PPAR alpha Antibody - #AF5301

Fig. 9 The nuclear transcription factor PPARα mediates T2D-induced specific reduction in the expression of osteocytic SERCA2 pump. a RNA-seq-based KEGG pathway analysis showing the top 10 enriched KEGG pathways. b, c GSEA analysis showing a significant enrichment of signaling events associated with PPARα and PPARDR1_Q2. d The PPARα and p-PPARα protein expression in osteocytes. e Immunohistochemical staining of osteocytic PPARα in diabetic and non-diabetic tibiae. f The SERCA2 expression in osteocytes treated with antagonists of PPARα (MK886 and GW6471), PPARβ/δ (GSK0660 and GSK3787), and PPARγ (T0070907 and GW9662). g The SERCA2 expression in HGHF-exposed osteocytes treated with agonists of PPARα (Fenofibrate and GW7647), PPARβ/δ (GW0742 and GW501516), and PPARγ (rosiglitazone and pioglitazone). h A schematic representation and the relative luciferase activities of three ATP2A2 promotor regions. i The relative luciferase activity assays of Seg#1, Seg#2 and Seg#3. j The relative luciferase activity in HGHF-treated osteocytes with PPARα silencing. k ChIP assays showing the PPARα enrichment on ATP2A2 promotor in normal and HGHF-treated osteocytes. l EMSA assays confirming the binding of PPARα to the ATP2A2 promoter region (−620 to −608 bp). The nuclear extract were incubated with biotin-labeled wild-type (WT-biotin) probe, unlabeled wild-type (WT) probe, and biotin-labeled mutated (Mut-biotin) probe. Red letters indicate substituted nucleotide sequences in the mutated probes (P1: −620 to −608 bp; P2: −1283 to −1277 bp). m, n Intracellular Ca2+ signaling and protein expression of osteocyte-related cytokines in HGHF-treated osteocytes with PPARα overexpression subjected to FSS. o, p Intracellular Ca2+ signaling and the expression of osteocyte-related cytokines in MLO-Y4 cells with lentiviral silencing of PPARα subjected to FSS. Graphs represent mean ± SD (d, f, g, i–k, m, o n = 6 biologically independent replicates; e n = 8 mice per group; l n = 3 independent replicates; n, p: n = 120 cells per group). a P value was obtained by one-tailed hypergeometric test. b, c P values were obtained by one-tailed permutation test. d–h, n, p ***P 

Figure 2. SF exacerbated lipid metabolism disorders in mice. (A) KO annotation for the DEGs in testis between DM-SF vs. DM mice. (B) Effect of SF on characteristic genes indicative of lipid homeostasis and fatty acid metabolism pathway shown by GSEA analysis. (C) KEGG pathway enrichment analysis of DEGs in CSR rat (GSE141699). (D) GSEA analysis showed that CSR was negatively associated with fatty acid metabolism and fatty acid degradation. (E) KEGG pathway enrichment analysis of DEGs in timed sleep restriction mice (GSE38921). (F) A chordal graph of enriched KEGG terms showed the relationship between DEGs and KEGG pathways related to lipid metabolism. (G) TG and T-CHO content in serum and testis homogenates (n = 6). (H) SREBP1 and PPARA protein levels in the testis and densitometric quantification (n = 6). (I) Relative mRNA levels of Srebp1, Acaca, Fasn, Ppara, Acox1, Acadm, and Cpt1a in the testis (n = 6). Data shown in graphs represent the means ± SD; GAPDH was used as an internal control; ∗P < 0.05; NS, not significant.

Fig. 5. USP7 inhibition mitigated PGC1β/PPARα related cardiometabolic signaling pathway in the hearts of diabetic mice and NMCMs treated with HG+PA or H9c2 cells treated with PA. (A) Representative Western blot and quantification of PGC1β, PPARα, CD36 and CPT1 expression in the heart of a diabetic mouse treated with P5091. n = 5 in each group. *P

Fig. 5: Ythdf2 and CPT-1a function as downstream of MIAT in cardiac hypertrophy. H9c2 cells transfected with MIAT, MIAT + siYthdf2, siMIAT, siMIAT+Ythdf2 (A–E). A, B Western blot analysis and relative protein levels of ANP, BNP, β-MHC, PPARα and CPT-1a. C, D Phalloidin staining and the relative cell surface area: F-actin were stained with fluorescent phalloidin (red) and the nuclei were stained with DAPI (blue). Scale bar: 100 um. E RT-qPCR of the relative mRNA expression levels of ANP, BNP, and β-MHC, PPARα, CPT-1a, MIAT and Ythdf2. H9c2 cells transfected with Ythdf2, Ythdf2+siMIAT, siYthdf2, siYthdf2+MIAT (F–J). F, G Western blot analysis and relative protein levels of ANP, BNP, and β-MHC, PPARα and CPT-1a. H, I Phalloidin staining and the relative cell surface area: F-actin were stained with fluorescent phalloidin (red) and the nuclei were stained with DAPI (blue). Scale bar: 100 um. J RT-qPCR of the relative mRNA expression levels of ANP, BNP, β-MHC, PPARα, CPT-1a, MIAT and Ythdf2. ∗∗∗p