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Expression of MIP-1alpha mRNA in Kupffer Cells and Serum MIP-1alpha Post Portal Vein Transfusion / 대한이식학회지
The Journal of the Korean Society for Transplantation ; : 167-171, 2002.
Artigo em Coreano | WPRIM | ID: wpr-15823
ABSTRACT

PURPOSE:

Portal vein transfusion (PVT) has been known to induce immunosuppression or tolerance and Kupffer cell was identified to play an important role in the phenomenon. The purposes of this study were investigating PVT effect on gene regulation in Kupffer cells and subsequent change in serum cytokine.

METHODS:

For investigating the effect of PVT, Kupffer cells were isolated from the mice (BalbC) of six groups; 1 hour sham operation (S), 1 hour portal vein saline injection (PVS), 1 hour PVT, 24 hour S, 24 hour PVS, and 24 hour PVT groups. Each group was composed of 3 mice. Total RNAs isolated from Kupffer cells were subjected to RT-PCR differential display. The bands of 24 hour group showing increased expression was cloned for the sequencing analysis.

RESULTS:

Macrophage inflammatory protein 1 alpha (MIP-1alpha) was identified from the bands of increased expression. In PVT groups, increased expression of MIP-1alpha mRNA in Kupffer cells coincided with elevated serum level of MIP-1alpha.

CONCLUSION:

MIP-1alpha may be one of the important cytokines involved in PVT induced immunosuppression or tolerance.
Assuntos

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Veia Porta / RNA / RNA Mensageiro / Citocinas / Terapia de Imunossupressão / Células Clonais / Quimiocina CCL3 / Células de Kupffer Limite: Animais Idioma: Coreano Revista: The Journal of the Korean Society for Transplantation Ano de publicação: 2002 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Veia Porta / RNA / RNA Mensageiro / Citocinas / Terapia de Imunossupressão / Células Clonais / Quimiocina CCL3 / Células de Kupffer Limite: Animais Idioma: Coreano Revista: The Journal of the Korean Society for Transplantation Ano de publicação: 2002 Tipo de documento: Artigo