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Functional imaging of Rel expression in inflammatory processes using bioluminescence imaging system in transgenic mice.

Yang X, Jing H, Zhao K, Sun R, Liu Z, Ying Y, Ci L, Kuang Y, Huang F, Wang Z, Fei J - PLoS ONE (2013)

Bottom Line: Revealing the dynamic expression of c-Rel in disease processes in vivo is critical for understanding c-Rel functions and for developing anti-inflammatory drugs.Luciferase expression could be tracked in living mice by the method of bioluminescence imaging in a variety of inflammatory processes, including LPS induced sepsis and EAE disease model.These results indicate that the B6-Tg(c-Rel-luc)(Mlit) mouse is a valuable animal model to study Rel expression in physiological and pathological processes, and the effects of various drug treatments in vivo.

View Article: PubMed Central - PubMed

Affiliation: School of Life Science and Technology, Tongji University, Shanghai, China.

ABSTRACT
c-Rel plays important roles in many inflammatory diseases. Revealing the dynamic expression of c-Rel in disease processes in vivo is critical for understanding c-Rel functions and for developing anti-inflammatory drugs. In this paper, a transgenic mouse line, B6-Tg(c-Rel-luc)(Mlit), which incorporated the transgene firefly luciferase driven by a 14.5-kb fragment containing mouse c-Rel gene Rel promoter, was generated to monitor Rel expression in vivo. Luciferase expression could be tracked in living mice by the method of bioluminescence imaging in a variety of inflammatory processes, including LPS induced sepsis and EAE disease model. The luciferase expression in transgenic mice was comparable to the endogenous Rel expression and could be suppressed by administration of anti-inflammatory drug dexamethasone or aspirin. These results indicate that the B6-Tg(c-Rel-luc)(Mlit) mouse is a valuable animal model to study Rel expression in physiological and pathological processes, and the effects of various drug treatments in vivo.

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Luciferase expression in B6-Tg(c-Rel-luc)8Mlit mice of MOG induced experimental autoimmune encephalomyelitis (EAE) model.(A) Female B6-Tg(c-Rel-luc)8Mlit mice were treated with CFA and with or without emulsionized MOG. Images were captured at day −1, 8, 10, 12, 14, 16, 18, 20, 22, 24, 26 and 30; (B) The quantification of luciferase activity; (C) The changes in body weight of EAE and control mice; (D) The clinical scores of EAE and control mice, n = 7; (E, F) Mouse spinal cord sections stained with H&E. (E) Section from the control mouse; (F) Section from the EAE mouse. The infiltration of inflammatory leukocytes was indicated by the blue arrow. (G, H) Mouse spinal cord sections stained with LFB. (G) Section from the control mouse; (H) Section from the EAE mouse. The demyelination in the white matter was marked by the yellow arrow. *p<0.05; **p<0.01.
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pone-0057632-g005: Luciferase expression in B6-Tg(c-Rel-luc)8Mlit mice of MOG induced experimental autoimmune encephalomyelitis (EAE) model.(A) Female B6-Tg(c-Rel-luc)8Mlit mice were treated with CFA and with or without emulsionized MOG. Images were captured at day −1, 8, 10, 12, 14, 16, 18, 20, 22, 24, 26 and 30; (B) The quantification of luciferase activity; (C) The changes in body weight of EAE and control mice; (D) The clinical scores of EAE and control mice, n = 7; (E, F) Mouse spinal cord sections stained with H&E. (E) Section from the control mouse; (F) Section from the EAE mouse. The infiltration of inflammatory leukocytes was indicated by the blue arrow. (G, H) Mouse spinal cord sections stained with LFB. (G) Section from the control mouse; (H) Section from the EAE mouse. The demyelination in the white matter was marked by the yellow arrow. *p<0.05; **p<0.01.

Mentions: To validate if B6-Tg(c-Rel-luc)8Mlit mice could be used in the research of chronic inflammatory disease, we studied the dynamic change of luciferase expression in EAE model. Compared with the control group, the luciferase signal was observed at the dorsum area of EAE mice, from day 8 after MOG challenge, and then was maintained high and waved during the whole disease process (Fig. 5A). Compared with the control group, the EAE group’s body weight reduced sharply starting at day 12 when the clinical symptom emerged (Fig. 5C). The development of the disease was confirmed by hematoxylin & eosin staining (HE) and luxol fast blue (LFB) staining at day 16, 4 days after the disease onset and near the peak of clinical activity. The HE-stained spinal cord sections were presented in Fig. 5E, F. The results exhibited massive infiltration of inflammatory leukocytes in the EAE group. Accompanied by the inflammatory leukocytes accumulation, the demyelination in the white matter was obvious by LFB staining (Fig. 5G, H). It is notable that the change of luciferase signal intensity (Fig. 5B) was much earlier than that of clinical score (Fig. 5D), which suggested that the luciferase activity of the transgenic mouse model could be an indicator to determine the initial development and severity of EAE disease.


Functional imaging of Rel expression in inflammatory processes using bioluminescence imaging system in transgenic mice.

Yang X, Jing H, Zhao K, Sun R, Liu Z, Ying Y, Ci L, Kuang Y, Huang F, Wang Z, Fei J - PLoS ONE (2013)

Luciferase expression in B6-Tg(c-Rel-luc)8Mlit mice of MOG induced experimental autoimmune encephalomyelitis (EAE) model.(A) Female B6-Tg(c-Rel-luc)8Mlit mice were treated with CFA and with or without emulsionized MOG. Images were captured at day −1, 8, 10, 12, 14, 16, 18, 20, 22, 24, 26 and 30; (B) The quantification of luciferase activity; (C) The changes in body weight of EAE and control mice; (D) The clinical scores of EAE and control mice, n = 7; (E, F) Mouse spinal cord sections stained with H&E. (E) Section from the control mouse; (F) Section from the EAE mouse. The infiltration of inflammatory leukocytes was indicated by the blue arrow. (G, H) Mouse spinal cord sections stained with LFB. (G) Section from the control mouse; (H) Section from the EAE mouse. The demyelination in the white matter was marked by the yellow arrow. *p<0.05; **p<0.01.
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3585201&req=5

pone-0057632-g005: Luciferase expression in B6-Tg(c-Rel-luc)8Mlit mice of MOG induced experimental autoimmune encephalomyelitis (EAE) model.(A) Female B6-Tg(c-Rel-luc)8Mlit mice were treated with CFA and with or without emulsionized MOG. Images were captured at day −1, 8, 10, 12, 14, 16, 18, 20, 22, 24, 26 and 30; (B) The quantification of luciferase activity; (C) The changes in body weight of EAE and control mice; (D) The clinical scores of EAE and control mice, n = 7; (E, F) Mouse spinal cord sections stained with H&E. (E) Section from the control mouse; (F) Section from the EAE mouse. The infiltration of inflammatory leukocytes was indicated by the blue arrow. (G, H) Mouse spinal cord sections stained with LFB. (G) Section from the control mouse; (H) Section from the EAE mouse. The demyelination in the white matter was marked by the yellow arrow. *p<0.05; **p<0.01.
Mentions: To validate if B6-Tg(c-Rel-luc)8Mlit mice could be used in the research of chronic inflammatory disease, we studied the dynamic change of luciferase expression in EAE model. Compared with the control group, the luciferase signal was observed at the dorsum area of EAE mice, from day 8 after MOG challenge, and then was maintained high and waved during the whole disease process (Fig. 5A). Compared with the control group, the EAE group’s body weight reduced sharply starting at day 12 when the clinical symptom emerged (Fig. 5C). The development of the disease was confirmed by hematoxylin & eosin staining (HE) and luxol fast blue (LFB) staining at day 16, 4 days after the disease onset and near the peak of clinical activity. The HE-stained spinal cord sections were presented in Fig. 5E, F. The results exhibited massive infiltration of inflammatory leukocytes in the EAE group. Accompanied by the inflammatory leukocytes accumulation, the demyelination in the white matter was obvious by LFB staining (Fig. 5G, H). It is notable that the change of luciferase signal intensity (Fig. 5B) was much earlier than that of clinical score (Fig. 5D), which suggested that the luciferase activity of the transgenic mouse model could be an indicator to determine the initial development and severity of EAE disease.

Bottom Line: Revealing the dynamic expression of c-Rel in disease processes in vivo is critical for understanding c-Rel functions and for developing anti-inflammatory drugs.Luciferase expression could be tracked in living mice by the method of bioluminescence imaging in a variety of inflammatory processes, including LPS induced sepsis and EAE disease model.These results indicate that the B6-Tg(c-Rel-luc)(Mlit) mouse is a valuable animal model to study Rel expression in physiological and pathological processes, and the effects of various drug treatments in vivo.

View Article: PubMed Central - PubMed

Affiliation: School of Life Science and Technology, Tongji University, Shanghai, China.

ABSTRACT
c-Rel plays important roles in many inflammatory diseases. Revealing the dynamic expression of c-Rel in disease processes in vivo is critical for understanding c-Rel functions and for developing anti-inflammatory drugs. In this paper, a transgenic mouse line, B6-Tg(c-Rel-luc)(Mlit), which incorporated the transgene firefly luciferase driven by a 14.5-kb fragment containing mouse c-Rel gene Rel promoter, was generated to monitor Rel expression in vivo. Luciferase expression could be tracked in living mice by the method of bioluminescence imaging in a variety of inflammatory processes, including LPS induced sepsis and EAE disease model. The luciferase expression in transgenic mice was comparable to the endogenous Rel expression and could be suppressed by administration of anti-inflammatory drug dexamethasone or aspirin. These results indicate that the B6-Tg(c-Rel-luc)(Mlit) mouse is a valuable animal model to study Rel expression in physiological and pathological processes, and the effects of various drug treatments in vivo.

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Related in: MedlinePlus