Results: 5

1.
Fig. 4

Fig. 4. TNFα infusion into the DG reduces neurogenesis. From: Differential roles of TNFR1 and TNFR2 signaling in adult hippocampal neurogenesis.

(A) Schematic representation of the experimental paradigms in vivo. (B) TNFα infusion into the DG significantly reduced the number of BrdU-labeled cells as well as (C) the number of BrdU-labeled cells that had turned into Dcx- and/or NeuN-positive neurons. *p<0.05, compared with control groups. n=4–5 in figures B and C.

Zhiguo Chen, et al. Brain Behav Immun. 2013 May;30:45-53.
2.
Fig. 1

Fig. 1. TNFα treatment decreases neuron production in mouse, human and monkey NSC cultures. From: Differential roles of TNFR1 and TNFR2 signaling in adult hippocampal neurogenesis.

(A) Treatment with conditioned medium of LPS-activated primary mouse microglia culture significantly inhibited differentiation of mouse NSCs to Dcx-positive cells. The percentage of Dcx-positive cells was normalized to sham-treated control culture. t=3.28; df=4; p=0.03. Ctl, control; MG-CM, conditioned medium from microglia culture. (B) Mouse NSCs were treated with individual cytokine in differentiation medium for 5 days. The proportion of cells positive for Dcx was scored. F(5,12)=15.8; p<0.0001. (C–D) Human (C) and Monkey (D) NSCs were cultured in differentiation medium with or without individual cytokines for 10 days and the fractions of cells positive for Dcx or Ki67 were scored. (C), Dcx: F(5.34)=30.3, p<0.0001; Ki67: F(5,34)=4.5, p=0.002; (D), Dcx: F(5, 17)=11.9, p<0.0001; Ki67: F(5,17)=11.3, p<0.0001. (B–D), Dunnett comparison with control groups. *p<0.05; #0.05<p<0.1.

Zhiguo Chen, et al. Brain Behav Immun. 2013 May;30:45-53.
3.
Fig. 5

Fig. 5. Effects of TNFR1- or TNFR2-mediated Signaling on hippocampal neurogenesis in radiation-induced inflammation. From: Differential roles of TNFR1 and TNFR2 signaling in adult hippocampal neurogenesis.

(A) Schematic representation of the experimental paradigm. (B, C) Representative pictures of Dcx-positive alone (B), Dcx/NeuN-double positive (C), and NeuN-positive alone (C) cells. (D) The numbers of BrdU-labeled cells in the DG were scored using stereology. Under control conditions without irradiation, TNFR1−/− and TNFα−/− mice showed an increased number of BrdU-positive cells and TNFR2−/− mice exhibited a reduced number of BrdU-positive cells, compared with that of wild-type mice. In the irradiated mice, no significant difference was observed in the total number of BrdU-positive cells between the genotypes. (E) The numbers of BrdU-labeled cells that had turned into neurons (Dcx- and/or NeuN-positive cells) were scored. Under control conditions without irradiation, more new neurons in TNFR1−/− and TNFα−/− and fewer new neurons in TNFR2−/− mice were observed. In the irradiated groups, TNFR2−/− and TNFα−/− mice exhibited a reduced number of new neurons, whereas TNFR1−/− mice did not show a measurable change, compared to that of wild-type mice. *p<0.05, compared with naïve wild-type groups in figures D and E; ap<0.05, compared with irradiated wild-type group in figure E. n=8 in figures D and E. Scale bar: 10 µm.

Zhiguo Chen, et al. Brain Behav Immun. 2013 May;30:45-53.
4.
Fig. 2

Fig. 2. Differential roles of TNFR1- and TNFR2-mediated signaling in vitro. From: Differential roles of TNFR1 and TNFR2 signaling in adult hippocampal neurogenesis.

(A) Wild-type, TNFR1−/−, and TNFR2−/− NSCs were grown as neurospheres with or without TNFα treatment and sphere sizes over a course of 6 days were plotted. The results of statistical analysis were listed in Table 1. (B) Representative pictures of NSCs with or without TNFα treatment on day 6. Scale bar: 50µm. (C–H) Deficiency of TNFR1 or TNFR2 alters cell cycle progression. NSCs of the different genotypes were subjected to flow cytometric analysis. (C) Cell debris was excluded on the FSC versus SSC plot. FSC, forward scatter; SSC, side scatter. (D) The gated cells were further analyzed on the PI-Area versus PI-Width plot to select for the singlets. (E) Standard cell cycle analysis was performed based on the histogram showing the proportion of cells at the G1, S, and G2/M phases. A representative sample from the wild-type NSCs without TNFα treatment was shown. (F–H) The fractions of cells at G1 (F), S (G), and G2/M (H) phases were compared between each genotype with or without TNFα treatment. (I–J) NSCs were cultured as monolayer and differentiated for 5 days with or without TNFα treatment. The proportions of cells positive for Dcx (I), or GFAP (J) were scored. n=5 in figure A; n=3 in figures F–J. *p<0.05, compared between the indicated groups; ap<0.05, compared with vehicle-treated wild-type.

Zhiguo Chen, et al. Brain Behav Immun. 2013 May;30:45-53.
5.
Fig. 3

Fig. 3. TNFα reduces neuron production through activating NF-κB pathway in Nestin-positive cells as well as induced apoptosis of Dcx-positive cells. From: Differential roles of TNFR1 and TNFR2 signaling in adult hippocampal neurogenesis.

(A) NSCs were differentiated for 6 days in the presence of 20 ng/ml TNFα in combination with Caspase 3 inhibitor (2 µM, 6 days), or Caspase 9 inhibitor (2 µM, 6 days), or following SN50 treatment (25 µg/ml) for 30 mins. Treatment with SN50 or Caspase 3 inhibitor could reverse the inhibitory effect of TNFα on neuron production. F(4,15)=7.7; p=0.0014. Casp3 In, Caspase 3 inhibitor; Casp9 In, Caspase 9 inhibitor. (B) Representative pictures of Dcx-positive cells. (C) NSCs were differentiated for 3 days prior to addition of TNFα (20 ng/ml) for 30 or 60 mins. After TNFα treatment, NF-κB translocated from cytoplasm to nucleus, as evidenced by p65 staining. (D, E) Co-labeling of p65 with Nestin and Dcx revealed that Nestin- but not Dcx-positive cells responded to TNFα treatment by activating NF-κB signaling cascades. F(2,6)=14.5; p=0.005. (F, G) NSCs were differentiated for 3 days followed by treatment with TNFα for 8 hrs. The proportions of Dcx-, and Nestin-positive cells co-labeled with cleaved Caspase 3 were scored. TNFα treatment resulted in increased apoptosis of Dcx-positive cells. t=4.93; df=4; p=0.008. A representative picture of cells with TNFα treatment for 8 hrs was shown in F. *p<0.05, compared between indicated groups in (A) or with respective control groups in (E) and (G). n=3–4 in figures A, E and G. Scale bars: 20 µm.

Zhiguo Chen, et al. Brain Behav Immun. 2013 May;30:45-53.

Supplemental Content

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...
Write to the Help Desk