• Medientyp: E-Artikel
  • Titel: Intratracheal administration of cyclooxygenase-1-transduced adipose tissue-derived stem cells ameliorates monocrotaline-induced pulmonary hypertension in rats
  • Beteiligte: Somanna, Naveen K.; Wörner, Philipp M.; Murthy, Subramanyam N.; Pankey, Edward A.; Schächtele, Deborah J.; St. Hilaire, Rose-Claire; Jansen, David; Chaffin, Abigail E.; Nossaman, Bobby D.; Alt, Eckhard U.; Kadowitz, Philip J.; Izadpanah, Reza
  • Erschienen: American Physiological Society, 2014
  • Erschienen in: American Journal of Physiology-Heart and Circulatory Physiology, 307 (2014) 8, Seite H1187-H1195
  • Sprache: Englisch
  • DOI: 10.1152/ajpheart.00589.2013
  • ISSN: 0363-6135; 1522-1539
  • Schlagwörter: Physiology (medical) ; Cardiology and Cardiovascular Medicine ; Physiology
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  • Beschreibung: The effect of intratracheal administration of cyclooxygenase-1 (COX-1)-modified adipose stem cells (ASCs) on monocrotaline-induced pulmonary hypertension (MCT-PH) was investigated in the rat. The COX-1 gene was cloned from rat intestinal cells, fused with a hemagglutanin (HA) tag, and cloned into a lentiviral vector. The COX-1 lentiviral vector was shown to enhance COX-1 protein expression and inhibit proliferation of vascular smooth muscle cells without increasing apoptosis. Human ASCs transfected with the COX-1 lentiviral vector (ASCCOX-1) display enhanced COX-1 activity while exhibiting similar differentiation potential compared with untransduced (native) ASCs. PH was induced in rats with MCT, and the rats were subsequently treated with intratracheal injection of ASCCOX-1 or untransduced ASCs. The intratracheal administration of ASCCOX-1 3 × 106 cells on day 14 after MCT treatment significantly attenuated MCT-induced PH when hemodynamic values were measured on day 35 after MCT treatment whereas administration of untransduced ASCs had no significant effect. These results indicate that intratracheally administered ASCCOX-1 persisted for at least 21 days in the lung and attenuate MCT-induced PH and right ventricular hypertrophy. In addition, vasodilator responses to the nitric oxide donor sodium nitroprusside were not altered by the presence of ASCCOX-1 in the lung. These data emphasize the effectiveness of ASCCOX-1 in the treatment of experimentally induced PH.
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