Vascular Endothelial Growth Factor Bioactivity and Its Receptors in Patients with Acute Respiratory Distress Syndrome.
10.4132/KoreanJPathol.2011.45.2.139
- Author:
Simona GURZU
1
;
Ioan JUNG
;
Leonard AZAMFIREI
;
Bong Young SHIN
;
Raluca SOLOMON
;
Daria DEMIAN
;
Judith KOVACS
;
Han Kyeom KIM
Author Information
1. Department of Pathology, University of Medicine and Pharmacy of Targu-Mures, Targu Mures, Romania. simonagurzu@yahoo.com
- Publication Type:Original Article
- Keywords:
Respiratory distress syndrome, adult;
Vascular endothelial growth factor;
Pneumocytes;
Hyaline membranes
- MeSH:
Antibodies;
Biopsy;
Down-Regulation;
Endothelial Cells;
Epithelium;
Humans;
Hyalin;
Lung;
Macrophages;
Macrophages, Alveolar;
Membranes;
Pneumocytes;
Respiratory Distress Syndrome, Adult;
Vascular Endothelial Growth Factor A
- From:Korean Journal of Pathology
2011;45(2):139-145
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Pathogenesis of acute respiratory distress syndrome (ARDS) is a controversial issue. Few studies have analyzed the possible role of vascular endothelial growth factor (VEGF) and its receptors in this lesion. METHODS: We compared the immunohistochemical expression of VEGF, its receptors (VEGFR1, VEGFR2) and CD68, in normal lungs and lungs with ARDS. Fifty necropsy cases and 12 lung biopsies with ARDS were analyzed. In total, eight cases were in the early stage and 54 cases were in late stage of ARDS. In addition, the serum level of VEGF165 was also determined. RESULTS: In normal lungs, all antibodies marked the endothelial cells (EC) and pneumocytes (PC), except for CD68, which was expressed in the alveolar macrophages. In early ARDS, the intensity of VEGF165 and VEGFR2 decreased in both EC and PC. VEGF121 was absent in PC but its expression increased in bronchial epithelium. VEGFR1 was expressed in the integral PC. In late ARDS, VEGF165 down-regulation was more significant in PC and EC but its intensity increased in hyaline membranes (HM). In some cases, HM were CD68 positive. The serum level of VEGF165 was up-regulated, while VEGF165 intensity in PC decreased and the HM appeared in alveolar spaces. CONCLUSIONS: Sporadic positivity of HM for CD68 and decreasing of VEGF165 expression in EC proved that VEGF165 is produced by PC, destroyed macrophages, and extravasated serum.
