Vascular Endothelial Growth Factor Bioactivity and Its Receptors in Patients with Acute Respiratory Distress Syndrome
Gurzu Simona, Jung Ioan, Azamfirei Leonard, Shin Bong-Young, Solomon Raluca, Demian Daria, Kovacs Judith, 김한겸,
소속 상세정보
( Gurzu Simona )
Romania University of Medicine and Pharmacy of Targu-Mures Department of Pathology
( Jung Ioan )
Romania University of Medicine and Pharmacy of Targu-Mures Department of Pathology
( Azamfirei Leonard )
Romania University of Medicine and Pharmacy of Targu-Mures Department of Intensive Care
( Shin Bong-Young )
Korea University College of Medicine Department of Pathology
( Solomon Raluca )
Romania University of Medicine and Pharmacy of Targu-Mures Department of Intensive Care
( Demian Daria )
Romania University of Medicine and Pharmacy of Targu-Mures Department of Pathology
( Kovacs Judith )
Romania University of Medicine and Pharmacy of Targu-Mures Department of Intensive Care
김한겸 ( Kim Han-Kyeom )
Korea University College of Medicine Department of Pathology
KMID : 0357920110450020139
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.
키워드
Respiratory distress syndrome; adult; Vascular endothelial growth factor; Pneumocytes; Hyaline membranes
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