Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasminogen is the zymogen form of the serine proteinase plasmin. Although plasmin functions primarily as a fibrinolytic enzyme, recent evidence from numerous laboratories indicates that plasmin is also active in extracellular-matrix (ECM) proteolysis. The role of plasmin in ECM degradation suggests that activation of plasminogen may be regulated by interaction with components of the ECM. In the current study, we have investigated binding and kinetic interactions between plasminogen, plasminogen activators and ECM synthesized by either vascular smooth muscle cells (SMCECM) or endothelial cells (ECECM). We report binding of plasminogen, tissue-type plasminogen activator (t-PA) and urinary-type plasminogen activator (u-PA) to intact SMCECM with concentrations of ligand yielding half-maximal binding (B50) of 34, 5 and 15 nM, respectively. ECECM bound only plasminogen and t-PA, with B50 values of 32 nM and 10 nM, respectively. The initial rate of t-PA-catalyzed plasminogen activation was enhanced 41-fold in the presence of SMCECM and 27-fold on ECECM. In contrast, u-PA-catalyzed activation on SMCECM and ECECM was increased only 1.5-fold or 3-fold, respectively. These data suggest that the ECM may provide an alternative surface for assembly and regulation of plasminogen activation.
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PMID:Comparison of plasminogen binding and activation on extracellular matrices produced by vascular smooth muscle and endothelial cells. 781 84

Behavioral sensitization or reverse tolerance induced by repeated treatment of psychostimulants, such as amphetamine and cocaine, has been widely used as an animal model for schizophrenia. This phenomenon may result from almost eternally lasting plastic functional adaptation in the brain. Such long-lasting plasticity must accompany anatomical and morphological neural changes. Histological studies revealed that chronic treatment of psychostimulants induced thickness, elongation and an increased branch number of neurites and dendrites in cortices and accumbens, and an increased spine density. These changes may seem a positive adaptation for neural transmission, however, similar histological changes were seen after toxicity of methamphetamine as deafferation compensation. Therefore, further studies are needed to establish the significance of these morphological changes induced by chronic psychostimulants. On the other hand, neuromolecular studies showed increased phosphorylation of neuromodulin, increased expression of tissue-type plasminogen activator, synaptotagmin IV and arc, which are assumed to play roles in neural outgrowth and synaptogenesis. Although all of these histological and neuromolecular findings may suggest reorganization of the neural network should grow along with behavioral sensitization, more solid evidence is indispensable to confirm it.
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PMID:[Is there solid evidence for reorganization of the neural network associated with development of behavioral sensitization to psychostimulants?]. 1046 75

There are few studies of neural implants in spinal cord injury (SCI) focused on supporting directed axon growth. In this study, we fabricated a macroporous poly (lactic acid) (PLA) foam with oriented inner channels. Amorphous foam without linear channels served as a control in an acute SCI injury model, and the effectiveness of foam with linear channels was further investigated in a chronic SCI model. Implants were placed into a 2 mm hemisection lesion cavity at the T8 spinal cord level in adult rats. Two weeks post-implantation, tissue sections including the implants were examined using antibodies against GFAP, p75, ED-1, laminin, GAP-43, and CGRP. Foam implants were well-integrated with the host spinal cord. In linear foams, numerous DAPI-stained cells were found within the inner channels. Schwann cells but not astrocytes had migrated within the channels. Intense laminin staining was observed throughout the extracellular matrix substrate. GAP-43- and CGRP-positive axons grew through the implants following the linear channels. In the amorphous control foams, DAPI staining distributed evenly through the pores. However, the growth of GAP-43 or CGRP-positive axons was misguided and impeded at the entrance area of the foam. Higher numbers of GAP-43 and CGRP-positive axons grew into linear foam implants after chronic SCI than acute SCI. These results suggest the potential application of linear foam implants in cell and axon guidance for SCI repair, especially for chronic SCI.
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PMID:Evaluation of cellular organization and axonal regeneration through linear PLA foam implants in acute and chronic spinal cord injury. 1750 92