Figure 1: TLR2 activation induces mitochondrial mutations in RASFC in vitro. | Scientific Reports

Figure 1: TLR2 activation induces mitochondrial mutations in RASFC in vitro.

From: Resolution of TLR2-induced inflammation through manipulation of metabolic pathways in Rheumatoid Arthritis

Figure 1

(a) Bar graphs representing increased mtDNA mutation frequency in RA ex vivo explants (n = 7) and RASFC (n = 6) in response to Pam3CSK4 (1 μg/ml) stimulation for 24 hrs. (b) Representative transmission microscopy images of RASFC mitochondria under basal or Pam3CSK4 (1 μg/ml) stimulated conditions. Regular shaped mitochondria are seen in resting cells, in contrast to larger more dense (red arrows) mitochondria and a higher frequency of elongated mitochondria (blue arrow). Scale bar represents 500 nm. (c) Bar graph demonstrating 17 genes dysregulated in response to 24 hr incubation with Pam3CSK4 (1 μg/mL) as assessed by RT2 PCR Profiler Microarray (n = 3). Dashed line represents no change (1). Data is expressed as up- or down-regulation compared to basal control. Data is normalised to housekeepers: β-Actin, B2M, GAPDH, HPRT1 and RPLP0. (d) (i) Representative scatter plots demonstrating Annexin-V/7-AAD double staining in RASFC in response to Pam3CSK4 (1 μg/ml) stimulation for 24 hrs and (ii) representative bar graphs showing percentage of live, early apoptotic and late apoptotic cells under basal control or Pam3CSK4 stimulated conditions (n = 3). Non-parametric data was analysed using Wilcoxin Signed Rank test and parametric data was analysed using paired t-test and is represented as Mean ± SEM, *p < 0.05, **p < 0.01 significantly different to control.

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