Receptor protein tyrosine phosphatase beta (RPTPbeta) is expressed as soluble and receptor forms with common extracellular regions consisting of a carbonic anhydrase domain (C), a fibronectin type III repeat (F), and a unique region called S. We showed previously that a recombinant Fc fusion protein with the C domain (beta C) binds to contactin and supports neuronal adhesion and neurite growth. As a substrate, betaCFS was less effective in supporting cell adhesion, but it was a more effective promoter of neurite outgrowth than betaCF. betaS had no effect by itself, but it potentiated neurite growth when mixed with betaCF. Neurite outgrowth induced by betaCFS was inhibited by antibodies against Nr-CAM and contactin, and these cell adhesion molecules formed a complex that bound betaCFS. NIH-3T3 cells transfected to express betaCFS on their surfaces induced neuronal differentiation in culture. These results suggest that binding of glial RPTPbeta to the contactin/Nr-CAM complex is important for neurite growth and neuronal differentiation.
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http://dx.doi.org/10.1083/jcb.136.4.907 | DOI Listing |
Brain Pathol
January 2025
The Ritchie Centre, Hudson Institute of Medical Research, Translational Research Facility, Clayton, VIC, Australia.
The last pregnancy trimester is critical for fetal brain development but is a vulnerable period if the pregnancy is compromised by fetal growth restriction (FGR). The impact of FGR on the maturational development of neuronal morphology is not known, however, studies in fetal sheep allow longitudinal analysis in a long gestation species. Here we compared hippocampal neuron dendritogenesis in FGR and control fetal sheep at three timepoints equivalent to the third trimester of pregnancy, complemented by magnetic resonance image for brain volume, and electrophysiology for synaptic function.
View Article and Find Full Text PDFNeurorehabil Neural Repair
January 2025
Department of Neurosurgery, Faculty of Medicine, Medical Center-University of Freiburg, Freiburg, Germany.
Background: Spinal cord injury (SCI) can impair motor, sensory, and autonomic function. The formation of the glial scar comprises protective as well as inhibitory neurite outgrowth properties operated by the deposition of chondroitin sulfate proteoglycans (CSPG). Chondroitinase ABC (ChABC) can degrade CSPG and foster neuroaxonal plasticity as a therapeutic approach to restore locomotor function after SCI.
View Article and Find Full Text PDFBiomolecules
December 2024
Department of Anesthesiology and Perioperative Medicine, University of Rochester, 601 Elmwood Ave, Box 604, Rochester, NY 14620, USA.
Astrocytes play critical roles in supporting structural and metabolic homeostasis in the central nervous system (CNS). CNS injury leads to the development of a range of reactive phenotypes in astrocytes whose molecular determinants are poorly understood. Finding ways to modulate astrocytic injury responses and leverage a pro-recovery phenotype holds promise in treating CNS injury.
View Article and Find Full Text PDFInt Immunopharmacol
January 2025
Department of Oral and Maxillofacial Surgery, State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education School and Hospital of Stomatology, Wuhan University, Wuhan, Hubei, China. Electronic address:
Background: Pain and disability are primary concerns for temporomandibular joint osteoarthritis (TMJOA) patients, and the efficacy of current treatments remains controversial. Overactive osteoclasts are associated with subchondral bone degeneration and pain in OA. The vacuolar H+-ATPase (V-ATPase) is crucial for differentiation and function in osteoclasts, but its role in TMJOA is not well defined.
View Article and Find Full Text PDFCommun Biol
January 2025
Division of Geriatrics, Department of Medicine, SMPH, University of Wisconsin-Madison, Madison, WI, USA.
Changes in brain mitochondrial metabolism are coincident with functional decline; however, direct links between the two have not been established. Here, we show that mitochondrial targeting via the adiponectin receptor activator AdipoRon (AR) clears neurofibrillary tangles (NFTs) and rescues neuronal tauopathy-associated defects. AR reduced levels of phospho-tau and lowered NFT burden by a mechanism involving the energy-sensing kinase AMPK and the growth-sensing kinase GSK3b.
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