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Increased erythropoietin production after myocardial infarction in mice
  1. M Mengozzi1,
  2. R Latini1,*,
  3. M Salio1,
  4. A Sfacteria2,
  5. G Piedimonte2,
  6. J G Gerwien3,
  7. M Leist3,
  8. A L Siren4,
  9. P Ghezzi1,,
  10. S Chimenti1
  1. 1Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy
  2. 2Department of Veterinary of Public Health, University of Messina, Messina, Italy
  3. 3H Lundbeck A/S, Valby, Denmark
  4. 4Max Planck Institute for Experimental Medicine and Departments of Neurology and Psychiatry, Goettingen, Germany
  1. Correspondence to:
    Professor Roberto Latini
    Istituto Mario Negri, Via Eritrea, 62, 20157 Milan, Italy; latini{at}marionegri.it

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In addition to its role as the main regulator of erythropoiesis, erythropoietin has a wide range of protective, antiapoptotic activities in vitro and in vivo, particularly in the brain and, as more recently shown, in the heart.1

Of note, erythropoietin is not exclusively produced by fetal liver and adult kidney but is expressed also in the brain, where it can be induced by hypoxia or ischaemia. Several studies underline the potential role of erythropoietin in mediating hypoxic–ischaemic preconditioning in the brain.1 On the other hand, the heart has never been described as a site for erythropoietin production. However, hypoxia inducible factor 1 (HIF-1), the main transcriptional regulator of erythropoietin, is induced by hypoxia in myocardial cells in vivo and in vitro.1 HIF-1 has recently been reported to mediate hypoxic preconditioning in the heart.2 We investigated whether, as in the brain, erythropoietin is produced in mouse ischaemic heart.3

MATERIALS AND METHODS

After permanent coronary artery occlusion (CAO), CD1 mice were killed.4 For immunohistochemistry, the portion of heart below the ligature was formalin fixed, paraffin embedded, cut into 5 µm thick sections, and processed as previously described (antierythropoietin: H-162, 1:100; Santa Cruz Biotechnology, Santa Cruz, …

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