells may be mediated by the activation of the nuclear receptor.

We recently examined the expression of PPAR-γ in normal lung tissues by reverse transcriptase-polymerase chain reaction (RT-PCR), Western blot analysis, and immunohistochemistry.2By using RT-PCR, we detected the expression of PPAR-γ messenger RNA in two of three normal lung tissues. By Western blot analysis, we detected the expression of PPAR-γ protein in three of five normal lung tissues. Immunohistochemistry demonstrated that PPAR-γ expression was detected in four of six normal lung tissues. In addition, we graded the intensity and extent of expression of immunoreactive PPAR-γ for each tissue specimen on a scale of 0 to 4 according to the grading methodology previously described.3 As a result, immunoreactive PPAR-γ was weakly expressed in bronchial epithelial cells, type I pneumocytes, and vascular endothelial cells (mean ± SD immunohistologic scores were 1.0 ± 0.3, 1.2 ± 0.4, 0.8 ± 0.3, respectively). However, we found the moderate expression of immunoreactive PPAR-γ in type II pneumocytes (mean immunohistologic score was 1.8 ± 0.6), suggesting that type II pneumocytes may be target cells in which PPAR-γ is activated by TZD.

In conclusion, we would like to support the hypothesis that TZD inhibits MCP-1 secretion in interleukin-1β-treated human lung epithelial cells through activation of PPAR-γ.

Momoi, A, Murao, K, Imachi, H, et al (2001) Inhibition of monocyte chemoattractant protein-1 expression in cytokine-treated human epithelial cells by thiazolidinedione.Chest120,1293-1300. [CrossRef]
 
Inoue, K, Kawahito, Y, Yamada, R, et al Expression of peroxisome proliferator-activated receptor (PPAR)-γ in human lung cancer.Anticancer Res2002;21,2471-2476
 
Sano, H, Hla, T, Maier, JAM, et al In vivocyclooxygenase expression in synovial tissues of patients with rheumatoid arthritis and osteoarthritis and rats with adjuvant and streptococcal cell wall arthritis.J Clin Invest1992;89,97-108. [CrossRef]
 

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References

Momoi, A, Murao, K, Imachi, H, et al (2001) Inhibition of monocyte chemoattractant protein-1 expression in cytokine-treated human epithelial cells by thiazolidinedione.Chest120,1293-1300. [CrossRef]
 
Inoue, K, Kawahito, Y, Yamada, R, et al Expression of peroxisome proliferator-activated receptor (PPAR)-γ in human lung cancer.Anticancer Res2002;21,2471-2476
 
Sano, H, Hla, T, Maier, JAM, et al In vivocyclooxygenase expression in synovial tissues of patients with rheumatoid arthritis and osteoarthritis and rats with adjuvant and streptococcal cell wall arthritis.J Clin Invest1992;89,97-108. [CrossRef]
 
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