Fig 1: Effects of rHGF gene-modified BM-MSCs on the mRNA expression of selected hepatic proteins.The quantitative data of the HNF-4α, CK18 and ALB mRNA expression in different groups are shown a. All the data are displayed as the means ± SDs. Quantitative analyses of the above markers are illustrated in b–d, with the data expressed as a ratio of β-actin expression. The mRNA expression was highest in the HGF-BM-MSC-treated group relative to the HGF, BM-MSC and control groups (all *p < 0.05, **p < 0.01)
Fig 2: Analysis of hepatic protein markers in mouse MSCs following 23 days of hepatic differentiation. Green immunofluorescence staining of ALB, AFP and CK19 in undifferentiated MSC control, 2D and 3D groups. Nuclei were stained blue with DAPI. Scale bars, 100 µm. MSCs, mesenchymal stem cells; ALB, albumin; AFP, α-fetoprotein; CK19, cytokeratin-19.
Fig 3: Validation of microarray data with RT-qPCR. Microarray and RT-qPCR for (A) ALB, (B) IL-8, (C) CD44, (D) CCL2, (E) HGF, (F) CFTR, (G) HIST1H2BN, (H) MAPK11 and (I) NTRK2. RT-qPCR results were consistent with the microarray data, and the P-values were calculated by Student's t-test. ▲P<0.05, ▲▲P<0.01. RT-qPCR, reverse transcription-quantitative PCR; ALB, albumin; IL, interleukin; CCL2, C-C motif chemokine ligand 2; HGF, hepatocyte growth factor; CFTR, cystic fibrosis transmembrane conductance regulator; HIST1H2BN, histone cluster 1 H2B family member n; MAPK11, mitogen-activated protein kinase 11; NTRK2, neurotrophic receptor tyrosine kinase 2.
Fig 4: Orthotopic livertumor targeting of Pt NPs in vivo.a Anatomical location (left) and MIR imaging (right) of orthotopic liver tumors in 5 nude mice; b NIR image of tumors 1–3 d after intravenous injection with 1 mg kg−1 ICG-conjugated Pt NPs (1, 2, 3) or 1 mg kg−1 ICG-conjugated chem-Pt NPs (HSA prepared Pt NPs; 4, 5), c Three dimensional reconstruction of the NIR images of the orthotopic liver tumor models treated with 1 mg kg−1 ICG-conjugated Pt NPs (1, 2, 3); d Anatomical location (left) and MIR imaging (right) of the orthotopic liver tumors; e NIR image of a tumor 1–2d after intravenous injection with 1 mg kg−1 ICG-conjugated Pt NPs (1) or 1 mg kg−1 albumin bound Paclitaxol (Abraxane)-ICG (2) treatment. f Three dimensional reconstruction of the NIR image of the tumor after treatment with 1 mg kg−1 ICG-conjugated Pt NPs (1). All red circles indicate the tumor location.
Fig 5: Hepatocyte-specific inhibition of IL11 cis-signaling protects mice against HFMCD diet-induced NASH.a Schematic of HFMCD feeding regimen for AAV8-Alb-Cre injected Il11ra1loxP/loxP (conditional knockout; CKO) mice for experiments shown in (b–k). Il11ra1loxP/loxP mice were intravenously injected with either AAV8-Alb-Null or AAV8-Alb-Cre to delete Il11ra1 specifically in hepatocytes 3 weeks prior to the start of HFMCD diet. b Western blots of hepatic IL11RA and GAPDH (n = 3 mice/group). c Body weight (shown as a percentage (%) of initial body weight). d Representative gross anatomy, H&E-stained (scale bars, 50 µm), and Masson’s Trichrome (scale bars, 100 µm) images of livers. Representative dataset from n = 5 mice/group is shown for gross anatomy; representative dataset from n = 4 mice/group is shown for H&E-stained and Masson’s Trichrome images. e Hepatic triglycerides content. f Serum ALT levels. g Serum AST levels. h Hepatic GSH content. i Hepatic collagen levels. j Heatmap showing hepatic mRNA expression of pro-inflammatory markers (Tnfa, Ccl2, Ccl5) and fibrotic markers (Col1a1, Col1a2, Col3a1, Acta2). Values are shown in Supplementary Fig. 8c and d. k Western blots showing hepatic ERK and JNK activation status (n = 3 mice/group). c, e–j NCD (n = 5 mice/group), HFMCD (n = 6 mice/group). c Data are shown as mean ± SD, two-way ANOVA with Tukey’s correction, statistical significance (P values) are shown for comparison between WT HFMCD and CKO HFMCD; e–i data are shown as box-and-whisker with median (middle line), 25th–75th percentiles (box), and min–max values (whiskers); two-way ANOVA with Tukey’s correction. Source data are provided as a Source data file.
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