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J Urol. 2014 Jun;191(6):1906-12. doi: 10.1016/j.juro.2014.01.013. Epub 2014 Feb 8.

A paracrine mechanism involving renal tubular cells, adipocytes and macrophages promotes kidney stone formation in a simulated metabolic syndrome environment.

Author information

1
Department of Nephro-urology, Nagoya City University Graduate School of Medical Sciences, Aichi, Japan; Department of Urology, Changzhou Second Hospital, Nanjing Medical University, Nanjing, People's Republic of China.
2
Department of Nephro-urology, Nagoya City University Graduate School of Medical Sciences, Aichi, Japan.
3
Department of Nephro-urology, Nagoya City University Graduate School of Medical Sciences, Aichi, Japan. Electronic address: a-okada@med.nagoya-cu.ac.jp.
4
Department of Urology, Changzhou Second Hospital, Nanjing Medical University, Nanjing, People's Republic of China.

Abstract

PURPOSE:

We developed an in vitro system composed of renal tubular cells, adipocytes and macrophages to simulate metabolic syndrome conditions. We investigated the molecular communication mechanism of these cells and their involvement in kidney stone formation.

MATERIALS AND METHODS:

Mouse renal tubular cells (M-1) were cocultured with adipocytes (3T3-L1) and/or macrophages (RAW264.7). Calcium oxalate monohydrate crystals were exposed to M-1 cells after 48-hour coculture and the number of calcium oxalate monohydrate crystals adherent to the cells was quantified. The expression of cocultured medium and M-1 cell inflammatory factors was analyzed by enzyme-linked immunosorbent assay and quantitative polymerase chain reaction, respectively.

RESULTS:

The inflammatory markers MCP-1, OPN and TNF-α were markedly up-regulated in cocultured M-1 cells. OPN expression increased in M-1 cells cocultured with RAW264.7 cells while MCP-1 and TNF-α were over expressed in M-1 cells cocultured with 3T3-L1 cells. Coculturing M-1 cells simultaneously with 3T3-L1 and RAW264.7 cells resulted in a significant increase in calcium oxalate monohydrate crystal adherence to M-1 cells.

CONCLUSIONS:

Inflammatory cytokine changes were induced by coculturing renal tubular cells with adipocytes and/or macrophages without direct contact, indicating that crosstalk between adipocytes/macrophages and renal tubular cells was mediated by soluble factors. The susceptibility to urolithiasis of patients with metabolic syndrome might be due to aggravated inflammation of renal tubular cells triggered by a paracrine mechanism involving these 3 cell types.

KEYWORDS:

inflammation; kidney; metabolic syndrome X; obesity; urolithiasis

PMID:
24518782
DOI:
10.1016/j.juro.2014.01.013
[Indexed for MEDLINE]
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