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. Author manuscript; available in PMC: 2022 Feb 1.
Published in final edited form as: Circ Heart Fail. 2021 Feb 1;14(2):e007279. doi: 10.1161/CIRCHEARTFAILURE.120.007279

Figure 5: Deletion of mineralocorticoid receptor in smooth muscle cells (SMC-MR-KO) reduces pressure overload-induced cardiac inflammation.

Figure 5:

Leukocytes were quantified from LV tissue 4 weeks after TAC by flow cytometry. (A) Total leukocytes (CD45+), (B) T cells (CD45+/CD11b−/CD3+) and (C) myeloid cells (CD45+/CD3−/CD11b+) were compared between Shams, MR-intact TAC or SMC-MR-KO TAC mice. Results of quantitative RT-PCR for inflammatory gene expression in the LV: (D) monocyte chemoattractant protein-1 (MCP-1), (E) regulated on activation, normal T cell expressed and secreted (RANTES), (F) interleukin 1 beta (IL1-B), (G) interleukin 6 (IL-6), and (H) tumor necrosis factor alpha (TNFα). Results of quantitative RT-PCR for adhesion molecules (I) intercellular adhesion molecule 1 (ICAM1), (J) vascular cell adhesion protein 1 (VCAM1), and (K) endothelial-leukocyte adhesion molecule (E-selectin). A-C: Sham n=9: (MR-intact Sham n=5, SMC-MR-KO Sham n=4), MR-intact TAC n=8, SMC-MR-KO TAC n=6. D-K: MR-intact Sham n=3, MR-intact TAC n=6, SMC-MR-KO Sham n=3, SMC-MR-KO TAC n=6. A-C: One-way ANOVA with Tukey post-hoc test. D-K: Two-way ANOVA with Tukey post-hoc test.