Brief Article
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World J Gastroenterol. Sep 7, 2011; 17(33): 3830-3835
Published online Sep 7, 2011. doi: 10.3748/wjg.v17.i33.3830
YKL-40 expression in CD14+ liver cells in acute and chronic injury
Oscar Pizano-Martínez, Irinea Yañez-Sánchez, Pilar Alatorre-Carranza, Alejandra Miranda-Díaz, Pablo C Ortiz-Lazareno, Trinidad García-Iglesias, Adrian Daneri-Navarro, Mónica Vázquez-Del Mercado, Mary Fafutis-Morris, Vidal Delgado-Rizo
Oscar Pizano-Martínez, Irinea Yañez-Sánchez, Pilar Alatorre-Carranza, Alejandra Miranda-Díaz, Trinidad García-Iglesias, Adrian Daneri-Navarro, Mónica Vázquez-Del Mercado, Mary Fafutis-Morris, Vidal Delgado-Rizo, Department of Physiology, CUCS, University of Guadalajara, Guadalajara, Jalisco 44340, México
Pablo C Ortiz-Lazareno, Division of Immunology, Centro de Investigación Biomédica de Occidente-IMSS. Guadalajara, Jalisco 44340, México
Author contributions: Pizano-Martínez O and Yañez-Sánchez I contributed equally to this work; Pizano-Martínez O, Yañez-Sánchez I, and Delgado-Rizo V designed the research; Pizano-Martínez O, Miranda-Diaz A, Ortiz-Lazareno PC and García-Iglesias T performed the research; Daneri-Navarro A, Vázquez-Del Mercado M and Fafutis-Morris M contributed new reagents and analytic equipment; Pizano-Martínez O, Yañez-Sánchez I and Delgado-Rizo V analyzed the data; and Pizano-Martínez O, Yañez-Sánchez I, Alatorre-Carranza P and Delgado-Rizo V wrote the paper.
Supported by Complementary support CONACyT 90361
Correspondence to: Dr. Vidal Delgado-Rizo, Department of Physiology, CUCS, University of Guadalajara, Sierra Mojada 950, Col. Independencia, Building P second level, Guadalajara, Jalisco 44340, México. vidalrizo@gmail.com
Telephone: +52-33-10585307 Fax: +52-33-10585307
Received: October 28, 2010
Revised: January 17, 2011
Accepted: January 24, 2011
Published online: September 7, 2011
Abstract

AIM: To demonstrate that CD14+ cells are an important source of the growth factor YKL-40 in acute and chronic liver damage.

METHODS: Rats were inoculated with one dose of CCl4 to induce acute damage. Liver biopsies were obtained at 0, 6, 12, 24, 48 and 72 h. For chronic damage, CCl4 was administered three days per week for 6 or 8 wk. Tissue samples were collected, and cellular populations were isolated by liver digestion and purified by cell sorting. YKL-40 mRNA and protein expression were evaluated by real-time polymerase chain reaction and western blot.

RESULTS: Acute liver damage induced a rapid increase of YKL-40 mRNA beginning at 12 h. Expression peaked at 24 h, with a 26-fold increase over basal levels. By 72 h however, YKL-40 expression levels had nearly returned to control levels. On the other hand, chronic damage induced a sustained increase in YKL-40 expression, with 7- and 9-fold higher levels at 6 and 8 wk, respectively. The pattern of YKL-40 expression in different subpopulations showed that CD14+ cells, which include Kupffer cells, are a source of YKL-40 after acute damage at 72 h [0.09 relative expression units (REU)] as well as after chronic injury at 6 wk (0.11 REU). Hepatocytes, in turn, accounted for 0.06 and 0.01 REU after 72 h (acute) or 6 wk (chronic), respectively. The rest of the CD14- cells (including T lymphocytes, B lymphocytes, natural killer and natural killer T cells) yielded 0.07 and 0.15 REU at 72 h and 6 wk, respectively. YKL-40 protein expression in liver was detected at 72 h as well as 6 and 8 wk, with the highest expression relative to controls (11-fold; P≤ 0.05) seen at 6 wk. Macrophages were stimulated by lipopolysaccharide. We demonstrate that under these conditions, these cells showed maximum expression of YKL-40 at 12 h, with P < 0.05 compared with controls.

CONCLUSION: Hepatic CD14+ cells are an YKL-40 mRNA and protein source in acute and chronic liver injury, with expression patterns similar to growth factors implicated in inflammation-fibrogenesis.

Keywords: YKL-40, Kupffer cells, Liver cirrhosis, CD14+ cells