The Expression of Vascular Endothelial Growth Factor (VEGF)in Aplastic Anemia.
- Author:
Na Ri LEE
1
;
Eun Kee SONG
;
Hyun Jung YOON
;
Ho Kyung LEE
;
Jae Yong KWAK
;
Chang Yeol YIM
;
Myoung Ja CHUNG
;
Hyun LIM
;
Sam Im CHOI
Author Information
1. Department of Internal Medicine, Chonbuk National University Medical School, Chonbuk, Korea. jykwak@moak.chonbuk.ac.kr
- Publication Type:Original Article
- Keywords:
Aplastic anemia;
VEGF (Vascular endothelial growth factor);
MVD (microvessel density)
- MeSH:
Anemia, Aplastic*;
Antigens, CD34;
Biopsy;
Bone Marrow;
Cytoplasm;
Extracellular Matrix;
Hematopoietic Stem Cells;
Histiocytes;
Humans;
Immunohistochemistry;
Megakaryocytes;
Microvessels;
Paraffin;
Plasma;
Plasma Cells;
Vascular Endothelial Growth Factor A*
- From:Korean Journal of Hematology
2003;38(3):157-163
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Vascular endothelial growth factor (VEGF) is a potent angiogenic peptide with biologic effects that include regulation of hematopoietic stem cell development, extracellular matrix remodeling, and inflammatory cytokine generation. VEGF plasma levels are elevated in circulation during tumor growth and bone marrow proliferative status. In this study, to investigate the role of VEGF expression in patients with aplastic anemia (AA), VEGF protein expression and microvessel density (MVD) were evaluated. METHODS: Immunohistochemical staining for detecting VEGF protein was performed by the labeled avidin-biotin method on the formalin-fixed and paraffin embedded bone marrow biopsy samples of 25 patients with severe AA and 10 normal controls. Microvessels were scored in at least 3 areas (x200 fields) of the highest MVD in representative sections of each bone marrow biopsy specimen using immunohistochemistry for CD34 antigen. RESULTS: In AA, megakaryocytes and histiocytes expressed less intense cytoplasmic VEGF than in control (P < 0.05). However, plasma cells had higher VEGF immunoreactivity in AA than in control. MVD was significantly lower in patients with AA (21.43+/-7.24), compared to controls (27.65+/-3.44) (P < 0.05). MVD had a strong correlation with bone marrow cellularity. Also, the degree of VEGF immunoreactivity was correlated with bone marrow cellularity and MVD. CONCLUSION: Angiogenesis as assessed by MVD and VEGF expression seems to have a role in the pathogenesis of AA.
