The molecular mechanisms of androgen receptor in nephrolithiasis

Ziyu Fang1, Yonghan Peng1, Ling Li1

  • 1Department of Urology, Changhai Hospital, The Second Military Medical University, No.168 Changhai Road, Shanghai 200433, Republic of China.

Gene
|March 25, 2017
PubMed
Abstract

Insights

Androgen receptor (AR) mechanisms in kidney stone (nephrolithiasis) formation were studied. Key genes like CCL2 and CD44 were identified as potentially critical in nephrolithiasis development.

Area of Science:

  • Molecular biology
  • Genomics
  • Nephrology

Background:

  • Nephrolithiasis, or kidney stone disease, affects millions globally.
  • The role of the androgen receptor (AR) in nephrolithiasis pathogenesis remains incompletely understood.
  • Investigating AR's molecular mechanisms can reveal novel therapeutic targets.

Purpose of the Study:

  • To elucidate the molecular mechanisms of androgen receptor (AR) in nephrolithiasis.
  • To identify key genes and pathways regulated by AR in kidney cells.

Main Methods:

  • Human kidney (HK-2) cells were manipulated to overexpress (DEC-AR) or knockdown (sh-AR) the androgen receptor.
  • Gene expression profiling (microarray) was performed to identify differentially expressed genes (DEGs).
  • Protein-protein interaction (PPI) networks and pathway enrichment analyses were conducted on identified DEGs.

Main Results:

  • AR manipulation significantly altered gene expression in HK-2 cells.
  • 64 downregulated and 63 upregulated negatively correlated DEGs were identified in DEC-AR cells.
  • DEGs were implicated in cell differentiation, immune response, and pathways including rheumatoid arthritis and TNF signaling.

Conclusions:

  • The study identified key negatively correlated differentially expressed genes (DEGs) in AR-modulated kidney cells.
  • Genes such as CCL2, CD44, MMP1, and MMP9 are highlighted as potentially critical players in nephrolithiasis.
  • These findings provide insights into AR's role and potential therapeutic targets for kidney stone disease.

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