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Lung and Heart Biology of the Dp16 Mouse Model of down Syndrome: Implications for Studying Cardiopulmonary Disease.
Colvin, Kelley L; Nguyen, Kathleen; Boncella, Katie L; Goodman, Desiree M; Elliott, Robert J; Harral, Julie W; Bilodeaux, Jill; Smith, Bradford J; Yeager, Michael E.
Afiliación
  • Colvin KL; Linda Crnic Institute for Down Syndrome, University of Colorado, Aurora, CO 80045, USA.
  • Nguyen K; Department of Bioengineering, University of Colorado Denver, Anschutz Medical Campus, Aurora, CO 80045, USA.
  • Boncella KL; Department of Bioengineering, University of Colorado Denver, Anschutz Medical Campus, Aurora, CO 80045, USA.
  • Goodman DM; Linda Crnic Institute for Down Syndrome, University of Colorado, Aurora, CO 80045, USA.
  • Elliott RJ; Department of Bioengineering, University of Colorado Denver, Anschutz Medical Campus, Aurora, CO 80045, USA.
  • Harral JW; Department of Medicine, University of Colorado, Aurora, CO 80045, USA.
  • Bilodeaux J; Department of Bioengineering, University of Colorado Denver, Anschutz Medical Campus, Aurora, CO 80045, USA.
  • Smith BJ; Department of Bioengineering, University of Colorado Denver, Anschutz Medical Campus, Aurora, CO 80045, USA.
  • Yeager ME; Section of Pediatric Pulmonary and Sleep Medicine, Department of Pediatrics, School of Medicine, University of Colorado, Aurora, CO 80045, USA.
Genes (Basel) ; 14(9)2023 Sep 19.
Article en En | MEDLINE | ID: mdl-37761959
(1) Background: We sought to investigate the baseline lung and heart biology of the Dp16 mouse model of Down syndrome (DS) as a prelude to the investigation of recurrent respiratory tract infection. (2) Methods: In controls vs. Dp16 mice, we compared peripheral blood cell and plasma analytes. We examined baseline gene expression in lungs and hearts for key parameters related to susceptibility of lung infection. We investigated lung and heart protein expression and performed lung morphometry. Finally, and for the first time each in a model of DS, we performed pulmonary function testing and a hemodynamic assessment of cardiac function. (3) Results: Dp16 mice circulate unique blood plasma cytokines and chemokines. Dp16 mouse lungs over-express the mRNA of triplicated genes, but not necessarily corresponding proteins. We found a sex-specific decrease in the protein expression of interferon α receptors, yet an increased signal transducer and activator of transcription (STAT)-3 and phospho-STAT3. Platelet-activating factor receptor protein was not elevated in Dp16 mice. The lungs of Dp16 mice showed increased stiffness and mean linear intercept and contained bronchus-associated lymphoid tissue. The heart ventricles of Dp16 mice displayed hypotonicity. Finally, Dp16 mice required more ketamine to achieve an anesthetized state. (4) Conclusions: The Dp16 mouse model of DS displays key aspects of lung heart biology akin to people with DS. As such, it has the potential to be an extremely valuable model of recurrent severe respiratory tract infection in DS.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Infecciones del Sistema Respiratorio / Síndrome de Down Tipo de estudio: Prognostic_studies Límite: Animals / Female / Humans / Male Idioma: En Revista: Genes (Basel) Año: 2023 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Suiza
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Infecciones del Sistema Respiratorio / Síndrome de Down Tipo de estudio: Prognostic_studies Límite: Animals / Female / Humans / Male Idioma: En Revista: Genes (Basel) Año: 2023 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Suiza