Cell-specific expression of fibronectin and EIIIA and EIIIB splice variants after oxygen injury
| العنوان: | Cell-specific expression of fibronectin and EIIIA and EIIIB splice variants after oxygen injury |
|---|---|
| المؤلفون: | Robert A. Sinkin, Stuart Horowitz, William M. Maniscalco, Patricia R. Chess, Liana Toia, Richard H. Watkins |
| المصدر: | American Journal of Physiology-Lung Cellular and Molecular Physiology. 274:L599-L609 |
| بيانات النشر: | American Physiological Society, 1998. |
| سنة النشر: | 1998 |
| مصطلحات موضوعية: | Male, Pulmonary and Respiratory Medicine, Pulmonary Circulation, Pathology, medicine.medical_specialty, Physiology, Proteolipids, DNA, Recombinant, Biology, Isomerism, Physiology (medical), Gene expression, medicine, Animals, splice, RNA, Messenger, Lung, Hyperoxia, Messenger RNA, Genetic Variation, Pulmonary Surfactants, Cell Biology, respiratory system, Immunohistochemistry, Fibronectins, Cell biology, Oxygen, Pulmonary Alveoli, Endothelial stem cell, Fibronectin, biology.protein, Endothelium, Vascular, Rabbits, medicine.symptom, Protein C, medicine.drug |
| الوصف: | Cellular fibronectin (cFN) expression is characteristic of injured tissues. Unlike plasma FN, cFN mRNA often contains the EIIIA or EIIIB domains. We examined the lung cell-specific expression of total cFN mRNA and the EIIIA and EIIIB splice variants in rabbits after acute oxygen injury. By in situ hybridization, control lung had low cFN mRNA. After exposure to >95% oxygen, mRNAs for total cFN and EIIIA were noted primarily in alveolar macrophages and large-vessel endothelial cells. By 3–5 days recovery, cFN and EIIIA mRNA abundance was increased in alveolar septal cells (i.e., alveolar epithelial, interstitial, or endothelial cells) and in some large-vessel endothelial cells but was low in bronchial epithelial cells. During recovery, EIIIB mRNA was low in alveolar septal cells but was noted mainly in chondrocytes. Immunostaining for EIIIA increased during recovery, paralleling the in situ hybridizations. Because FN may modulate alveolar type II cell phenotype, we investigated type II cell cFN mRNA expression in vivo. During recovery, neither isolated type II cells nor cells with surfactant protein C mRNA in vivo contained FN mRNA. In summary, these data suggest that cFN with the EIIIA domain has a role in alveolar cell recovery from oxygen injury and that type II cells do not express cFN during recovery. |
| تدمد: | 1522-1504 1040-0605 |
| DOI: | 10.1152/ajplung.1998.274.4.l599 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::42548f7564e0883865c967082c67a7d3 https://doi.org/10.1152/ajplung.1998.274.4.l599 |
| رقم الانضمام: | edsair.doi.dedup.....42548f7564e0883865c967082c67a7d3 |
| قاعدة البيانات: | OpenAIRE |
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Unlike plasma FN, cFN mRNA often contains the EIIIA or EIIIB domains. We examined the lung cell-specific expression of total cFN mRNA and the EIIIA and EIIIB splice variants in rabbits after acute oxygen injury. By in situ hybridization, control lung had low cFN mRNA. After exposure to >95% oxygen, mRNAs for total cFN and EIIIA were noted primarily in alveolar macrophages and large-vessel endothelial cells. By 3–5 days recovery, cFN and EIIIA mRNA abundance was increased in alveolar septal cells (i.e., alveolar epithelial, interstitial, or endothelial cells) and in some large-vessel endothelial cells but was low in bronchial epithelial cells. During recovery, EIIIB mRNA was low in alveolar septal cells but was noted mainly in chondrocytes. Immunostaining for EIIIA increased during recovery, paralleling the in situ hybridizations. Because FN may modulate alveolar type II cell phenotype, we investigated type II cell cFN mRNA expression in vivo. 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