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. Author manuscript; available in PMC: 2021 Aug 1.
Published in final edited form as: Diabetologia. 2020 May 18;63(8):1564–1575. doi: 10.1007/s00125-020-05168-7

Fig. 5.

Fig. 5

A subset of pericytes in AktTg islets differentiates into myofibroblasts. (a, b) Representative confocal images of an NG2-tdTomato wild-type islet (WT, a) and NG2-tdTomato-AktTg islet (AktTg, b) showing tdTomato-labelled pericytes and periostin immunostaining (green). Cell nuclei are shown in blue. (a′ and b′) Higher magnification images of regions within dashed boxes. In wild-type islets, periostin is present in the interface between endocrine/exocrine tissue but not expressed by pericytes, while tdTomato-labelled pericytes in AktTg islets express periostin.

(c, d) Representative confocal images of regions in islets from NG2-tdTomato-AktTg mice showing tdTomato-labelled pericytes and collagen type I (green, c) and fibronectin immunostaining (green, d). Cell nuclei are shown in blue. tdTomato-labelled pericytes synthesising collagen I and fibronectin can be seen, as well as accumulation of these ECM proteins in their extracellular space. (e) Quantification of the fraction of tdTomato-positive cells that express the pericytic markers NG2, PDGFRβ and αSMA, ECM proteins fibronectin and collagen type I, and (myo)fibroblast markers vimentin and periostin in wild-type (white) and NG2-tdTomato-AktTg mice (grey). *p<0.05 (unpaired t test; n=3 confocal planes/islet, 5 islets/mouse, 2 mice/genotype). Scale bars, 20 μm (a, b) and 10 μm (c, d).