Supplementary Materials

Supplementary Materials for:

Obligatory role for GPER in cardiovascular aging and disease

Matthias R. Meyer,* Natalie C. Fredette, Christoph Daniel, Geetanjali Sharma, Kerstin Amann, Jeffrey B. Arterburn, Matthias Barton,* Eric R. Prossnitz*

*Corresponding author. Email: matthias.meyer{at}triemli.zuerich.ch (M.R.M.); barton{at}access.uzh.ch (M.B.); eprossnitz{at}salud.unm.edu (E.R.P.)

This PDF file includes:

  • Fig. S1. Contribution of Nox activity to vascular reactivity in young (4-month-old) wild-type and Gper−/− mice.
  • Fig. S2. Endothelium-independent, NO-mediated vasodilation in young (4-month-old) and aged (24-month-old) wild-type and Gper−/−mice.
  • Fig. S3. Effect of Gper deletion on LV hypertrophy and fibrosis in adult mice.
  • Fig. S4. Determination of GPER protein in cultured VSMCs isolated from wild-type and Gper−/− mice.
  • Fig. S5. Ang II–induced ⋅O2 ‾ generation in VSMCs isolated from wild-type and Gper−/− mice.
  • Fig. S6. Effect of G36, a small-molecule GRB, on ⋅O2 ‾ generation in a cell-free system.
  • Fig. S7. Endothelium-independent, NO-mediated vasodilation in wild-type and Gper−/− mice with Ang II–induced hypertension.
  • Table S1. Echocardiographic measurements and hemodynamic parameters in aged (24-month-old) wild-type and Gper−/− mice.

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Citation: M. R. Meyer, N. C. Fredette, C. Daniel, G. Sharma, K. Amann, J. B. Arterburn, M. Barton, E. R. Prossnitz, Obligatory role for GPER in cardiovascular aging and disease. Sci. Signal. 9, ra105 (2016).

© 2016 American Association for the Advancement of Science