title: Expression of lysophosphatidic acid receptor 1 and relation with cell proliferation, apoptosis, and angiogenesis on preneoplastic changes induced by cadmium chloride in the rat ventral prostate.
abstract: BACKGROUND
  Lysophosphatidic acid (LPA) is a phospholipid growth factor involved in cell proliferation, differentiation, migration, inflammation, angiogenesis, wound healing, cancer invasion, and survival. This study was directed to evaluate the immunoexpression of LPA-1, cell proliferation, apoptosis, and angiogenesis markers in preneoplastic lesions induced with cadmium chloride in rat prostate.
  
  
  METHODS
  The following parameters were calculated in ventral prostate of normal rats and rats that received Cd in drinking water during 24 months: percentages of cells immunoreactive to LPA-1 (LILPA1), PCNA (LIPCNA), MCM7 (LIMCM7), ubiquitin (LIUBI), apoptotic cells (LIAPO), and p53 (LIp53); volume fraction of Bcl-2 (VFBcl-2); and length of microvessels per unit of volume (LVMV/mm3). Data were analyzed using Student's t-test and Pearson correlation test.
  
  
  RESULTS
  The LILPA1 in dysplastic lesions and normal epithelium of Cd-treated rats was significantly higher than those in the control group. Markers of proliferation were significantly increased in dysplastic lesions, whereas some apoptotic markers were significantly decreased. No significant differences between groups were found in VFBcl-2. Dysplastic lesions showed a significant increase of LIp53. The length of microvessels per unit of volume was elevated in dysplastic acini. Statistically significant correlations were found only between LILPA1 and LIUBI.
  
  
  CONCLUSIONS
  Our results suggest that LPA-1 might be implicated in dysplastic lesions induced by cadmium chloride development. More studies are needed to confirm its potential contribution to the disease.
authors: Histology Laboratory, Institute of Applied Molecular Medicine, Department of Basic Medical Sciences, School of Medicine, CEU-San Pablo University, Madrid, Spain. arriazun@ceu.es
authors: Riánsares
authors: R
authors: Arriazu
authors: Esther
authors: E
authors: Durán
authors: José M
authors: JM
authors: Pozuelo
authors: Luis
authors: L
authors: Santamaria
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology; D019256:Cadmium Chloride / Q000633:toxicity; D048708:Cell Growth Processes / Q000187:drug effects / Q000502:physiology; D008297:Male; D055806:Microvessels / Q000378:metabolism / Q000473:pathology; D064168:Minichromosome Maintenance Complex Component 7 / Q000235:genetics / Q000378:metabolism; D009389:Neovascularization, Pathologic / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D011230:Precancerous Conditions / Q000139:chemically induced / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D018809:Proliferating Cell Nuclear Antigen / Q000235:genetics / Q000378:metabolism; D011467:Prostate / Q000098:blood supply / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology*; D011471:Prostatic Neoplasms / Q000098:blood supply / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D049368:Receptors, Lysophosphatidic Acid / Q000096:biosynthesis* / Q000235:genetics / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism; D025801:Ubiquitin / Q000235:genetics / Q000378:metabolism
chemical_list: D018809:Proliferating Cell Nuclear Antigen; D019253:Proto-Oncogene Proteins c-bcl-2; D049368:Receptors, Lysophosphatidic Acid; D016159:Tumor Suppressor Protein p53; D025801:Ubiquitin; C512202:MCM7 protein, rat; D064168:Minichromosome Maintenance Complex Component 7; D019256:Cadmium Chloride