ReviewRespiratory physiology & neurobiology2009
Role of plasminogen activator in spinal cord remodeling after spinal cord injury.
Review in Respiratory physiology & neurobiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Plasminogen degrades α-synuclein, Tau and TDP-43 and decreases dopaminergic neurodegeneration in mouse models of Parkinson's disease.Scientific reports · 2024Article
- Respiratory plasticity following spinal cord injury: perspectives from mouse to man.Neural regeneration research · 2022Review
- Effects of Growth Hormone Treatment and Rehabilitation in Incomplete Chronic Traumatic Spinal Cord Injury: Insight from Proteome Analysis.Journal of personalized medicine · 2020Article
- Short-term inhibition of fibrinolytic system restores locomotor function after spinal cord injury in mice.Scientific reports · 2019Article
- Circadian rhythm and sleep-wake systems share the dynamic extracellular synaptic milieu.Neurobiology of sleep and circadian rhythms · 2018Review
- A murine model of cervical spinal cord injury to study post-lesional respiratory neuroplasticity.Journal of visualized experiments : JoVE · 2014Article
- Axonal regrowth after spinal cord injury via chondroitinase and the tissue plasminogen activator (tPA)/plasmin system.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Plasminogen activator promotes recovery following spinal cord injury.Cellular and molecular neurobiology · 2011Article
- The phrenic motor nucleus in the adult mouse.Experimental neurology · 2010Article
- Neuromuscular adaptations to respiratory muscle inactivity.Respiratory physiology & neurobiology · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Plasminogen activators play an active role in synaptic plasticity associated with the crossed phrenic phenomenon (CPP) and recovery of respiratory function following spinal cord injury. A genetic approach has been used to identify molecular mechanisms underlying this synaptic plasticity. Knockout mice lacking different genes in the plasminogen activator/plasmin system demonstrate that expression of urokinase plasminogen activator (uPA) is required during the critical 1-2h delay period following C2-hemisection for the acquisition of a good CPP response. uPA knockout mice fail to show the structural remodeling of phrenic motorneuron synapses that underlie the CPP response. Potential mechanisms by which uPA may promote phrenic motorneuron synaptic plasticity have been explored. Expression of uPA receptors, uPAR and LRP-1, are both up-regulated in the ipsilateral phrenic motor nucleus (PMN) following C2-hemisection. A comparison of microarray data and real-time PCR analysis of mRNAs induced in the PMN after hemisection indicate potential cell signaling pathways downstream of uPA's interaction with these cell surface receptors in the PMN. Knowledge of these uPA-mediated signaling pathways may identify potential means for the pharmacological activation of the synaptic plasticity required for recovery of phrenic motorneuron activity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.