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Revista do Instituto de Medicina Tropical de São Paulo

On-line version ISSN 1678-9946

Rev. Inst. Med. trop. S. Paulo vol.35 no.3 São Paulo May/June 1993

http://dx.doi.org/10.1590/S0036-46651993000300006 

ORIGINAL ARTICLES

 

Aggregatory behaviour of platelets incubated with subcellular fractions of normal and chagasic human syncytiotrophoblast

 

Comportamento agregatório das plaquetas incubadas com frações subcelulares de sinciciotrofoblasto humano normal e chagásico

 

 

A.R. Eynard; S. Muñoz; L. Ruiz Moreno; M.E. Pasqualini; S.P. de Fabro

Address for correspondence

 

 


SUMMARY

The surface of human syncytiotrophoblast does not induce maternal blood platelet aggregation even though it is not an endothelium. It can be surmised that as occurs in endothelial injury the subcellular components of the syncytiotrophoblast may have pro-or antiaggregatory activity. During congenital Chagas' disease which is associated to trophoblast lesions, platelets may play a role in the development of T. cruzi-induced placentitis. In the present work the aggregatory behaviour of normal human blood platelets was recorded after their challenging with subcellular fractions of syncytiotrophoblast isolated from normal and chagasic women. Nuclear, Mitochondrial, Microsomal and Supernatant fractions isolated from normal and chagasic syncytiotrophoblast failed to induce per se any aggregatory reaction on platelets. When samples of platelet-rich plasma (PRP) were preincubated with normal and chagasic nuclear fractions and then stimulated with collagen at threshold level (CT-PRP) an inhibition of the aggregatory response was observed. Treatment of CT-PRP with normal and chagasic mitochondrial fractions induced inhibition of platelet aggregation whereas only chagasic fraction reduced latency time. Microsornal fraction from normal placentas showed no significant effects on platelet aggregation. It is concluded that subcellular fractions of normal human syncytiotrophoblast do not exhibit any effect on platelet aggregation, whereas those subcellular fractions enriched in intracellular membrane components isolated from chagasic placentas inhibit platelet aggregation.

Key words: Human congenital Chagas' disease; Human platelet aggregation; Trypanosoma cruzi; Chagas' disease; Placenta.


RESUMO

A superficie do sinciciotrofoblasto humano não induz agregação das plaquetas maternas apesar de não ser um endotélio. Lesões endoteliais propiciam o aparecimento de agregados plaquetários, o que nos leva a questionar se os componentes subcelulares do sinciciotrofoblasto também poderiam propiciar eventos semelhantes. Na doença de Chagas congênita, que está associada a lesões a nivel de trofoblasto, as plaquetas poderiam desempenhar algum papel no desenvolvimento da placentitis induzida pelo T. cruzi. Neste trabalho estudou-se o comportamento agregatório das plaquetas humanas normais expostas a frações subcelulares do sinciciotrofoblasto isolado de placentas de mulheres normais e chagásticas. As frações Nuclear, Mitocondrial, Microsomal e Sobrenadante isoladas do sincicitrofoblasto normal ou chagásico não induziram per se reação agregatória de plaquetas. Quando amostras de plasma rico em plaquetas (PRP) foram pré-incubadas com fração nuclear de placentas normais ou chagásicas e pós-estimuladas com doses limiares de colágeno (DLC-PRP) observou-se uma inibiçâo da resposta agregatória. O tratamento de DLC-PRP com fração Mitocondrial de trofoblasto normal e chagásico também induziu inibição da agregação plaquetária porém somente a fração chagásica diminuiu o tempo de latência. A fração Microsomal das placentas normais não provocou diferenças significativas na agregação plaquetária. Conclui-se que as frações subcelulares do sinciciotrofoblasto humano normal não tem ação significativa na agregação plaquetária, enquanto que a incubação com frações subcelulares de placentas chagásicas, enriquecidas em componentes membranosos intracelulares, induziu a inibiçâo da agregação plaquetária.


 

 

Full text available only in PDF format.

Texto completo disponível apenas em PDF.

 

 

ACKNOWLEDGMENTS

This work was partialy supported by grants of CONICOR (Cordoba) and CONICET (Argentina) to Drs. ARE and SPF. We are indebted to Dr. Martha Gonzalez Cremer for critical reading of the manuscript and to Dra. Martha Romano for her collaboration in the obtention of some of the placentae.

 

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Address for correspondence:
Dr. A.R. Eynard
II Catedra de Histologia e Instituto de Biologia Celular
Facultad de Ciencias Medicas; CONICET
Agencia Postal N. 4, 5000
Córdoba, ARGENTINA

Recebido para publicação em 16/09/1992
Aceito para publicação em 17/12/1992

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