Research Article

Antiangiogenic VEGF Isoform in Inflammatory Myopathies

Figure 4

Representative images of immunohistological distribution of VEGF-A, , and TGF-β in inflammatory myopathies. Consecutive sections, IBM. Regenerating fibres (asterisk), basophilic (1a) and reactive for foetal myosin heavy chain (1d), show VEGF-A (1b) upregulation, against basal expression of adjacent fibres. These fibres are strongly reactive (1c), in contrast with low or null reactivity of adjacent fibres, and show highly reactive foci. Small endomysial vessels are diffusely VEGF-A and reactive. A mild upregulation (1c: arrow) is observed in nonregenerating fibres displaying sarcolemmal and cytoplasmic HLA-ABC neoexpression (1e: arrow). Negative control slide. Consecutive sections, PM. Necrotic fibres, identified by deposits of the terminal complex of complement, or membranolytic attack complex (MAC) (2a: arrow), do not express neither VEGF-A (2b: arrow) nor (2c: arrow), appearing as unreactive pale elements. Mononuclear cells surrounding and partially invading the necrotic fibre (2c: asterisk) are strongly reactive for . Consecutive sections, IBM. Fibres with rimmed vacuoles (3a, arrows) show VEGF-A upregulation (3b, arrows), with occasional highly reactive foci, and upregulation with multiple spots of intense reactivity (3c, arrows). Mononuclear infiltrates show a scarce reactivity for VEGF-A (3b), whereas they strongly express . IBM. TGF-β (3d) is expressed on a large endomysial vessel (arrow) and inflammatory cells. Muscle fibres of smaller diameter show higher reactivity. On nonadjacent serial sections, localization of both VEGF isoforms is observed ((3e)-(3f)) in the vessel. The asterisk identifies a fibre surrounded by inflammatory cells. Consecutive sections, DM. Perifascicular atrophic fibres (arrows) show increased reactivity for angiogenic (3a) and antiangiogenic (3b) VEGF isoforms. Mononuclear cells also react for both isoforms.
219313.fig.004a
219313.fig.004b