Capacity of the extracellular matrix of the bone marrow to induce proliferation of myeloid cells in vitro in model of protein malnutrition in mice

被引:0
|
作者
Vituri, Cidonia de Lourdes [1 ]
Alvarez-Silva, Marcio [2 ]
Trentin, Andrea Goncalves [2 ]
Borelli, Primavera [3 ]
机构
[1] Univ Fed Santa Catarina, Dept Anal Clin, Ctr Ciencias Saude, BR-88010970 Florianopolis, SC, Brazil
[2] Univ Fed Santa Catarina, Dept Biol Celular Embriol & Genet, Ctr Ciencias Biol, BR-88010970 Florianopolis, SC, Brazil
[3] Univ Sao Paulo, Fac Ciencias Farmaceut, Dept Anal Clin & Toxicol, BR-05508 Sao Paulo, Brazil
来源
REVISTA BRASILEIRA DE CIENCIAS FARMACEUTICAS | 2008年 / 44卷 / 03期
关键词
Malnutrition experimental study; Extracellular matrix; Hematopoiesis; Bone marrow; Myeloid cells/proliferation;
D O I
暂无
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The aim of this study was to verify the capacity of the extracellular matrix (ECM) obtained from bone marrow of malnourished mice to sustain survival and to induce the proliferation of myeloid cells. We also verified the capacity of the tests to interact with in vitro hematopoietic cytokines. Male "Swiss" mice were submitted to protein malnutrition with a diet contents of 4% casein until they lost 20% of the original weight, while the group-control was kept with a diet content of 14% of casein. The bone marrow was extracted with 1.0 mg of aprotinin/mL in PBS. The proliferation tests were carried out with myeloid cell line FDCP-1, by the colorimetric method of reduction of the MTT. The obtained ECM from nourished and undernourished mice induced cellular proliferation in vitro. Tests performed with Il-3 and GM-CSF cytokines in a concentration of 10 and 500 rho g/mL displayed synergic and regulatory effects respectively. The ECM obtained from the malnourished group submitted to the binding to GM-CSF demonstrated higher cellular proliferation than the ECM obtained from the control group (p<0.05). The results suggest that the alterations in the composition of ECM of bone marrow caused by malnutrition might lead to modification of the GM-CSF activity modulation.
引用
收藏
页码:493 / 501
页数:9
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