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Expression of TRAIL (Apo-2L)/TRAIL Receptor System Related to Apoptosis at the Human Extraembryonic Tissues and Gestational Trophoblastic Disease / 대한산부인과학회잡지
Artigo em Coreano | WPRIM (Pacífico Ocidental) | ID: wpr-79243
Biblioteca responsável: WPRO
ABSTRACT
Human uterus has been known as a immune privileged site for the product of conception. At the feto-maternal interface, Fas system is a underlying main mechanism of maternal immune acceptance. To date, the TRAIL (TNF-related apoptosis-inducing ligand) system is known to be another pivotal mechanism.

OBJECTIVE:

To clarify the protein expression of TRAIL ligand and receptors in the normal and pathologic (preeclampsia, hydatidiform mole) placenta, chorioamnion, decidua.

METHODS:

we investigated the expression of TRAIL system in the above-mentioned tissues by using Western Hybridization.

RESULTS:

All tissues expressed TRAIL ligand and only a DcR2 among TRAIL receptors (DR4, DR5, DcR1, DcR2).

CONCLUSION:

we demonstrated the expression of TRAIL ligand and DcR2 protein at the feto-maternal interface of the normal and pathologic pregnancies. Further study regarding the expression of other receptors and quantitative analysis between normal and pathologic pregnancies should be followed.
Assuntos

Texto completo: Disponível Base de dados: WPRIM (Pacífico Ocidental) Assunto principal: Placenta / Útero / Apoptose / Decídua / Doença Trofoblástica Gestacional / Receptores do Ligante Indutor de Apoptose Relacionado a TNF / Fertilização Limite: Feminino / Humanos / Gravidez Idioma: Coreano Revista: Korean Journal of Obstetrics and Gynecology Ano de publicação: 2003 Tipo de documento: Artigo
Texto completo: Disponível Base de dados: WPRIM (Pacífico Ocidental) Assunto principal: Placenta / Útero / Apoptose / Decídua / Doença Trofoblástica Gestacional / Receptores do Ligante Indutor de Apoptose Relacionado a TNF / Fertilização Limite: Feminino / Humanos / Gravidez Idioma: Coreano Revista: Korean Journal of Obstetrics and Gynecology Ano de publicação: 2003 Tipo de documento: Artigo
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