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. 2023 Sep 28;80(10):308. doi: 10.1007/s00018-023-04961-y

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© The Author(s), under exclusive licence to Springer Nature Switzerland AG 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.

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Fig. 6 — PPARγ mediates myofibroblasts lipogenic pathway promoted by omentin-1. (a) The mRNA level of PPARγ in the reversible fibrotic lung tissue of mice detected by qPCR (n = 3). (b–d) Immunohistochemistry staining of PPARγ in the reversible and non-reversible fibrotic lung tissue of mice, scale bar = 50 μm (n = 3). (e) The correlation between PPARγ and omentin-1 mRNA levels in the reversible fibrosis model. (f) The mRNA level of PPARγ in fibroblasts detected by qPCR (n = 6). (g) Schematic for fibroblasts activated by stiff matrix transfected with specific plasmid or siRNA and treated with omentin-1. (h) The mRNA level of PPARγ in negative control (vector) or YAP plasmid transfected fibroblasts detected by qPCR (n = 4). (i) Western blot showing the inhibition or induction of PPARγ phosphorylation in response to YAP overexpression or knockdown treatment with/without omentin-1, GAPDH was used as the loading control (n = 3). (J) Schematic for fibroblasts activated by stiff matrix and treated with GW9662 (a selective PPARγ inhibitor) and omentin-1 (k) Immunofluorescent staining of α-SMA and PLIN2 in fibroblasts following omentin-1 and GW9662 treatment, scale bar = 25 μm (n = 3). (l, m) The mRNA level of Col 1, FN, α-SMA and PLIN2 in fibroblasts following omentin-1 and PPARγ inhibitor (GW9662) treatment detected by qPCR (n = 3)