Effects of Sulfur Dioxide on the Expressions of EGF, EGFR, and COX-2 in Airway of Asthmatic Rats
Abstract The pathogenesis of asthma involves a combination of genetic and environmental factors. The epidemiology studies have shown that $ SO_{2 } $might play an important role in the initiation or exacerbation of the asthma disease. To investigate the asthmatic molecular mechanisms exposed to $ SO...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Li, Ruijin [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2007 |
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| Schlagwörter: |
Epidermal Growth Factor Receptor |
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| Anmerkung: |
© Springer Science+Business Media, LLC 2007 |
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| Übergeordnetes Werk: |
Enthalten in: Archives of environmental contamination and toxicology - New York, NY : Springer, 1973, 54(2007), 4 vom: 26. Okt. |
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| Übergeordnetes Werk: |
volume:54 ; year:2007 ; number:4 ; day:26 ; month:10 |
| Links: |
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| DOI / URN: |
10.1007/s00244-007-9054-9 |
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| Katalog-ID: |
SPR002737175 |
|---|
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| 100 | 1 | |a Li, Ruijin |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Effects of Sulfur Dioxide on the Expressions of EGF, EGFR, and COX-2 in Airway of Asthmatic Rats |
| 264 | 1 | |c 2007 | |
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| 500 | |a © Springer Science+Business Media, LLC 2007 | ||
| 520 | |a Abstract The pathogenesis of asthma involves a combination of genetic and environmental factors. The epidemiology studies have shown that $ SO_{2 } $might play an important role in the initiation or exacerbation of the asthma disease. To investigate the asthmatic molecular mechanisms exposed to $ SO_{2} $, male Wistar rats were divided randomly into four equal groups of six animals each: (1) $ SO_{2} $ group, (2) ovalbumin (OVA) group (asthma group), (3) $ SO_{2 } $plus OVA group, and (4) control group. The rats were challenged by ovalbumin (OVA) or $ SO_{2} $ (5.6 mg/$ m^{3} $) inhalation alone or together. The mRNA and protein levels of asthma-related genes (EGF, EGFR, and COX-2) were analyzed in lungs and tracheas using real-time reverse transcription–polymerase chain reaction assay, radioimmunoassay method, and Western blot analysis, respectively. The results showed that inhaled $ SO_{2} $ alone increased the mRNA and protein expressions of three tested genes in lung and trachea tissues, but only the mRNA levels of EGFR and COX-2 in tracheas were significantly increased compared with the control. However, OVA exposure significantly induced the mRNA and protein expressions of EGF, EGFR, and COX-2 compared with the control. Meanwhile, OVA plus $ SO_{2} $ inhalation enhanced the mRNA and protein levels of these genes in rat airways, versus exposure to OVA alone. These results suggested that $ SO_{2} $ could increase the expressions of EGF, EGFR, and COX-2 on the transcription and translation levels in the lungs and tracheas from asthmatic rats, which might be one of the possible mechanisms by which $ SO_{2} $ pollution aggravates asthma disease. | ||
| 650 | 4 | |a Epidermal Growth Factor Receptor |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Epidermal Growth Factor |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Airway Remodel |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Epidermal Growth Factor Receptor mRNA |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Epidermal Growth Factor Level |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Meng, Ziqiang |4 aut | |
| 700 | 1 | |a Xie, Jingfang |4 aut | |
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2007 |
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10.1007/s00244-007-9054-9 doi (DE-627)SPR002737175 (SPR)s00244-007-9054-9-e DE-627 ger DE-627 rakwb eng Li, Ruijin verfasserin aut Effects of Sulfur Dioxide on the Expressions of EGF, EGFR, and COX-2 in Airway of Asthmatic Rats 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Science+Business Media, LLC 2007 Abstract The pathogenesis of asthma involves a combination of genetic and environmental factors. The epidemiology studies have shown that $ SO_{2 } $might play an important role in the initiation or exacerbation of the asthma disease. To investigate the asthmatic molecular mechanisms exposed to $ SO_{2} $, male Wistar rats were divided randomly into four equal groups of six animals each: (1) $ SO_{2} $ group, (2) ovalbumin (OVA) group (asthma group), (3) $ SO_{2 } $plus OVA group, and (4) control group. The rats were challenged by ovalbumin (OVA) or $ SO_{2} $ (5.6 mg/$ m^{3} $) inhalation alone or together. The mRNA and protein levels of asthma-related genes (EGF, EGFR, and COX-2) were analyzed in lungs and tracheas using real-time reverse transcription–polymerase chain reaction assay, radioimmunoassay method, and Western blot analysis, respectively. The results showed that inhaled $ SO_{2} $ alone increased the mRNA and protein expressions of three tested genes in lung and trachea tissues, but only the mRNA levels of EGFR and COX-2 in tracheas were significantly increased compared with the control. However, OVA exposure significantly induced the mRNA and protein expressions of EGF, EGFR, and COX-2 compared with the control. Meanwhile, OVA plus $ SO_{2} $ inhalation enhanced the mRNA and protein levels of these genes in rat airways, versus exposure to OVA alone. These results suggested that $ SO_{2} $ could increase the expressions of EGF, EGFR, and COX-2 on the transcription and translation levels in the lungs and tracheas from asthmatic rats, which might be one of the possible mechanisms by which $ SO_{2} $ pollution aggravates asthma disease. Epidermal Growth Factor Receptor (dpeaa)DE-He213 Epidermal Growth Factor (dpeaa)DE-He213 Airway Remodel (dpeaa)DE-He213 Epidermal Growth Factor Receptor mRNA (dpeaa)DE-He213 Epidermal Growth Factor Level (dpeaa)DE-He213 Meng, Ziqiang aut Xie, Jingfang aut Enthalten in Archives of environmental contamination and toxicology New York, NY : Springer, 1973 54(2007), 4 vom: 26. Okt. (DE-627)253390052 (DE-600)1458449-9 1432-0703 nnns volume:54 year:2007 number:4 day:26 month:10 https://dx.doi.org/10.1007/s00244-007-9054-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 54 2007 4 26 10 |
| spelling |
10.1007/s00244-007-9054-9 doi (DE-627)SPR002737175 (SPR)s00244-007-9054-9-e DE-627 ger DE-627 rakwb eng Li, Ruijin verfasserin aut Effects of Sulfur Dioxide on the Expressions of EGF, EGFR, and COX-2 in Airway of Asthmatic Rats 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Science+Business Media, LLC 2007 Abstract The pathogenesis of asthma involves a combination of genetic and environmental factors. The epidemiology studies have shown that $ SO_{2 } $might play an important role in the initiation or exacerbation of the asthma disease. To investigate the asthmatic molecular mechanisms exposed to $ SO_{2} $, male Wistar rats were divided randomly into four equal groups of six animals each: (1) $ SO_{2} $ group, (2) ovalbumin (OVA) group (asthma group), (3) $ SO_{2 } $plus OVA group, and (4) control group. The rats were challenged by ovalbumin (OVA) or $ SO_{2} $ (5.6 mg/$ m^{3} $) inhalation alone or together. The mRNA and protein levels of asthma-related genes (EGF, EGFR, and COX-2) were analyzed in lungs and tracheas using real-time reverse transcription–polymerase chain reaction assay, radioimmunoassay method, and Western blot analysis, respectively. The results showed that inhaled $ SO_{2} $ alone increased the mRNA and protein expressions of three tested genes in lung and trachea tissues, but only the mRNA levels of EGFR and COX-2 in tracheas were significantly increased compared with the control. However, OVA exposure significantly induced the mRNA and protein expressions of EGF, EGFR, and COX-2 compared with the control. Meanwhile, OVA plus $ SO_{2} $ inhalation enhanced the mRNA and protein levels of these genes in rat airways, versus exposure to OVA alone. These results suggested that $ SO_{2} $ could increase the expressions of EGF, EGFR, and COX-2 on the transcription and translation levels in the lungs and tracheas from asthmatic rats, which might be one of the possible mechanisms by which $ SO_{2} $ pollution aggravates asthma disease. Epidermal Growth Factor Receptor (dpeaa)DE-He213 Epidermal Growth Factor (dpeaa)DE-He213 Airway Remodel (dpeaa)DE-He213 Epidermal Growth Factor Receptor mRNA (dpeaa)DE-He213 Epidermal Growth Factor Level (dpeaa)DE-He213 Meng, Ziqiang aut Xie, Jingfang aut Enthalten in Archives of environmental contamination and toxicology New York, NY : Springer, 1973 54(2007), 4 vom: 26. Okt. (DE-627)253390052 (DE-600)1458449-9 1432-0703 nnns volume:54 year:2007 number:4 day:26 month:10 https://dx.doi.org/10.1007/s00244-007-9054-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 54 2007 4 26 10 |
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10.1007/s00244-007-9054-9 doi (DE-627)SPR002737175 (SPR)s00244-007-9054-9-e DE-627 ger DE-627 rakwb eng Li, Ruijin verfasserin aut Effects of Sulfur Dioxide on the Expressions of EGF, EGFR, and COX-2 in Airway of Asthmatic Rats 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Science+Business Media, LLC 2007 Abstract The pathogenesis of asthma involves a combination of genetic and environmental factors. The epidemiology studies have shown that $ SO_{2 } $might play an important role in the initiation or exacerbation of the asthma disease. To investigate the asthmatic molecular mechanisms exposed to $ SO_{2} $, male Wistar rats were divided randomly into four equal groups of six animals each: (1) $ SO_{2} $ group, (2) ovalbumin (OVA) group (asthma group), (3) $ SO_{2 } $plus OVA group, and (4) control group. The rats were challenged by ovalbumin (OVA) or $ SO_{2} $ (5.6 mg/$ m^{3} $) inhalation alone or together. The mRNA and protein levels of asthma-related genes (EGF, EGFR, and COX-2) were analyzed in lungs and tracheas using real-time reverse transcription–polymerase chain reaction assay, radioimmunoassay method, and Western blot analysis, respectively. The results showed that inhaled $ SO_{2} $ alone increased the mRNA and protein expressions of three tested genes in lung and trachea tissues, but only the mRNA levels of EGFR and COX-2 in tracheas were significantly increased compared with the control. However, OVA exposure significantly induced the mRNA and protein expressions of EGF, EGFR, and COX-2 compared with the control. Meanwhile, OVA plus $ SO_{2} $ inhalation enhanced the mRNA and protein levels of these genes in rat airways, versus exposure to OVA alone. These results suggested that $ SO_{2} $ could increase the expressions of EGF, EGFR, and COX-2 on the transcription and translation levels in the lungs and tracheas from asthmatic rats, which might be one of the possible mechanisms by which $ SO_{2} $ pollution aggravates asthma disease. Epidermal Growth Factor Receptor (dpeaa)DE-He213 Epidermal Growth Factor (dpeaa)DE-He213 Airway Remodel (dpeaa)DE-He213 Epidermal Growth Factor Receptor mRNA (dpeaa)DE-He213 Epidermal Growth Factor Level (dpeaa)DE-He213 Meng, Ziqiang aut Xie, Jingfang aut Enthalten in Archives of environmental contamination and toxicology New York, NY : Springer, 1973 54(2007), 4 vom: 26. Okt. (DE-627)253390052 (DE-600)1458449-9 1432-0703 nnns volume:54 year:2007 number:4 day:26 month:10 https://dx.doi.org/10.1007/s00244-007-9054-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 54 2007 4 26 10 |
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10.1007/s00244-007-9054-9 doi (DE-627)SPR002737175 (SPR)s00244-007-9054-9-e DE-627 ger DE-627 rakwb eng Li, Ruijin verfasserin aut Effects of Sulfur Dioxide on the Expressions of EGF, EGFR, and COX-2 in Airway of Asthmatic Rats 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Science+Business Media, LLC 2007 Abstract The pathogenesis of asthma involves a combination of genetic and environmental factors. The epidemiology studies have shown that $ SO_{2 } $might play an important role in the initiation or exacerbation of the asthma disease. To investigate the asthmatic molecular mechanisms exposed to $ SO_{2} $, male Wistar rats were divided randomly into four equal groups of six animals each: (1) $ SO_{2} $ group, (2) ovalbumin (OVA) group (asthma group), (3) $ SO_{2 } $plus OVA group, and (4) control group. The rats were challenged by ovalbumin (OVA) or $ SO_{2} $ (5.6 mg/$ m^{3} $) inhalation alone or together. The mRNA and protein levels of asthma-related genes (EGF, EGFR, and COX-2) were analyzed in lungs and tracheas using real-time reverse transcription–polymerase chain reaction assay, radioimmunoassay method, and Western blot analysis, respectively. The results showed that inhaled $ SO_{2} $ alone increased the mRNA and protein expressions of three tested genes in lung and trachea tissues, but only the mRNA levels of EGFR and COX-2 in tracheas were significantly increased compared with the control. However, OVA exposure significantly induced the mRNA and protein expressions of EGF, EGFR, and COX-2 compared with the control. Meanwhile, OVA plus $ SO_{2} $ inhalation enhanced the mRNA and protein levels of these genes in rat airways, versus exposure to OVA alone. These results suggested that $ SO_{2} $ could increase the expressions of EGF, EGFR, and COX-2 on the transcription and translation levels in the lungs and tracheas from asthmatic rats, which might be one of the possible mechanisms by which $ SO_{2} $ pollution aggravates asthma disease. Epidermal Growth Factor Receptor (dpeaa)DE-He213 Epidermal Growth Factor (dpeaa)DE-He213 Airway Remodel (dpeaa)DE-He213 Epidermal Growth Factor Receptor mRNA (dpeaa)DE-He213 Epidermal Growth Factor Level (dpeaa)DE-He213 Meng, Ziqiang aut Xie, Jingfang aut Enthalten in Archives of environmental contamination and toxicology New York, NY : Springer, 1973 54(2007), 4 vom: 26. Okt. (DE-627)253390052 (DE-600)1458449-9 1432-0703 nnns volume:54 year:2007 number:4 day:26 month:10 https://dx.doi.org/10.1007/s00244-007-9054-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 54 2007 4 26 10 |
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10.1007/s00244-007-9054-9 doi (DE-627)SPR002737175 (SPR)s00244-007-9054-9-e DE-627 ger DE-627 rakwb eng Li, Ruijin verfasserin aut Effects of Sulfur Dioxide on the Expressions of EGF, EGFR, and COX-2 in Airway of Asthmatic Rats 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Science+Business Media, LLC 2007 Abstract The pathogenesis of asthma involves a combination of genetic and environmental factors. The epidemiology studies have shown that $ SO_{2 } $might play an important role in the initiation or exacerbation of the asthma disease. To investigate the asthmatic molecular mechanisms exposed to $ SO_{2} $, male Wistar rats were divided randomly into four equal groups of six animals each: (1) $ SO_{2} $ group, (2) ovalbumin (OVA) group (asthma group), (3) $ SO_{2 } $plus OVA group, and (4) control group. The rats were challenged by ovalbumin (OVA) or $ SO_{2} $ (5.6 mg/$ m^{3} $) inhalation alone or together. The mRNA and protein levels of asthma-related genes (EGF, EGFR, and COX-2) were analyzed in lungs and tracheas using real-time reverse transcription–polymerase chain reaction assay, radioimmunoassay method, and Western blot analysis, respectively. The results showed that inhaled $ SO_{2} $ alone increased the mRNA and protein expressions of three tested genes in lung and trachea tissues, but only the mRNA levels of EGFR and COX-2 in tracheas were significantly increased compared with the control. However, OVA exposure significantly induced the mRNA and protein expressions of EGF, EGFR, and COX-2 compared with the control. Meanwhile, OVA plus $ SO_{2} $ inhalation enhanced the mRNA and protein levels of these genes in rat airways, versus exposure to OVA alone. These results suggested that $ SO_{2} $ could increase the expressions of EGF, EGFR, and COX-2 on the transcription and translation levels in the lungs and tracheas from asthmatic rats, which might be one of the possible mechanisms by which $ SO_{2} $ pollution aggravates asthma disease. Epidermal Growth Factor Receptor (dpeaa)DE-He213 Epidermal Growth Factor (dpeaa)DE-He213 Airway Remodel (dpeaa)DE-He213 Epidermal Growth Factor Receptor mRNA (dpeaa)DE-He213 Epidermal Growth Factor Level (dpeaa)DE-He213 Meng, Ziqiang aut Xie, Jingfang aut Enthalten in Archives of environmental contamination and toxicology New York, NY : Springer, 1973 54(2007), 4 vom: 26. Okt. (DE-627)253390052 (DE-600)1458449-9 1432-0703 nnns volume:54 year:2007 number:4 day:26 month:10 https://dx.doi.org/10.1007/s00244-007-9054-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 54 2007 4 26 10 |
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Enthalten in Archives of environmental contamination and toxicology 54(2007), 4 vom: 26. Okt. volume:54 year:2007 number:4 day:26 month:10 |
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Enthalten in Archives of environmental contamination and toxicology 54(2007), 4 vom: 26. Okt. volume:54 year:2007 number:4 day:26 month:10 |
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Epidermal Growth Factor Receptor Epidermal Growth Factor Airway Remodel Epidermal Growth Factor Receptor mRNA Epidermal Growth Factor Level |
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Li, Ruijin @@aut@@ Meng, Ziqiang @@aut@@ Xie, Jingfang @@aut@@ |
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The epidemiology studies have shown that $ SO_{2 } $might play an important role in the initiation or exacerbation of the asthma disease. To investigate the asthmatic molecular mechanisms exposed to $ SO_{2} $, male Wistar rats were divided randomly into four equal groups of six animals each: (1) $ SO_{2} $ group, (2) ovalbumin (OVA) group (asthma group), (3) $ SO_{2 } $plus OVA group, and (4) control group. The rats were challenged by ovalbumin (OVA) or $ SO_{2} $ (5.6 mg/$ m^{3} $) inhalation alone or together. The mRNA and protein levels of asthma-related genes (EGF, EGFR, and COX-2) were analyzed in lungs and tracheas using real-time reverse transcription–polymerase chain reaction assay, radioimmunoassay method, and Western blot analysis, respectively. The results showed that inhaled $ SO_{2} $ alone increased the mRNA and protein expressions of three tested genes in lung and trachea tissues, but only the mRNA levels of EGFR and COX-2 in tracheas were significantly increased compared with the control. However, OVA exposure significantly induced the mRNA and protein expressions of EGF, EGFR, and COX-2 compared with the control. Meanwhile, OVA plus $ SO_{2} $ inhalation enhanced the mRNA and protein levels of these genes in rat airways, versus exposure to OVA alone. These results suggested that $ SO_{2} $ could increase the expressions of EGF, EGFR, and COX-2 on the transcription and translation levels in the lungs and tracheas from asthmatic rats, which might be one of the possible mechanisms by which $ SO_{2} $ pollution aggravates asthma disease.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Epidermal Growth Factor Receptor</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Epidermal Growth Factor</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Airway Remodel</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Epidermal Growth Factor Receptor mRNA</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Epidermal Growth Factor Level</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Meng, Ziqiang</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Xie, Jingfang</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Archives of environmental contamination and toxicology</subfield><subfield code="d">New York, NY : Springer, 1973</subfield><subfield code="g">54(2007), 4 vom: 26. 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|
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Li, Ruijin |
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Li, Ruijin misc Epidermal Growth Factor Receptor misc Epidermal Growth Factor misc Airway Remodel misc Epidermal Growth Factor Receptor mRNA misc Epidermal Growth Factor Level Effects of Sulfur Dioxide on the Expressions of EGF, EGFR, and COX-2 in Airway of Asthmatic Rats |
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Effects of Sulfur Dioxide on the Expressions of EGF, EGFR, and COX-2 in Airway of Asthmatic Rats Epidermal Growth Factor Receptor (dpeaa)DE-He213 Epidermal Growth Factor (dpeaa)DE-He213 Airway Remodel (dpeaa)DE-He213 Epidermal Growth Factor Receptor mRNA (dpeaa)DE-He213 Epidermal Growth Factor Level (dpeaa)DE-He213 |
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misc Epidermal Growth Factor Receptor misc Epidermal Growth Factor misc Airway Remodel misc Epidermal Growth Factor Receptor mRNA misc Epidermal Growth Factor Level |
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Effects of Sulfur Dioxide on the Expressions of EGF, EGFR, and COX-2 in Airway of Asthmatic Rats |
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Effects of Sulfur Dioxide on the Expressions of EGF, EGFR, and COX-2 in Airway of Asthmatic Rats |
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10.1007/s00244-007-9054-9 |
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effects of sulfur dioxide on the expressions of egf, egfr, and cox-2 in airway of asthmatic rats |
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Effects of Sulfur Dioxide on the Expressions of EGF, EGFR, and COX-2 in Airway of Asthmatic Rats |
| abstract |
Abstract The pathogenesis of asthma involves a combination of genetic and environmental factors. The epidemiology studies have shown that $ SO_{2 } $might play an important role in the initiation or exacerbation of the asthma disease. To investigate the asthmatic molecular mechanisms exposed to $ SO_{2} $, male Wistar rats were divided randomly into four equal groups of six animals each: (1) $ SO_{2} $ group, (2) ovalbumin (OVA) group (asthma group), (3) $ SO_{2 } $plus OVA group, and (4) control group. The rats were challenged by ovalbumin (OVA) or $ SO_{2} $ (5.6 mg/$ m^{3} $) inhalation alone or together. The mRNA and protein levels of asthma-related genes (EGF, EGFR, and COX-2) were analyzed in lungs and tracheas using real-time reverse transcription–polymerase chain reaction assay, radioimmunoassay method, and Western blot analysis, respectively. The results showed that inhaled $ SO_{2} $ alone increased the mRNA and protein expressions of three tested genes in lung and trachea tissues, but only the mRNA levels of EGFR and COX-2 in tracheas were significantly increased compared with the control. However, OVA exposure significantly induced the mRNA and protein expressions of EGF, EGFR, and COX-2 compared with the control. Meanwhile, OVA plus $ SO_{2} $ inhalation enhanced the mRNA and protein levels of these genes in rat airways, versus exposure to OVA alone. These results suggested that $ SO_{2} $ could increase the expressions of EGF, EGFR, and COX-2 on the transcription and translation levels in the lungs and tracheas from asthmatic rats, which might be one of the possible mechanisms by which $ SO_{2} $ pollution aggravates asthma disease. © Springer Science+Business Media, LLC 2007 |
| abstractGer |
Abstract The pathogenesis of asthma involves a combination of genetic and environmental factors. The epidemiology studies have shown that $ SO_{2 } $might play an important role in the initiation or exacerbation of the asthma disease. To investigate the asthmatic molecular mechanisms exposed to $ SO_{2} $, male Wistar rats were divided randomly into four equal groups of six animals each: (1) $ SO_{2} $ group, (2) ovalbumin (OVA) group (asthma group), (3) $ SO_{2 } $plus OVA group, and (4) control group. The rats were challenged by ovalbumin (OVA) or $ SO_{2} $ (5.6 mg/$ m^{3} $) inhalation alone or together. The mRNA and protein levels of asthma-related genes (EGF, EGFR, and COX-2) were analyzed in lungs and tracheas using real-time reverse transcription–polymerase chain reaction assay, radioimmunoassay method, and Western blot analysis, respectively. The results showed that inhaled $ SO_{2} $ alone increased the mRNA and protein expressions of three tested genes in lung and trachea tissues, but only the mRNA levels of EGFR and COX-2 in tracheas were significantly increased compared with the control. However, OVA exposure significantly induced the mRNA and protein expressions of EGF, EGFR, and COX-2 compared with the control. Meanwhile, OVA plus $ SO_{2} $ inhalation enhanced the mRNA and protein levels of these genes in rat airways, versus exposure to OVA alone. These results suggested that $ SO_{2} $ could increase the expressions of EGF, EGFR, and COX-2 on the transcription and translation levels in the lungs and tracheas from asthmatic rats, which might be one of the possible mechanisms by which $ SO_{2} $ pollution aggravates asthma disease. © Springer Science+Business Media, LLC 2007 |
| abstract_unstemmed |
Abstract The pathogenesis of asthma involves a combination of genetic and environmental factors. The epidemiology studies have shown that $ SO_{2 } $might play an important role in the initiation or exacerbation of the asthma disease. To investigate the asthmatic molecular mechanisms exposed to $ SO_{2} $, male Wistar rats were divided randomly into four equal groups of six animals each: (1) $ SO_{2} $ group, (2) ovalbumin (OVA) group (asthma group), (3) $ SO_{2 } $plus OVA group, and (4) control group. The rats were challenged by ovalbumin (OVA) or $ SO_{2} $ (5.6 mg/$ m^{3} $) inhalation alone or together. The mRNA and protein levels of asthma-related genes (EGF, EGFR, and COX-2) were analyzed in lungs and tracheas using real-time reverse transcription–polymerase chain reaction assay, radioimmunoassay method, and Western blot analysis, respectively. The results showed that inhaled $ SO_{2} $ alone increased the mRNA and protein expressions of three tested genes in lung and trachea tissues, but only the mRNA levels of EGFR and COX-2 in tracheas were significantly increased compared with the control. However, OVA exposure significantly induced the mRNA and protein expressions of EGF, EGFR, and COX-2 compared with the control. Meanwhile, OVA plus $ SO_{2} $ inhalation enhanced the mRNA and protein levels of these genes in rat airways, versus exposure to OVA alone. These results suggested that $ SO_{2} $ could increase the expressions of EGF, EGFR, and COX-2 on the transcription and translation levels in the lungs and tracheas from asthmatic rats, which might be one of the possible mechanisms by which $ SO_{2} $ pollution aggravates asthma disease. © Springer Science+Business Media, LLC 2007 |
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4 |
| title_short |
Effects of Sulfur Dioxide on the Expressions of EGF, EGFR, and COX-2 in Airway of Asthmatic Rats |
| url |
https://dx.doi.org/10.1007/s00244-007-9054-9 |
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Meng, Ziqiang Xie, Jingfang |
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| doi_str |
10.1007/s00244-007-9054-9 |
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2024-07-03T14:52:39.790Z |
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| score |
7.402231 |