title: YKL-40 expression in CD14⁺ liver cells in acute and chronic injury.
abstract: OBJECTIVE
  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 CCl(4) to induce acute damage. Liver biopsies were obtained at 0, 6, 12, 24, 48 and 72 h. For chronic damage, CCl(4) 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.
  
  
  CONCLUSIONS
  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.
authors: Department of Physiology, CUCS, University of Guadalajara, Guadalajara, Jalisco 44340, México.
authors: Oscar
authors: O
authors: Pizano-Martínez
authors: Irinea
authors: I
authors: Yañez-Sánchez
authors: Pilar
authors: P
authors: Alatorre-Carranza
authors: Alejandra
authors: A
authors: Miranda-Díaz
authors: Pablo C
authors: PC
authors: Ortiz-Lazareno
authors: Trinidad
authors: T
authors: García-Iglesias
authors: Adrian
authors: A
authors: Daneri-Navarro
authors: Mónica
authors: M
authors: Vázquez-Del Mercado
authors: Mary
authors: M
authors: Fafutis-Morris
authors: Vidal
authors: V
authors: Delgado-Rizo
mesh_terms: D054392:Adipokines / Q000378:metabolism; D000818:Animals; D002478:Cells, Cultured; D000071451:Chitinase-3-Like Protein 1; D016326:Extracellular Matrix Proteins / Q000235:genetics / Q000378:metabolism*; D006023:Glycoproteins / Q000235:genetics / Q000378:metabolism*; D006133:Growth Substances / Q000378:metabolism; D022781:Hepatocytes / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D037102:Lectins / Q000378:metabolism; D018950:Lipopolysaccharide Receptors / Q000378:metabolism*; D008099:Liver / Q000166:cytology / Q000378:metabolism* / Q000473:pathology*; D016676:Macrophages, Alveolar / Q000502:physiology; D008297:Male; D051381:Rats; D017208:Rats, Wistar
chemical_list: D054392:Adipokines; C084533:CHI3L1 protein, human; C507621:CHI3L1 protein, rat; D000071451:Chitinase-3-Like Protein 1; D016326:Extracellular Matrix Proteins; D006023:Glycoproteins; D006133:Growth Substances; D037102:Lectins; D018950:Lipopolysaccharide Receptors