title: Leptin does not induce hypertrophy, cell cycle alterations, or production of MCP-1 in cultured rat and mouse cardiomyocytes.
abstract: BACKGROUND
  Leptin has been proposed as an important mediator in cardiovascular pathophysiology. Patients with congestive heart failure (CHF) present high plasma leptin levels. CHF is generally preceded by myocardial remodeling involving hypertrophy, necrosis, and apoptosis.
  
  
  OBJECTIVE
  To investigate whether leptin causes hypertrophy or cell cycle alterations, or induces MCP-1 synthesis in cardiomyocytes.
  
  
  METHODS
  Primary cultures of neonatal rat cardiomyocytes (PC) and murine cell line HL-1 were used. RT-PCR was used to identify Ob-Rb gene expression. Metabolic activity and proliferation of cardiomyocytes was studied using MTT and BrdU uptake, while apoptosis was assayed with Hoechst dye vital staining and flow cytometry. Measurement of the cell surface area was used to determine hypertrophy. MCP-1 levels were measured by ELISA.
  
  
  RESULTS
  RT-PCR showed Ob-Rb mRNA expression in HL-1 cells. Exposure to leptin induced no changes in metabolic activity, proliferation, and apoptotic rates, and did not alter cell cycle in cardiomyocytes. Leptin did not increase cell size of cardiomyocytes, and MCP-1 synthesis was not detected in PC and HL-1 cells treated with leptin.
  
  
  CONCLUSIONS
  This work shows that leptin does not induce changes in viability, proliferation, size or apoptosis of rat neonatal and HL-1 cardiomyocytes, and it does not induce MCP-1 secretion in these cells.
authors.affiliation: Research Unit in Cardiology, University Clinical Hospital of Santiago de Compostela, Santiago de Compostela, Spain.
authors.forename: Roberto
authors.initials: R
authors.lastname: Piñieiro
authors.forename: María J
authors.initials: MJ
authors.lastname: Iglesias
authors.forename: Sonia
authors.initials: S
authors.lastname: Eiras
authors.forename: Juan
authors.initials: J
authors.lastname: Viñuela
authors.forename: Francisca
authors.initials: F
authors.lastname: Lago
authors.forename: José R
authors.initials: JR
authors.lastname: González-Juanatey
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D006690:Bisbenzimidazole / Q000737:chemistry; D002453:Cell Cycle / Q000187:drug effects; D048708:Cell Growth Processes / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000096:biosynthesis* / Q000235:genetics; D005260:Female; D020738:Leptin / Q000494:pharmacology*; D008297:Male; D051379:Mice; D008856:Microscopy, Fluorescence; D032383:Myocytes, Cardiac / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D011956:Receptors, Cell Surface / Q000096:biosynthesis / Q000235:genetics; D054411:Receptors, Leptin; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D020738:Leptin; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin; C515447:leptin receptor, mouse; D006690:Bisbenzimidazole