pparγ agonist rosiglitazone rosi  (Cayman Chemical)

Journal: bioRxiv

Article Title: Diet-induced hyperplastic expansion in subcutaneous adipose tissue and protection against adipose progenitor exhaustion in female mice are lost with ovariectomy

doi: 10.1101/2024.09.05.611480

Figure Lengend Snippet: A) Male and female mice were treated with rosiglitazone or vehicle for 8 weeks; ovx and sham mice were treated with rosi for 8 weeks. Body composition was measured weekly using TD-NMR. B) Mechanism of rosiglitazone action on APCs. Whole- body fat accumulation over 8 weeks vehicle or rosi treatment in C) female, D) male, and E) ovariectomized and sham operated mice, measured via TD-NMR. F) sWAT and G) vWAT weight relative to body weight in male and female vehicle or rosi treated mice. H) sWAT to vWAT ratio in male and female vehicle or rosi treated mice. J) sWAT and K) vWAT weight relative to body weight in rosi treated ovx and sham mice. L) sWAT to vWAT ratio for rosi treated ovx and sham mice (n=5-6). *p<0.05, **p<0.01, ****p<0.0001.

Article Snippet: In a subset of mice, adipogenesis was stimulated pharmacologically by oral administration of the PPARγ agonist, rosiglitazone (15mg/kg/day) (Rosi; TCI Chemicals, R0106) or a vehicle control consisting of 1% methylcellulose (Veh; Sigma Aldrich, M0512) in 50% sweetened condensed milk, for 8 weeks.

Techniques:

Journal: Hepatology Communications

Article Title: PNPLA3 I148M Variant Impairs Liver X Receptor Signaling and Cholesterol Homeostasis in Human Hepatic Stellate Cells

doi: 10.1002/hep4.1395

Figure Lengend Snippet: LXR transcriptional activity is lower due to impaired PPARγ1 functionality in HSCs carrying PNPLA3 I148M. LX‐2 cells stably overexpressing WT or I148M PNPLA3 transiently transfected with either LXRE, AP‐1, or PPRE plasmids to measure LXR, AP‐1, or PPARγ transcriptional activity, respectively. After 48 hours, luciferase activity (expressed as percentage) was measured using a luminometer and normalized to total protein content, as described in Materials and Methods. All bar graphs show mean values ± SD. (A) LXRE‐luciferase activity was measured either in untreated HSCs or in the presence of nuclear receptor LXR (LXRE+LXR) for 24 hours. (B) AP‐1‐luciferase activity was measured either in untreated HSCs or in the presence of the synthetic LXR agonist T09 for 24 hours. (C) PPARγ‐luciferase activity was measured in untreated (PPRE) or previously treated HSCs with either T09 (PPRE+T09) or rosiglitazone (PPRE+ROSI) for 24 hours. (D) LXRE‐luciferase activity was measured in untreated (LXRE) or in pretreated HSCs with either 10 nM of T09 (LXRE+T09) or rosiglitazone (LXRE+ROSI) for 24 hours. All bar graphs are representative of four independent transfections performed in triplicates. * P < 0.05, ** P < 0.01, and *** P < 0.001, as indicated in the bar graphs. Open bars refer to PNPLA3 WT HSCs and closed bars to I148M HSCs (n = 3 for each genotype).

Article Snippet: For cell culture treatments, cells deprived of FBS for 24 hours were stimulated with 10 μM of specific LXR agonist (T0901317 [T09]; Sigma‐Aldrich), inverse agonist (SR9238; Tocris), antagonist (GSK2033; Tocris), and PPARγ agonist (rosiglitazone [ROSI]; Sigma‐Aldrich) for an additional 24 hours.

Techniques: Activity Assay, Stable Transfection, Transfection, Luciferase

Journal: Hepatology Communications

Article Title: PNPLA3 I148M Variant Impairs Liver X Receptor Signaling and Cholesterol Homeostasis in Human Hepatic Stellate Cells

doi: 10.1002/hep4.1395

Figure Lengend Snippet: LXR agonist T09 alone restores ABCA1 and attenuates inflammatory and fibrogenic markers independently from PPARγ in HSCs with the PNPLA3 I148M variant. LX‐2 stable overexpressing WT or I148M PNPLA3 untreated or treated for 24 hours with either T09 (+T09) or the combination T09 and ROSI (+T09+Rosi). mRNA expression of (A) ABCA1, (B) collagen1α1, (C) PPARγ1 and (D) CCL5 and analyzed by RT‐PCR and normalized to 18s. White bars show untreated HSCs, gray bars show HSCs treated with T09, and black bars show HSCs treated with T09 or the combination (+T09+Rosi). All bar graphs show mean values ± SD. * P < 0.05, ** P < 0.01, and *** P < 0.001 versus untreated WT or I148M HSCs (n = 3 for each genotype).

Article Snippet: For cell culture treatments, cells deprived of FBS for 24 hours were stimulated with 10 μM of specific LXR agonist (T0901317 [T09]; Sigma‐Aldrich), inverse agonist (SR9238; Tocris), antagonist (GSK2033; Tocris), and PPARγ agonist (rosiglitazone [ROSI]; Sigma‐Aldrich) for an additional 24 hours.

Techniques: Variant Assay, Expressing, Reverse Transcription Polymerase Chain Reaction

Journal: The Journal of Neuroscience

Article Title: Activation of PPARγ Ameliorates Spatial Cognitive Deficits through Restoring Expression of AMPA Receptors in Seipin Knock-Out Mice

doi: 10.1523/JNEUROSCI.3280-15.2016

Figure Lengend Snippet: Neuronal seipin deficiency reduces hippocampal PPARγ level. A, Representative images of seipin immunostaining in hippocampal CA1 region of control mice and seipin-nKO mice. str-R, Stratum radiatum; str-P, stratum pyramidale; str-O, stratum oriens. Arrows indicate seipin-immunopositive cells. Scale bars, 50 μm. B, Bars show the levels of hippocampal PPARγ in seipin-sKO mice and WT mice, seipin-nKO mice and control mice, or seipin-aKO mice and a-control mice treated with vehicle or rosi for 3 d. The densitometric values for Western blots of protein are normalized to the amounts of GAPDH and normalized again by control values. **p < 0.01 versus WT mice or control mice (two-way ANOVA).

Article Snippet: Drug administration The PPARγ agonist rosiglitazone (rosi; Enzo) was dissolved in dimethyl sulfoxide (DMSO) and then diluted in 0.9% saline to a final concentration of 0.5% DMSO.

Techniques: Immunostaining, Control, Western Blot