Protein kinase A-dependent substance P expression by pituitary adenylate cyclase-activating polypeptide in rat sensory neuronal cell line ND7/23 cells.
Bibliographic Information
- Other Title
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- 脳下垂体アデニル酸シクラーゼ活性化ポリペプチドによるラット知覚神経細胞株ND7/23でのプロテインキナーゼA依存的サブスタンスP発現誘導(発表論文抄録(2012))
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Abstract
The neurotrophic effects of pituitary adenylate cyclase-activating polypeptide (PACAP) on rat sensory neuronal cell line ND7/23 cells were investigated. PACAP caused a concentration-dependent increase in the number of neurite-bearing cells and the expression of the substance P precursor (PPT) mRNA in 24h. The effects of PACAP were mimicked by vasoactive intestinal polypeptide with lower potency and dibutyryl-cyclic AMP, and inhibited by inhibitors of protein kinase A, ERK kinase or p38 kinase, KT5720, U0126, or SB203580, respectively. In a PPT promoter luciferase reporter assay, the increase of PPT mRNA was the result of an increase in PPT gene transcriptional activity by PACAP. The increasing effects of PACAP on PPT mRNA were similarly observed in primary cultured rat dorsal root ganglion cells. Thus, PACAP could induce differentiation-like phenomena in sensory neurons in a cAMP-, protein kinase A-, ERK kinase-, and p38 kinase-dependent manner. These results provide evidence of the neurotrophic action of PACAP, which may function to rescue damaged neurons or to switch the neuronal phenotype in injured or inflamed sensory neurons.
The neurotrophic effects of pituitary adenylate cyclase-activating polypeptide (PACAP) on rat sensory neuronal cell line ND7/23 cells were investigated. PACAP caused a concentration-dependent increase in the number of neurite-bearing cells and the expression of the substance P precursor (PPT) mRNA in 24h. The effects of PACAP were mimicked by vasoactive intestinal polypeptide with lower potency and dibutyryl-cyclic AMP, and inhibited by inhibitors of protein kinase A, ERK kinase or p38 kinase, KT5720, U0126, or SB203580, respectively. In a PPT promoter luciferase reporter assay, the increase of PPT mRNA was the result of an increase in PPT gene transcriptional activity by PACAP. The increasing effects of PACAP on PPT mRNA were similarly observed in primary cultured rat dorsal root ganglion cells. Thus, PACAP could induce differentiation-like phenomena in sensory neurons in a cAMP-, protein kinase A-, ERK kinase-, and p38 kinase-dependent manner. These results provide evidence of the neurotrophic action of PACAP, which may function to rescue damaged neurons or to switch the neuronal phenotype in injured or inflamed sensory neurons.
Journal
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- Annual report of the Faculty of Pharmacy & Pharmaceutical Sciences, Fukuyama University
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Annual report of the Faculty of Pharmacy & Pharmaceutical Sciences, Fukuyama University (31), 41-42, 2013-12-25
福山大学薬学部
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Keywords
- Animals
- Cell Differentiation
- Cells, Cultured
- Cyclic AMP-Dependent Protein Kinases
- Extracellular Signal-Regulated MAP Kinases
- Ganglia, Spinal
- Gene Expression Regulation
- Genes, Reporter
- Hybrid Cells
- Male
- Neurites
- Phenotype
- Pituitary Adenylate Cyclase-Activating Polypeptide
- Protein Kinase Inhibitors
- Protein Precursors
- RNA, Messenger
- Rats
- Rats, Wistar
- Recombinant Fusion Proteins
- Reverse Transcriptase Polymerase Chain Reaction
- Sensory Receptor Cells
- Signal Transduction
- Substance P
- Tachykinins
- Transcription, Genetic
- p38 Mitogen-Activated Protein Kinases
Details 詳細情報について
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- CRID
- 1050845762531907328
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- NII Article ID
- 120006373256
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- NII Book ID
- AN10064550
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- ISSN
- 0288724X
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- Text Lang
- en
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- Article Type
- departmental bulletin paper
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- Data Source
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- IRDB
- CiNii Articles