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Fig. 1 | Molecular Medicine

Fig. 1

From: Hypertension Exacerbates Coronary Artery Disease in Transgenic Hyperlipidemic Dahl Salt-sensitive Hypertensive Rats

Fig. 1

Composite of two end-stage Tg53 proximal coronary (≈200 micron) lesion phenotypes. (A) Low magnification Masson trichrome-stained section reveals an occlusive, thrombosed lesion (1) and an occlusive complication-prone non-thrombosed lesion (2) in the right ventricle (RV). Boxed lesion 1 (B–D) and lesion 2 (E–H) are further analyzed in adjacent serial sections; RA, right atrium; bar = 200 microns. (B) High magnification of occlusive plaque 1 reveals endothelialized thrombus and few smooth muscle cells in the lesion-side media, in contrast to abundant smooth muscle cells in the non-lesion-side media. (C) PTAH stained fibrin in thrombosed plaque. (D) MMP3 immunostaining at the base () of thrombosed plaque. (E) High-magnification of lesion 2 shows few smooth muscle cells in the plaque and lesion-side media, acellular plaque core with large extracellular lipid deposits; significant amount of collagen (dark blue) in the lesion-side media; minimal collagen in plaque core (pale blue) and in non-lesion side media. (F) No PTAH-stained fibrin in plaque 2. (G) Marked MMP3 immunostaining in plaque 2 core (); few stained cells in media. (H) Negative TIMP3 immunostaining in plaque 2 corroborates specificity of MMP3 immunostaining (D, G). (I) Occlusive distal coronary (≈160 microns) lesion with minimal MMP3 immunostaining (identical to (D, G)) restricted to macrophage-foam cells () in the lesion and media; *, non-specific staining of red blood cells; bar = 20 microns. Note: (↔), residual lumen; , plaque; (m), media; (thr) thrombosed plaque.

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