Calcitriol downregulates fibroblast growth factor receptor 1 through histone deacetylase activation in HL-1 atrial myocytes

Figures

• 

  Fig. 1. Fibroblast growth factor (FGF) receptor (FGFR) protein and mRNA expressions in control and calcitriol-treated HL-1 cells. (a) Representative immunoblots and average data (n = 6) of FGFR1, FGFR2, FGFR3, and FGFR4 from control and calcitriol (1 and 10 nM)-treated HL-1 cells, and (b) FGFR1 mRNA from control and calcitriol (10 nM)-treated HL-1 cells (n = 6). *** p < 0.005

• 

  Fig. 2. Phosphorylated extracellular signal-regulated kinase (p-ERK) protein and β-myosin heavy chain (β-MHC) mRNA expressions in control and calcitriol-treated HL-1 cells without and with fibroblast growth factor (FGF)-2 incubation. (a) FGF-2 (25 ng/mL) was administered for 30 min to study ERK phosphorylation (n = 6), or (b) for 48 h to evaluate β-MHC mRNA from control and calcitriol (10 nM)-treated HL-1 cells (n = 6). * p < 0.05, ** p < 0.01, *** p < 0.005

• 

  Fig. 3. Phosphorylated phospholipase Cγ (p-PLCγ) and nuclear factor of activated T cells (NFAT) protein expressions in control and fibroblast growth factor (FGF)-2-treated HL-1 cells. (a) Representative immunoblots and average data (n = 6) of p-PLCγ in total cell lysates, and (b) NFAT in nuclear and cytoplasmic extracts from HL-1 cells without and with FGF-2 (25 ng/mL) treatment for 30 min

• 

  Fig. 4. Effects of fibroblast growth factor (FGF) receptor 1 (FGFR1) knockdown on phosphorylated extracellular signal-regulated kinase (p-ERK) protein, and β-myosin heavy chain (β-MHC) mRNA expressions in HL-1 cells. (a) Representative immunoblots and average data (n = 6) of FGFR1 from control and FGFR1-knockdown cells (left panel). FGF-2 (25 ng/mL for 30 min) did not increase ERK phosphorylation in FGFR1-knockdown cells without and with calcitriol (10 nM) treatment (right panel). (b) FGF-2 (25 ng/mL for 48 h) did not increase β-MHC mRNA expression in FGFR1-knockdown cells (n = 6). * p < 0.05

• 

  Fig. 5. Nuclear and cytoplasmic histone deacetylase (HDAC) activities in control and calcitriol-treated HL-1 cells. Representative average data (n = 7) of HDAC activities in (a) nuclear and (b) cytoplasmic extracts from HL-1 cells without and with calcitriol (10 nM) treatment for 48 h. * p < 0.05

• 

  Fig. 6. Chromatin immunoprecipitation (ChIP) assay of acetyl-histone H4 (Ac-H4) and histone deacetylase (HDAC) in the fibroblast growth factor receptor 1 (FGFR1) promoter in control and calcitriol-treated HL-1 cells. Representative image and average data (n = 6) of (a) histone H4 acetylation, and (b) HDAC1, HDAC2, and HDAC3 binding to the FGFR1 promoter from control and calcitriol (10 nM)-treated HL-1 cells. * p < 0.05, *** p < 0.005

• 

  Fig. 7. Fibroblast growth factor receptor 1 (FGFR1) protein expression in control and calcitriol-treated HL-1 cells without and with suberanilohydroxamic acid (SAHA, a pan-HDAC inhibitor) treatment. Representative immunoblots and average data (n = 7) of FGFR1 from control and calcitriol (10 nM)-treated HL-1 cells without and with SAHA (1 μM) treatment. * p < 0.05, ** p < 0.01