agonist rosiglitazone  (MedChemExpress)

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: Journal of Inflammation Research

Article Title: Overexpression of Plakophilin2 Mitigates Capillary Leak Syndrome in Severe Acute Pancreatitis by Activating the p38/MAPK Signaling Pathway

doi: 10.2147/JIR.S459449

Figure Lengend Snippet: Rosiglitazone upregulates PKP2 and affects endothelial cell leakage. ( A ) Western blot analysis revealed that rosiglitazone markedly increased the expression levels of PKP2, p-p38/p38, and claudin1 proteins in HUVECs stimulated with LPS (data represent the results of three independent experiments). ( B ) Rosiglitazone significantly enhanced the mRNA expression of AQP3 and occludin in HUVECs stimulated with LPS (data represent the results of three independent experiments). ( C ) Following LPS stimulation, rosiglitazone significantly increased the protein expression of β-catenin and claudin1 in HUVECs with PKP2 knockdown (representative of three independent experiments). ( D ) Following LPS stimulation, the degree of porosity of the cytoskeleton in HUVECs with PKP2 knockdown was significantly improved by rosiglitazone (data represent the results of three independent experiments). ( E ) Rosiglitazone significantly decreased the permeability of HUVECs stimulated with LPS (data represent the results of three independent experiments). ( F ) Rosiglitazone significantly reduced the permeability of HUVECs with PKP2 knockdown upon LPS stimulation (data represent the results of three independent experiments). Rosiglitazone: agonist of PPARγ. *p < 0.05, **p < 0.01, ***p < 0.001, ****p <0.0001.

Article Snippet: 24 hours after transfection of PKP2 plasmid, HUVECs were treated with PPARγ agonist Rosiglitazone (10uM, HY-17386, MCE) and PPARγ antagonist GW9662 (10uM, HY-16578, MCE) 2 hours prior.

Techniques: Western Blot, Expressing, Knockdown, Permeability

Journal: Journal of Inflammation Research

Article Title: Overexpression of Plakophilin2 Mitigates Capillary Leak Syndrome in Severe Acute Pancreatitis by Activating the p38/MAPK Signaling Pathway

doi: 10.2147/JIR.S459449

Figure Lengend Snippet: Targeting PKP2 using GW9662 leads to the downregulation of the P38/MAPK signaling pathway. ( A ) Western blot analysis revealed that GW9662 markedly reduced the production of the PKP2 protein in HUVECs stimulated with LPS (data represent the results of three independent experiments). ( B ) GW9662 significantly reduced the mRNA expression of connexin43 and AQP3 in HUVECs overexpressing PKP2 upon LPS stimulation (data represent the results of three independent experiments). ( C ) In the presence of LPS, GW9662 substantially reduced the protein levels of ZO-1, p-p38/p38, and claudin1 in HUVECs overexpressing PKP2 and simultaneously enhanced cell permeability (data represent the results of three independent experiments). ( D ) After LPS stimulation, GW9662 induced cytoskeletal disruption in HUVECs overexpressing PKP2 (data represent the results of three independent experiments). ( E ) GW9662 increased the permeability of HUVECs overexpressing PKP2 upon LPS stimulation (data represent the results of three independent experiments). ( F ) GW9662 decreased the immunofluorescence intensity of claudin1 in HUVECs overexpressing PKP2 following LPS stimulation (data represent the results of three independent experiments). GW9662: antagonist of PPARγ. *p < 0.05, **p < 0.01, ***p < 0.001, ****p <0.0001.

Article Snippet: 24 hours after transfection of PKP2 plasmid, HUVECs were treated with PPARγ agonist Rosiglitazone (10uM, HY-17386, MCE) and PPARγ antagonist GW9662 (10uM, HY-16578, MCE) 2 hours prior.

Techniques: Western Blot, Expressing, Permeability, Disruption, Immunofluorescence