ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
A model for sealing plasmalemmal damage in neurons and other eukaryotic cells.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Polyethylene Glycol: The Future of Posttraumatic Nerve Repair? Systemic Review.International journal of molecular sciences · 2019Pooled it
- TEMPOL Enhances Polyethylene Glycol Axon Fusion Following Sciatic Nerve Transection in Adult Rats.ACS chemical neuroscience · 2026Article
- Wound Repair of the Cell Membrane: Lessons fromCells · 2024Review
- Article
- Femtosecond laser microdissection for isolation of regenerating C. elegans neurons for single-cell RNA sequencing.Nature methods · 2023Article
- Repair of traumatic lesions to the plasmalemma of neurons and other cells: Commonalities, conflicts, and controversies.Frontiers in physiology · 2023Review
- The cellular response to plasma membrane disruption for nanomaterial delivery.Nano convergence · 2022Review
- Short-term transcriptomic response to plasma membrane injury.Scientific reports · 2021Article
- The Cofilin/Limk1 Pathway Controls the Growth Rate of Both Developing and Regenerating Motor Axons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Effect of exogenous spastin combined with polyethylene glycol on sciatic nerve injury.Neural regeneration research · 2019Article
- Polyethylene glycol (PEG) and other bioactive solutions with neurorrhaphy for rapid and dramatic repair of peripheral nerve lesions by PEG-fusion.Journal of neuroscience methods · 2019Article
- Cardiomyocyte lethality by multidirectional stimuli.Medical & biological engineering & computing · 2018Article
- MRI-based assessment of function and dysfunction in myelinated axons.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Cellular mechanisms and signals that coordinate plasma membrane repair.Cellular and molecular life sciences : CMLS · 2018Review
- Polyethylene glycol solutions rapidly restore and maintain axonal continuity, neuromuscular structures, and behaviors lost after sciatic nerve transections in female rats.Journal of neuroscience research · 2018Article
- Ca2+/calmodulin-dependent protein kinase II and Dimethyl Sulfoxide affect the sealing frequencies of transected hippocampal neurons.Journal of neuroscience research · 2018Article
- Intracellular cAMP Sensor EPAC: Physiology, Pathophysiology, and Therapeutics Development.Physiological reviews · 2018Review
- Self-repairing cells: How single cells heal membrane ruptures and restore lost structures.Science (New York, N.Y.) · 2017Review
- [Changes of endogenous Spastin expression after sciatic nerve injury in rats].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2017Article
- Repair of traumatic plasmalemmal damage to neurons and other eukaryotic cells.Neural regeneration research · 2016Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Plasmalemmal repair is necessary for survival of damaged eukaryotic cells. Ca(2+) influx through plasmalemmal disruptions activates calpain, vesicle accumulation at lesion sites, and membrane fusion proteins; Ca(2+) influx also initiates competing apoptotic pathways. Using the formation of a dye barrier (seal) to assess plasmalemmal repair, we now report that B104 hippocampal cells with neurites transected nearer (<50 μm) to the soma seal at a lower frequency and slower rate compared to cells with neurites transected farther (>50 μm) from the soma. Analogs of cAMP, including protein kinase A (PKA)-specific and Epac-specific cAMP, each increase the frequency and rate of sealing and can even initiate sealing in the absence of Ca(2+) influx at both transection distances. Furthermore, Epac activates a cAMP-dependent, PKA-independent, pathway involved in plasmalemmal sealing. The frequency and rate of plasmalemmal sealing are decreased by a small molecule inhibitor of PKA targeted to its catalytic subunit (KT5720), a peptide inhibitor targeted to its regulatory subunits (PKI), an inhibitor of a novel PKC (an nPKCη pseudosubstrate fragment), and an antioxidant (melatonin). Given these and other data, we propose a model for redundant parallel pathways of Ca(2+)-dependent plasmalemmal sealing of injured neurons mediated in part by nPKCs, cytosolic oxidation, and cAMP activation of PKA and Epac. We also propose that the evolutionary origin of these pathways and substances was to repair plasmalemmal damage in eukaryotic cells. Greater understanding of vesicle interactions, proteins, and pathways involved in plasmalemmal sealing should suggest novel neuroprotective treatments for traumatic nerve injuries and neurodegenerative disorders.
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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.