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TRPA1 and TRPV1 contribute to propofol-mediated antagonism of U46619-induced constriction in murine coronary arteries - Fig 3

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posted on 2017-06-23, 17:49 authored by Pritam Sinharoy, Ian N. Bratz, Sayantani Sinha, Loral E. Showalter, Spencer R. Andrei, Derek S. Damron

A and B: Representative immunoblot images depicting the expression of TRPA1 and TRPV1 in TRPA1- TRPV1 co-transfected F-11 cells (F-11 V1/A1), MCAECs and non-transfected F-11 cells (F-11 NT). Alpha Tubulin was used as loading control. C: Fluorescent activated cell-sorting (FACS) analysis of MCAECs exposed to isotype control sera (grey traces), specific-TRPA1 antisera (black traces) or specific-TRPV1 antisera (black traces). D: FACS analysis of MCAECs co-stained with both TRPA1 and TRPV1 antisera depicting % of cell population co-expressing TRPA1 and TRPV1. Cells co-stained with rabbit and mouse isotype control antisera were used as a negative control. E: Immunocytochemical localization of TRPA1 and TRPV1 in MCAECs. Green represents TRPA1 localization, red represents TRPV1 localization and yellow represents (merged) the co-localization of TRPA1 and TRPV1 (top row). There was no immunoreactivity for TRPA1 or TRPV1 in aortic endothelial cells obtained from TRPAV-/- mice and CD- 31 staining with and without DAPI was used as an endothelial cell marker (middle row). MCAECs stained with DAPI (blue), Alexa Fluor 488 or Alexa Fluor 647 only were used as negative controls (bottom row). n = 5 different cell lysates or plates of cells.

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