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Screening of Differentially Displayed Genes Correlative to Diabetes with and without Chinese Herb Astragalus Membranaceus Treatment
Author(s) -
Zhao Hanfang,
Wu Yi,
Huang Shenglin
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.lb71
Subject(s) - gene , biology , transforming growth factor , diabetes mellitus , fibrosis , transfection , gene expression , messenger rna , plasmid , bioinformatics , medicine , microbiology and biotechnology , endocrinology , genetics
The worst consequence of Diabetes mellitus (DM) at the terminal stage is irreversible renal fibrosis. Several clinical researches have indicated that Chinese herb Astragalus membranaceus (AM) has ability to defer the progression of DM. In this work, we studied the molecular mechanism of AM to defer renal fibrosis. A rat model of type 1 DM with two groups was built: diabetes with (DA group) and without (D group) AM treatment. The total RNA from renal tissues was used for gene chip analysis and some differentially displayed genes were confirmed by real‐time PCR. Two hundred and one differentially displayed genes have been found in the chip with 4096 genes, in which 126 genes were up‐regulated and 75 genes were down‐regulated. One of expression down‐regulated genes is Latent Transforming Factor Binding Protein 1 (LTBP1). An interference plasmid of psilencer‐shLTBP1 was constructed and transfected into HK2 cells. The changes of gene expression of LTBP1, TGF¦Â1, collagenI and collagenIII were detected by RT‐PCR. In psilencer‐shLTBP1 transfected HK2 cells, mRNA expression of LTBP1, TGF¦Â1, collagenI and collagenIII were down‐regulated by 59%, 45%, 50% and 75% respectively. Our results suggest that LTBP1 can regulate the expression of TGF¦Â1 which improves the synthesis of collagen. LTBP1 itself may be a fibrosis associated factor. Our findings provide new insights into the molecular mechanism of AM to defer renal fibrosis via regulating LTBP1 expression.