ABSTRACT
The neurotrophin brain-derived neurotrophic factor (BDNF), which acts as a transducer, is responsible for improving cerebral stroke, neuropathic pain, and depression. Exercise can alter extracellular nucleotide levels and purinergic receptors in central nervous system (CNS) structures. This inevitably activates or inhibits the expression of BDNF via purinergic receptors, particularly the P2X receptor (P2XR), to alleviate pathological progression. In addition, the significant involvement of sensitive P2X4R in mediating increased BDNF and p38-MAPK for intracerebral hemorrhage and pain hypersensitivity has been reported. Moreover, archetypal P2X7R blockade induces mouse antidepressant-like behavior and analgesia by BDNF release. This review summarizes BDNF-mediated neural effects via purinergic receptors, speculates that P2X4R and P2X7R could be priming molecules in exercise-mediated changes in BDNF, and provides strategies for the protective mechanism of exercise in neurogenic disease.
Subject(s)
Neuralgia , Stroke , Animals , Mice , Antidepressive Agents , Brain-Derived Neurotrophic Factor , Neuroprotection , Receptors, Purinergic P2X4 , Receptors, Purinergic P2X7/metabolismABSTRACT
Sarcopenia is characterized by the loss of muscle mass and strength, and one of its major molecular mechanisms is muscle protein turnover. Quinoa, the grain-like food crop, is a health nutrient used to treat diseases that predispose individuals to muscle wasting, including cardiovascular disorders, diabetes mellitus, and cancer. Quinoa secondary metabolites have recently been demonstrated to regulate protein turnover (including protein synthesis and degradation), a main biological process within muscle cells, through diverse signals (such as the p38 MAPK, TNF-α, and IGF-1/PI3K/Akt/FOXO pathways). Here, we describe how quinoa functions in the main pathway of protein synthesis and degradation, screen promising pharmacological components in nutritional applications, and provide guidance for the effects of quinoa products in sarcopenia.
Subject(s)
Chenopodium quinoa , Sarcopenia , Forkhead Box Protein O1 , Humans , Insulin-Like Growth Factor I , Muscle, Skeletal , Nutrients , Phosphatidylinositol 3-Kinases , Proto-Oncogene Proteins c-akt , Sarcopenia/drug therapy , Signal TransductionABSTRACT
A novel bovine cDNA has been isolated by EST assembly and subsequently confirmed by using RT-PCR and designated bovine A Proliferation-Inducing Ligand belonging to TNF family (bAPRIL). The open reading frame (ORF) of this cDNA covers 753 bp, encoding 250 amino acids. The functional soluble part of bAPRIL (bsAPRIL) shows 97% and 92% identity with its pig and human counterparts, respectively, at the level of the primary protein structure. The bAPRIL genomic sequence consists of six exons and five introns, is approximately 1.8 kb in size, and maps to bovine chromosome 19q. Real-time quantitative PCR (qPCR) analysis revealed that bAPRIL is predominantly expressed in bovine lymphoid tissues spleen. The predicted three-dimensional (3D) structure of the bsAPRIL monomer analyzed by "comparative protein modelling" revealed that it is very similar to its mouse counterpart. The bsAPRIL and EGFP/bsAPRIL were efficiently expression in Escherichia coli BL21 (DE3) and its expression was confirmed by SDS-PAGE and Western blotting analysis. After purification, the EGFP/bsAPRIL fusion protein obtained similar fluorescence spectrum to those of EGFP. Laser scanning confocal microscopy analysis showed EGFP/bsAPRIL could bind to its receptor. In vitro, bsAPRIL could promote the proliferation of bovine or mouse splenic B cells together with/without SAC or anti-mouse IgM. Furthermore, compared to mouse soluble APRIL, the bovine soluble APRIL has the similar proliferation to mouse B cell. Those findings indicated that bsAPRIL plays an important role in proliferation of bovine B cells and has functional cross-reactivity among cow and other mammalians. Therefore, APRIL may be a potential immunologic factor for enhancing immunological efficacy in animals.