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Amyloid precursor-like protein 2 C-terminal fragments upregulate S100A9 gene and protein expression in BV2 cells.

Li G, Chen H, Cheng L, Zhao R, Zhao J, Xu Y - Neural Regen Res (2014)

Bottom Line: Reverse transcription-PCR, western blot assay and immunocytochemistry revealed that S100A9 protein and mRNA expression was greater in BV2 cells after CTF transfection than after mock transfection with an empty vector.Furthermore, transfection of full-length APLP2-751 resulted in low levels of S100A9 protein expression.Our results show that APLP2-CTFs upregulate S100A9 protein and mRNA expression in BV2 cells, and identify a novel pathway involved in neuronal injury and apoptosis, and repair and protection in Alzheimer's disease.

View Article: PubMed Central - PubMed

Affiliation: Department of Psychology, Yanbian Brain Hospital, Yanji, Jilin Province, China.

ABSTRACT
The murine microglial cell line BV2 has neuroprotective effects, but is toxic to neurons by secreting inflammatory cytokines, and is an important target in the treatment of nerve inflammation and neurodegenerative diseases. In the present study, we observed the effects of transfecting three amyloid precursor-like protein 2 (APLP2) C-terminal fragments (CTFs; C57, C50 and C31) in the pEGFP-N1 vector on S100A9 expression in BV2 cells. Reverse transcription-PCR, western blot assay and immunocytochemistry revealed that S100A9 protein and mRNA expression was greater in BV2 cells after CTF transfection than after mock transfection with an empty vector. Furthermore, transfection of full-length APLP2-751 resulted in low levels of S100A9 protein expression. Our results show that APLP2-CTFs upregulate S100A9 protein and mRNA expression in BV2 cells, and identify a novel pathway involved in neuronal injury and apoptosis, and repair and protection in Alzheimer's disease.

No MeSH data available.


Related in: MedlinePlus

Effects of transfection with APLP2-CTFs (C57, C50, C31) on S100A9 protein expression in BV2 cells (immunocytochemical staining; laser scanning confocal microscope, × 100).S100A9-positive cells (arrows) were visualized with Alexa Flour 555-conjugated secondary antibody (red). Nuclei were stained with DAPI (blue). Among successfully transfected cells (green), S100A9 protein expression was notably stronger in all three APLP2-CTF-transfected groups than in the mock transfected group.
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Figure 2: Effects of transfection with APLP2-CTFs (C57, C50, C31) on S100A9 protein expression in BV2 cells (immunocytochemical staining; laser scanning confocal microscope, × 100).S100A9-positive cells (arrows) were visualized with Alexa Flour 555-conjugated secondary antibody (red). Nuclei were stained with DAPI (blue). Among successfully transfected cells (green), S100A9 protein expression was notably stronger in all three APLP2-CTF-transfected groups than in the mock transfected group.

Mentions: Immunocytochemical staining confirmed that S100A9 was induced by APLP2-CTFs (Figure 2).


Amyloid precursor-like protein 2 C-terminal fragments upregulate S100A9 gene and protein expression in BV2 cells.

Li G, Chen H, Cheng L, Zhao R, Zhao J, Xu Y - Neural Regen Res (2014)

Effects of transfection with APLP2-CTFs (C57, C50, C31) on S100A9 protein expression in BV2 cells (immunocytochemical staining; laser scanning confocal microscope, × 100).S100A9-positive cells (arrows) were visualized with Alexa Flour 555-conjugated secondary antibody (red). Nuclei were stained with DAPI (blue). Among successfully transfected cells (green), S100A9 protein expression was notably stronger in all three APLP2-CTF-transfected groups than in the mock transfected group.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4281433&req=5

Figure 2: Effects of transfection with APLP2-CTFs (C57, C50, C31) on S100A9 protein expression in BV2 cells (immunocytochemical staining; laser scanning confocal microscope, × 100).S100A9-positive cells (arrows) were visualized with Alexa Flour 555-conjugated secondary antibody (red). Nuclei were stained with DAPI (blue). Among successfully transfected cells (green), S100A9 protein expression was notably stronger in all three APLP2-CTF-transfected groups than in the mock transfected group.
Mentions: Immunocytochemical staining confirmed that S100A9 was induced by APLP2-CTFs (Figure 2).

Bottom Line: Reverse transcription-PCR, western blot assay and immunocytochemistry revealed that S100A9 protein and mRNA expression was greater in BV2 cells after CTF transfection than after mock transfection with an empty vector.Furthermore, transfection of full-length APLP2-751 resulted in low levels of S100A9 protein expression.Our results show that APLP2-CTFs upregulate S100A9 protein and mRNA expression in BV2 cells, and identify a novel pathway involved in neuronal injury and apoptosis, and repair and protection in Alzheimer's disease.

View Article: PubMed Central - PubMed

Affiliation: Department of Psychology, Yanbian Brain Hospital, Yanji, Jilin Province, China.

ABSTRACT
The murine microglial cell line BV2 has neuroprotective effects, but is toxic to neurons by secreting inflammatory cytokines, and is an important target in the treatment of nerve inflammation and neurodegenerative diseases. In the present study, we observed the effects of transfecting three amyloid precursor-like protein 2 (APLP2) C-terminal fragments (CTFs; C57, C50 and C31) in the pEGFP-N1 vector on S100A9 expression in BV2 cells. Reverse transcription-PCR, western blot assay and immunocytochemistry revealed that S100A9 protein and mRNA expression was greater in BV2 cells after CTF transfection than after mock transfection with an empty vector. Furthermore, transfection of full-length APLP2-751 resulted in low levels of S100A9 protein expression. Our results show that APLP2-CTFs upregulate S100A9 protein and mRNA expression in BV2 cells, and identify a novel pathway involved in neuronal injury and apoptosis, and repair and protection in Alzheimer's disease.

No MeSH data available.


Related in: MedlinePlus