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. 2009 Apr 28;4(4):e5351. doi: 10.1371/journal.pone.0005351

Figure 6. Inhibition of aggregate formation (A–C) and amyloid oligomer formation (D–E) by overexpression of HSPB8 in HSPB5 R120G TG mice (R120G TG) at 30 weeks of age.

Figure 6

(A) Representative pictures of the immunohistochemistry are shown. The aggregates containing the mutant HSPB5 R120G protein are observed in R120G TG mice, and the overexpression of HSPB8 reduced the aggregates in samples from HSPB8 TG mice (tTA/HSPB8/HSPB5 R120G triple TG; Triple TG). (B) Typical picture of the filter assay for the detection of the aggregates. (C) Quantitative analysis of the aggregates containing mutant HSPB5 R120G protein (n = 4 mice). (D) Effect of HSPB8 overexpression on amyloid oligomer formation (green). (E) Amyloid oligomer levels were measured by fluorescence intensity. The overexpression of HSPB8 reduced the HSPB5 R120G-induced amyloid oligomer formation (Triple TG). Values shown are the -fold increase relative to NTG mice, whose value was set to 1 (n = 4 mice). To distinguish the cardiomyocytes, cardiac troponin I was stained (red)(A and D). *** p<0.001 vs. NTG mice; ### p<0.001 vs. R120G TG mice.