Journal: The veterinary quarterly

Article Title: Multiple roles of LncRNA-BMNCR on cell proliferation and apoptosis by targeting miR-145/CBFB axis in BMECs.

doi: 10.1080/01652176.2023.2262525

Figure Lengend Snippet: Figure 2. BMNCR Facilitated proliferation and attenuated apoptosis in BMECs. (A) qRT-PCR detected the expression efficiency of BMNCR after transfected three BMNCR siRNAs, respectively. (B) The expression levels of inflammation-related cytokines were validated by RT‐qPCR after treated siBMNCR for 48 h. (C) CCK8 assay exploring the function of BMNCR on the viability of BMECs. (D) EdU assay detected the number of BMECs treated with siBMNCR. (E) The proportion of EdU positive cells was counted by ImageJ. (F) Cell apoptosis was determined by flow cytometry after transfected with siBMNCR. (G) Distribution map of BMECs apoptosis. (H) Cell apoptosis index was counted by the sum of early and late apoptosis. Data are means ± SE of n = 3 independent experiments, each performed in triplicate, and normalized to GAPDH. *, p < .05 and **, p < .01.

Article Snippet: Finally, cells were stained using the Cell Proliferation Assay Kit (C0075S, Beyotime, Shanghai, China), and images were collected on the Inverted Fluorescence Microscope (DMi8, Leica, Germany).

Techniques: Quantitative RT-PCR, Expressing, Transfection, CCK-8 Assay, EdU Assay, Flow Cytometry

Journal: The veterinary quarterly

Article Title: Multiple roles of LncRNA-BMNCR on cell proliferation and apoptosis by targeting miR-145/CBFB axis in BMECs.

doi: 10.1080/01652176.2023.2262525

Figure Lengend Snippet: Figure 4. Functional roles of miR-145 on proliferation and apoptosis of BMECs. (A) qRT-PCR detected the overexpression (mimic) or Interference (inhibitor) efficiency of miR-145. The expression levels of inflammation-related cytokines were validated by RT‐qPCR after treated miR-145 mimic (B) or miR-145 inhibitor (C). (D) EdU assay detected the number of BMECs after treated with miR-145 mimic or inhibitor. (E) The proportion of EdU positive cells was counted by ImageJ. (F) Cell apoptosis was determined by flow cytometry after transfected with miR-145 mimic or inhibitor. (G) Distribution map of BMECs apoptosis. (H) Cell apoptosis index was counted by the sum of early and late apoptosis. Data are means ± SE of n = 3 independent exper iments, each performed in triplicate, and normalized to GAPDH. *, p < .05 and **, p < .01.

Article Snippet: Finally, cells were stained using the Cell Proliferation Assay Kit (C0075S, Beyotime, Shanghai, China), and images were collected on the Inverted Fluorescence Microscope (DMi8, Leica, Germany).

Techniques: Functional Assay, Quantitative RT-PCR, Over Expression, Expressing, EdU Assay, Flow Cytometry, Transfection

Journal: The veterinary quarterly

Article Title: Multiple roles of LncRNA-BMNCR on cell proliferation and apoptosis by targeting miR-145/CBFB axis in BMECs.

doi: 10.1080/01652176.2023.2262525

Figure Lengend Snippet: Figure 7. CBFB could modulate proliferation and apoptosis in BMECs. (A) qRT-PCR detected the expression efficiency of CBFB after transfected three siRNAs of CBFB, respectively. After transfected siCBFB into BMECs for 48 h, (B) mRNA level of CBFB was explored by qRT-PCR. (C) The protein level of CBFB was explored by Western blot. (D) The relative protein level of CBFB was calculated by ImageJ. (E) The expression levels of inflammation-related cytokines were validated by RT‐qPCR after treated siCBFB into BMECs for 48h. (F) EdU assay detected the number of BMECs treated with siCBFB. (G) The proportion of EdU positive cells was counted by ImageJ. (H) Cell apoptosis was determined by flow cytometry after transfected with siCBFB. (I) Distribution map of BMECs apoptosis. (J) Cell apoptosis index was counted by the sum of early and late apoptosis. Data are means ± SE of n = 3 independent experiments, each performed in triplicate, and normalized to GAPDH. *, p < .05 and **, p < .01.

Article Snippet: Finally, cells were stained using the Cell Proliferation Assay Kit (C0075S, Beyotime, Shanghai, China), and images were collected on the Inverted Fluorescence Microscope (DMi8, Leica, Germany).

Techniques: Quantitative RT-PCR, Expressing, Transfection, Western Blot, EdU Assay, Flow Cytometry

Journal: Molecular carcinogenesis

Article Title: IL-33 Promotes Growth and Liver Metastasis of Colorectal Cancer in Mice by Remodeling the Tumor Microenvironment and Inducing Angiogenesis

doi: 10.1002/mc.22491

Figure Lengend Snippet: IL-33 enhanced tumor growth. (A) Proliferation of MC38-Vector and MC38-IL33 cells in tissue culture. (B and C) Weights (grams) of primary tumors derived from MC38-Vector or MC38-IL33 cells 6 weeks after cecal implantation (B) or subcutaneous injection (C). ***P <0.001. (D) Incidence of primary tumor growth in cecum of C57Bl/6 mice implanted with MC38-Vector or MC38-IL33 cells (n =20). (E) H&E images (400×) and primary cecal tumor sections stained with anti Ki67 and cleaved caspase-3 antibodies. (F) Immunoblot analysis of total protein extracts from MC38-Vector and MC38-IL33 clones with antibodies against PCNA and cleaved caspase-3. (G) Serum levels of IL-33 in mice bearing MC38-Vector or MC38-IL33 tumors analyzed by ELISA.

Article Snippet: Endogenous peroxidases were blocked with 3% H 2 O 2 for 15 min. Nonspecific epitopes were blocked with normal horse serum (Jackson ImmunoResearch, West Grove, PA) for 1 h. The sections were incubated overnight at 4°C with antibodies against one of the following proteins: LOX, MMP9, MMP2, LYVE1, VEGF, and S100A8 (all from Abcam, Cambridge, MA), S100A9, IL-33 (R&D Systems, Minneapolis, MN), cleaved Caspase-3 (Cell Signaling Technology, Danvers, MA), Ki67 (OriGene Technologies, Rockville, MD).

Techniques: Plasmid Preparation, Derivative Assay, Injection, Staining, Western Blot, Clone Assay, Enzyme-linked Immunosorbent Assay