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Over-expression of Mxi1 represses renal epithelial tubulogenesis through the reduction of matrix metalloproteinase 9.

Abstract：

:Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary renal disease. ADPKD is characterized by cyst development that leads to abnormal kidney structure. Renal tubules are a fundamental unit of architecture, so controls of tubular growth and formation are important for proper kidney function. The molecular mechanisms of tubulogenesis are being actively studied as the basis of diagnosis and treatment of ADPKD. Mxi1 is a member of the MAD family of proteins that functions in terminal differentiation, inhibition of cell cycle progression and tumor suppression, while the Myc protein, which is antagonized by Mxi1, causes renal cystogenesis. Based on these molecular relationships, the present study implicated Mxi1 with ADPKD be demonstrating that curtailed Mxi1 gene expression caused cyst formation in Mxi1-deficient mice. To ascertain whether Mxi1 affects renal epithelial cell tubulogenesis, three-dimensional cultures (3D culture) of mIMCD-3 cells and stably Mxi1 over-expressed mIMCD-3 cells were established. The results indicated that over-expression of the Mxi1 gene plays a role in the regulation of tubulogenesis by regulating some genes participating in renal epithelial branching tubulogenesis such as matrix metalloproteinase 9 (MMP9), integrins, fibronectin, and E-cadherin. The results support the suggestion that over-expression of Mxi1 can suppress renal epithelial tubulogenesis. In particular, MMP9 is greatly affected by the expression level of Mxi1. It can be concluded that mIMCD-3 cells that stably over-express Mxi1 fail to form renal epithelial tubules because of abnormally reduced expression of MMP9.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Song SA,Yoo KH,Ko JY,Kim BH,Yook YJ,Park JH

doi

10.1016/j.bbrc.2012.02.002

subject

Has Abstract

pub_date

2012-03-16 00:00:00

pages

459-65

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(12)00220-3

journal_volume

419

pub_type

杂志文章

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