Journal: Biochemical pharmacology

Article Title: A53T α-synuclein mutation increases susceptibility to postoperative delayed neurocognitive recovery via hippocampal Ang-(1-7)/MasR axis.

doi: 10.1016/j.bcp.2024.116261

Figure Lengend Snippet: Fig. 8. Activation of the Ang-(1–7)/MasR axes by AVE 0991 alleviated microglial activation and mitochondrial-dependent apoptosis in the hippocampus of the A53T mice after surgery trauma. (A) Fluorescent staining of Iba-1, a marker of microglia, and its relative density are displayed. Scale bars = 50 μm (n = 3). (B, C) Graphs representing the mRNA expression levels of M1 and M2 microglial biomarkers. (D) Western blot images showing the effects of AVE 0991 treatment on Bcl-2, Bax, Cyto-C, Fl-Cas3, and Cl-Cas3 protein expression (n = 4). Data are expressed as the mean ± SEM (one-way ANOVA). *P < 0.05, ** P < 0.01, ***P < 0.001, control (Con) vs. surgery (Sur); #P < 0.05, ## P < 0.01 ### P < 0.001, surgery (Sur) vs. surgery plus AVE 0991 (Sur + AVE).

Article Snippet: Primary antibodies against MasR, methylated protein phosphatase-2A (Me-PP2A), β-actin (sc-390453, sc-81603, and sc-47778; Santa Cruz Biotechnology), occludin, claudin 5 (33–1500 and 35–2500; Invitrogen), B-cell lymphoma 2 (Bcl-2), clathrin, phosphorylated α-syn (p-α-syn) (ab32124, ab21679, and ab51253; Abcam), Bcl-2like protein 4 (Bax), cytochrome c (Cyto-C) (50599–2-Ig and 10993–1- AP; Proteintech), full-length caspase-3 (Fl-Cas3), cleaved caspase-3 (ClCas3), protein phosphatase-2A C subunit (PP2A-C), caveolin-1 (Cav-1) (9662, 9661, 2038, and 3267; Cell Signaling Technology), sodium dependent lysophosphatidylcholine transporter (Mfsd2a), and ZO-1 (PA5-21049 and 61–7300; Invitrogen).

Techniques: Activation Assay, Staining, Marker, Expressing, Western Blot, Control

Journal: Molecular medicine reports

Article Title: Dental pulp stem cell‑derived extracellular vesicles loaded with hydrogels promote osteogenesis in rats with alveolar bone defects.

doi: 10.3892/mmr.2024.13393

Figure Lengend Snippet: Figure 2. DPSC‑EVs promoted EMT in HERS cells. (A) HERS cells were cultured and identified by detection of their markers (CK14 and vimentin) via immunofluorescence staining. (B) HERS cells were co‑cultured with DPSC‑EVs, and the uptake of DPSC‑EVs was monitored via confocal microscopy. (C) HERS cells were co‑cultured with different concentrations of DPSC‑EVs, and the optimal concentration of DPSC‑EVs was determined by performing a CCK‑8 assay. (D) The expression of EMT‑related proteins (E‑cadherin, vimentin and collagen I) in co‑cultured HERS cells was detected by Western blotting. (E) The expression of CK‑14 in co‑cultured HERS cells was assessed by immunofluorescence staining. (F) The expression of E‑cadherin in co‑cultured HERS cells was assessed by immunofluorescence staining. (G) The expression of Vimentin in co‑cultured HERS cells was assessed by immunofluorescence staining. The data from three independent experiments are presented as the mean ± SD. **P<0.01. EMT, epithelial‑mesenchymal transition; DPSC, dental pulp stem cell; EV, extracellular vesicle; HERS, Hertwig's epithelial root sheath.

Article Snippet: The sections were pre‐blocked with 5% bovine serum albumin (MilliporeSigma; cat. no. a7030‐5G) in PBS at 37 ̊C for 30 min and stained with the following primary antibodies: anti‐e‐cadherin (Proteintech Group, inc.; cat. no. 20874‐1‐aP; 1:200), anti‐vimentin (novus Biologicals, ltd.; Bio‐Techne; cat. no. nB300‐223SS; 1:200) and anti‐cyto‐ keratin 14 (cK14) antibody (Proteintech Group, inc.; cat. no. 10143‐1‐AP; 1:200) overnight at 4 ̊C.

Techniques: Cell Culture, Immunofluorescence, Staining, Confocal Microscopy, Concentration Assay, CCK-8 Assay, Expressing, Western Blot