| Autor: |
Khan SI; Department of Pharmacology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.; Department of Medicine, Monash University, Melbourne, Victoria, Australia.; Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia., Andrews KL; Department of Pharmacology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.; Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia., Jackson KL; Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia., Memon B; Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia., Jefferis AM; Department of Pharmacology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.; Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia., Lee MKS; Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia., Diep H; Department of Pharmacology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia., Wei Z; Department of Pharmacology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia., Drummond GR; Department of Physiology, Anatomy, and Microbiology, La Trobe University, Bundoora, Victoria, Australia., Head GA; Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia., Jennings GL; Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia.; Sydney Medical School, University of Sydney, Camperdown, New South Wales, Australia., Murphy AJ; Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia., Vinh A; Department of Physiology, Anatomy, and Microbiology, La Trobe University, Bundoora, Victoria, Australia., Sampson AK; Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia., Chin-Dusting JPF; Department of Pharmacology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.; Department of Medicine, Monash University, Melbourne, Victoria, Australia.; Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia. |
| Abstrakt: |
The essential role of the Y chromosome in male sex determination has largely overshadowed the possibility that it may exert other biologic roles. Here, we show that Y-chromosome lineage is a strong determinant of perivascular and renal T-cell infiltration in the stroke-prone spontaneously hypertensive rat, which, in turn, may influence vascular function and blood pressure (BP). We also show, for the first time to our knowledge, that augmented perivascular T-cell levels can directly instigate vascular dysfunction, and that the production of reactive oxygen species that stimulate cyclo-oxygenase underlies this. We thus provide strong evidence for the consideration of Y-chromosome lineage in the diagnosis and treatment of male hypertension, and point to the modulation of cardiovascular organ T-cell infiltration as a possible mechanism that underpins Y- chromosome regulation of BP.-Khan, S. I., Andrews, K. L., Jackson, K. L., Memon, B., Jefferis, A.-M., Lee, M. K. S., Diep, H., Wei, Z., Drummond, G. R., Head, G. A., Jennings, G. L., Murphy, A. J., Vinh, A., Sampson, A. K., Chin-Dusting, J. P. F. Y-chromosome lineage determines cardiovascular organ T-cell infiltration in the stroke-prone spontaneously hypertensive rat. |
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