Placenta growth factor (PIGF) mRNA expression in brain tumors

被引:66
作者
Nomura, M
Yamagishi, S
Harada, S
Yamashima, T
Yamashita, J
Yamamoto, H
机构
[1] Kanazawa Univ, Sch Med, Dept Neurosurg, Kanazawa, Ishikawa 9208641, Japan
[2] Kanazawa Univ, Sch Med, Dept Biochem, Kanazawa, Ishikawa 9208641, Japan
关键词
PIGF; VEGF; bFGF; brain tumor; mRNA; hypoxia;
D O I
10.1023/A:1006198422718
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
To investigate the relationship between placenta growth factor (PlGF) and brain tumor angiogenesis, we screened 36 primary and 3 metastatic brain tumors. We examined the expression of PlGF mRNA with respect to vasculature of various tumors which was determined by preoperative angiography. The expression of genes of the other angiogenic factors, vascular endothelial growth factor (VEGF), and basic fibroblast growth factor (bFGF) was also tested, and compared to that of PlGF. The primary tumors consisted of 16 meningiomas, 7 gliomas, 7 schwannomas, 4 pituitary adenomas, 1 germinoma, and 1 choriocarcinoma. Using a quantitative reverse transcription-polymerase chain reaction, the mRNA for PlGF(149) and PlGF(170) were detected in 25 out of 39 (64.1%) brain tumors. In primary brain tumors, PlGF mRNA eras expressed in all the hypervascular tumors, but only in 5 of 16 hypovascular tumors (31.3%). None of the 3 metastatic hypervascular tumors expressed PIGF mRNA. The VEGF and bFGF mRNA expression was both detected in 87.2% of the tumors examined. We conducted hypoxic experiments with cultured U-251MG human glioma cells to determine the mechanism of PlGF gene regulation. As the atmospheric oxygen concentration was decreased, the PlGF mRNA level in the U-251MG cells was markedly increased. These results suggest that PlGF may contribute to the pathogenesis of brain tumor angiogenesis.
引用
收藏
页码:123 / 130
页数:8
相关论文
共 22 条
[1]
Migration of human monocytes in response to vascular endothelial growth factor (VEGF) is mediated via the VEGF receptor flt-1 [J].
Barleon, B ;
Sozzani, S ;
Zhou, D ;
Weich, HA ;
Mantovani, A ;
Marme, D .
BLOOD, 1996, 87 (08) :3336-3343
[2]
DISTINCT PATTERNS OF EXPRESSION OF FIBROBLAST GROWTH-FACTORS AND THEIR RECEPTORS IN HUMAN ATHEROMA AND NONATHEROSCLEROTIC ARTERIES - ASSOCIATION OF ACIDIC FGF WITH PLAQUE MICROVESSELS AND MACROPHAGES [J].
BROGI, E ;
WINKLES, JA ;
UNDERWOOD, R ;
CLINTON, SK ;
ALBERTS, GF ;
LIBBY, P .
JOURNAL OF CLINICAL INVESTIGATION, 1993, 92 (05) :2408-2418
[3]
PURIFICATION AND CHARACTERIZATION OF A NATURALLY-OCCURRING VASCULAR ENDOTHELIAL GROWTH-FACTOR PLACENTA GROWTH-FACTOR HETERODIMER [J].
DISALVO, J ;
BAYNE, ML ;
CONN, G ;
KWOK, PW ;
TRIVEDI, PG ;
SODERMAN, DD ;
PALISI, TM ;
SULLIVAN, KA ;
THOMAS, KA .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1995, 270 (13) :7717-7723
[4]
PITUITARY FOLLICULAR CELLS SECRETE A NOVEL HEPARIN-BINDING GROWTH-FACTOR SPECIFIC FOR VASCULAR ENDOTHELIAL-CELLS [J].
FERRARA, N ;
HENZEL, WJ .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1989, 161 (02) :851-858
[5]
ANGIOGENESIS INVITRO [J].
FOLKMAN, J ;
HAUDENSCHILD, C .
NATURE, 1980, 288 (5791) :551-556
[6]
FOLKMAN J, 1992, J BIOL CHEM, V267, P10931
[7]
WHAT IS THE EVIDENCE THAT TUMORS ARE ANGIOGENESIS DEPENDENT [J].
FOLKMAN, J .
JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1990, 82 (01) :4-6
[8]
REGULATION OF ANGIOGENIC GROWTH-FACTOR EXPRESSION BY HYPOXIA, TRANSITION-METALS, AND CHELATING-AGENTS [J].
GLEADLE, JM ;
EBERT, BL ;
FIRTH, JD ;
RATCLIFFE, PJ .
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 1995, 268 (06) :C1362-C1368
[9]
ISOLATION AND CHARACTERIZATION OF A VASCULAR ENDOTHELIAL-CELL MITOGEN PRODUCED BY PITUITARY-DERIVED FOLLICULO STELLATE CELLS [J].
GOSPODAROWICZ, D ;
ABRAHAM, JA ;
SCHILLING, J .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1989, 86 (19) :7311-7315
[10]
A HEPARIN-BINDING FORM OF PLACENTA GROWTH-FACTOR (PLGF-2) IS EXPRESSED IN HUMAN UMBILICAL VEIN ENDOTHELIAL-CELLS AND IN PLACENTA [J].
HAUSER, S ;
WEICH, HA .
GROWTH FACTORS, 1993, 9 (04) :259-268