title: PAL31 may play an important role as inflammatory modulator in the repair process of the spinal cord injury rat.
abstract: Functional regeneration in a complete T8 transection model Cheng et al. (1996) and most recently, acidic fibroblast growth factor (aFGF; also known as FGF-1) involved in the repair process of the spinal cord injury (SCI) rat Tsai et al. (2008) have been reported. To further reveal the mechanism of the repair process of SCI, in additionally, we have identified a 30 kDa specific protein kinase A substrate induced at 6 days after SCI. However, the induction of the transducing signal was reduced in samples treated with aFGF. The 30 kDa protein was purified and identified by mass spectrometry as a novel protein, PAL31. The results of immunohistochemical study showed that PAL31 is abundantly expressed in the epicenter of the injured spinal cord and colocalizes with ED1-positive cells (macrophages) and CD8 T lymphocytes. Over-expression of PAL31 in RAW 264.7 cells resulted in the down-regulation of macrophage chemoattractant protein 1, inducible nitric oxide synthase, and signal transducer and activator of transcription-1. However, knockdown of PAL31 by small interfering RNA seems to lead to apoptosis when the cells were treated with inflammatory inducers. These experimental results suggest that PAL31 may involve in the modulation of the inflammatory response and, at the same time, prevent apoptosis process of macrophage after SCI.
authors.affiliation: The Institute of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei, Taiwan.
authors.forename: Li-Fen
authors.initials: LF
authors.lastname: Shen
authors.forename: Henrich
authors.initials: H
authors.lastname: Cheng
authors.forename: Ming-Chu
authors.initials: MC
authors.lastname: Tsai
authors.forename: Huai-Sheng
authors.initials: HS
authors.lastname: Kuo
authors.forename: Kin-Fu
authors.initials: KF
authors.lastname: Chak
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D018414:CD8-Positive T-Lymphocytes / Q000378:metabolism; D053148:Caspase 3 / Q000378:metabolism; D018797:Cell Cycle Proteins / Q000235:genetics / Q000302:isolation & purification / Q000378:metabolism*; D002461:Cell Line, Transformed; D018932:Chemokine CCL2 / Q000378:metabolism; D017868:Cyclic AMP-Dependent Protein Kinases / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D053331:Ectodysplasins / Q000378:metabolism; D015180:Electrophoresis, Gel, Two-Dimensional / Q000379:methods; D005260:Female; D016220:Fibroblast Growth Factor 1 / Q000378:metabolism; D005786:Gene Expression Regulation / Q000502:physiology; D020287:In Situ Nick-End Labeling / Q000379:methods; D008264:Macrophages / Q000166:cytology / Q000378:metabolism; D018832:Molecular Chaperones; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000302:isolation & purification / Q000378:metabolism*; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D009687:Nuclear Proteins / Q000235:genetics / Q000302:isolation & purification / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function / Q000502:physiology*; D050794:STAT1 Transcription Factor / Q000378:metabolism; D013116:Spinal Cord / Q000378:metabolism* / Q000473:pathology; D013119:Spinal Cord Injuries / Q000378:metabolism* / Q000473:pathology
chemical_list: C412378:Anp32b protein, rat; C491766:Ccl2 protein, rat; D018797:Cell Cycle Proteins; D018932:Chemokine CCL2; D016207:Cytokines; D053331:Ectodysplasins; D018832:Molecular Chaperones; D009419:Nerve Tissue Proteins; D009687:Nuclear Proteins; D050794:STAT1 Transcription Factor; D016220:Fibroblast Growth Factor 1; D052247:Nitric Oxide Synthase Type II; D017868:Cyclic AMP-Dependent Protein Kinases; D053148:Caspase 3