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STAT1 antisense oligonucleotides attenuate the proinflammatory cytokine release of alveolar macrophages in bleomycin-induced fibrosis.
Cell Mol Immunol. 2005 Jun; 2(3):211-7.CM

Abstract

To investigate the effect of signal transducers and activators of transcription 1 (STAT1) antisense oligonucleotides (ASON) on concentrations of TNF-alpha, IL-8, NO secreted by alveolar macrophages (AMs) in bleomycin-induced rat pulmonary fibrosis, five adult female Wistar rats were intratracheally instilled with bleomycin. After 7 days, the rats were killed by right ventricle of heart exsanguinations under ketamine anaesthesia and bronchoalveolar lavage (BAL) was performed to obtain AMs. AMs were divided into four groups, treated with STAT1 ASON, STAT1 sense oligonucleotides (SON), dexamethasone (DEX) and medium alone (control), respectively. AMs and media were collected after culture for 36 h. The mRNA and protein expressions of STAT1 and ICAM-1 in AMs were detected by RT-PCR and ELISA, respectively. The concentrations of TNF-alpha, IL-8, NO in cultured medium were detected. The STAT1 mRNA expression by AMs in the STAT1 ASON group was lower than those of AMs in the STAT1 SON group, the DEX group and the control group (p<0.05). Moreover, the STAT1 mRNA expression by AMs in the DEX group was also lower than those of AMs in the STAT1 SON group and the control group (p<0.05), but the STAT1 mRNA expression by AMs in the STAT1 SON group was not different from that of the control group (p>0.05). The protein expressions of STAT1 and ICAM-1 and the mRNA expression of ICAM-1 showed similar changes to the STAT1 mRNA expression by AMs. The concentrations of TNF-alpha, IL-8, NO in cultured medium from STAT1 ASON group were lower than those from STAT1 SON, DEX and the control groups (p<0.05). Moreover, the concentrations of TNF-alpha, IL-8, NO in cultured medium from DEX group were also lower than those from the control and STAT1 SON group (p<0.05), but no difference between STAT1 SON group and the control (p>0.05). The results suggest that STAT1 ASON could inhibit the secretion of TNF-alpha, IL-8, NO in AMs, and STAT1 could become a target of treating pulmonary fibrosis.

Authors+Show Affiliations

Department of Respiratory Medicine, the Affiliated Hospital of Luzhou Medical College, Luzhou 646000, China. fxm129@163.comNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

16212889

Citation

Fan, Xianming, and Zengli Wang. "STAT1 Antisense Oligonucleotides Attenuate the Proinflammatory Cytokine Release of Alveolar Macrophages in Bleomycin-induced Fibrosis." Cellular & Molecular Immunology, vol. 2, no. 3, 2005, pp. 211-7.
Fan X, Wang Z. STAT1 antisense oligonucleotides attenuate the proinflammatory cytokine release of alveolar macrophages in bleomycin-induced fibrosis. Cell Mol Immunol. 2005;2(3):211-7.
Fan, X., & Wang, Z. (2005). STAT1 antisense oligonucleotides attenuate the proinflammatory cytokine release of alveolar macrophages in bleomycin-induced fibrosis. Cellular & Molecular Immunology, 2(3), 211-7.
Fan X, Wang Z. STAT1 Antisense Oligonucleotides Attenuate the Proinflammatory Cytokine Release of Alveolar Macrophages in Bleomycin-induced Fibrosis. Cell Mol Immunol. 2005;2(3):211-7. PubMed PMID: 16212889.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - STAT1 antisense oligonucleotides attenuate the proinflammatory cytokine release of alveolar macrophages in bleomycin-induced fibrosis. AU - Fan,Xianming, AU - Wang,Zengli, PY - 2005/10/11/pubmed PY - 2006/1/7/medline PY - 2005/10/11/entrez SP - 211 EP - 7 JF - Cellular & molecular immunology JO - Cell Mol Immunol VL - 2 IS - 3 N2 - To investigate the effect of signal transducers and activators of transcription 1 (STAT1) antisense oligonucleotides (ASON) on concentrations of TNF-alpha, IL-8, NO secreted by alveolar macrophages (AMs) in bleomycin-induced rat pulmonary fibrosis, five adult female Wistar rats were intratracheally instilled with bleomycin. After 7 days, the rats were killed by right ventricle of heart exsanguinations under ketamine anaesthesia and bronchoalveolar lavage (BAL) was performed to obtain AMs. AMs were divided into four groups, treated with STAT1 ASON, STAT1 sense oligonucleotides (SON), dexamethasone (DEX) and medium alone (control), respectively. AMs and media were collected after culture for 36 h. The mRNA and protein expressions of STAT1 and ICAM-1 in AMs were detected by RT-PCR and ELISA, respectively. The concentrations of TNF-alpha, IL-8, NO in cultured medium were detected. The STAT1 mRNA expression by AMs in the STAT1 ASON group was lower than those of AMs in the STAT1 SON group, the DEX group and the control group (p<0.05). Moreover, the STAT1 mRNA expression by AMs in the DEX group was also lower than those of AMs in the STAT1 SON group and the control group (p<0.05), but the STAT1 mRNA expression by AMs in the STAT1 SON group was not different from that of the control group (p>0.05). The protein expressions of STAT1 and ICAM-1 and the mRNA expression of ICAM-1 showed similar changes to the STAT1 mRNA expression by AMs. The concentrations of TNF-alpha, IL-8, NO in cultured medium from STAT1 ASON group were lower than those from STAT1 SON, DEX and the control groups (p<0.05). Moreover, the concentrations of TNF-alpha, IL-8, NO in cultured medium from DEX group were also lower than those from the control and STAT1 SON group (p<0.05), but no difference between STAT1 SON group and the control (p>0.05). The results suggest that STAT1 ASON could inhibit the secretion of TNF-alpha, IL-8, NO in AMs, and STAT1 could become a target of treating pulmonary fibrosis. SN - 1672-7681 UR - https://www.unboundmedicine.com/medline/citation/16212889/STAT1_antisense_oligonucleotides_attenuate_the_proinflammatory_cytokine_release_of_alveolar_macrophages_in_bleomycin_induced_fibrosis_ L2 - http://www.cmi.ustc.edu.cn/2/3/211.pdf DB - PRIME DP - Unbound Medicine ER -