The Role of Basal Lamina in Axon Regeneration

1988 ◽  
pp. 361-383
Author(s):  
M. Berry ◽  
S. M. Hall ◽  
E. L. Rees ◽  
P. Yiu ◽  
J. Sievers
Keyword(s):  
Basal Lamina ◽  
Axon Regeneration

scholarly journals The Role of Lipids, Lipid Metabolism and Ectopic Lipid Accumulation in Axon Growth, Regeneration and Repair after CNS Injury and Disease

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1078
Author(s):  
Debasish Roy ◽  
Andrea Tedeschi
Keyword(s):  
Nervous System ◽  
Lipid Metabolism ◽  
Lipid Accumulation ◽  
Axon Regeneration ◽  
Axon Growth ◽  
The Body ◽  
Cns Repair ◽  
Cord Injury ◽  
Cns Trauma

Axons in the adult mammalian nervous system can extend over formidable distances, up to one meter or more in humans. During development, axonal and dendritic growth requires continuous addition of new membrane. Of the three major kinds of membrane lipids, phospholipids are the most abundant in all cell membranes, including neurons. Not only immature axons, but also severed axons in the adult require large amounts of lipids for axon regeneration to occur. Lipids also serve as energy storage, signaling molecules and they contribute to tissue physiology, as demonstrated by a variety of metabolic disorders in which harmful amounts of lipids accumulate in various tissues through the body. Detrimental changes in lipid metabolism and excess accumulation of lipids contribute to a lack of axon regeneration, poor neurological outcome and complications after a variety of central nervous system (CNS) trauma including brain and spinal cord injury. Recent evidence indicates that rewiring lipid metabolism can be manipulated for therapeutic gain, as it favors conditions for axon regeneration and CNS repair. Here, we review the role of lipids, lipid metabolism and ectopic lipid accumulation in axon growth, regeneration and CNS repair. In addition, we outline molecular and pharmacological strategies to fine-tune lipid composition and energy metabolism in neurons and non-neuronal cells that can be exploited to improve neurological recovery after CNS trauma and disease.

scholarly journals Role of basal lamina in neoplastic disorganization of tissue architecture.

1981 ◽  
Vol 78 (6) ◽  
pp. 3901-3905 ◽  
Author(s):  
D. E. Ingber ◽  
J. A. Madri ◽  
J. D. Jamieson
Keyword(s):  
Basal Lamina ◽  
Tissue Architecture

THE INTERACTION OF BLOOD ELEMENTS WITH ENDOCARDIAL ENDOTHELIUM DAMAGED BY LACTIC ACID

1987 ◽  
Author(s):  
G Carter ◽  
B J Gavin
Keyword(s):  
Lactic Acid ◽  
Basal Lamina ◽  
Myocardial Infarct ◽  
Transmission Electron ◽  
Rat Hearts ◽  
Cacodylate Buffer ◽  
Aortic Cannula ◽  
Endocardial Endothelium

It has already been demonstrated that ischaemic metabolites, which could diffuse frcm a myocardial infarct in vivo, can cause substantial damage to the endocardial endotheliun and this could predispose to mural thrombosis.To investigate the role of ischaemic metabolites in the pathogenesis of mural thrombosis, lactic acid (pH6.4) was passed through a two-way concentric catheter ligated into the left ventricle of isolated beating rat hearts that were perfused with oxygenated Krebs-Henseleit buffer (KHB) through an aortic cannula. After periods of 1, 2, and 4 hours, the lactic acid was followed for 10 minutes by 10 mis of whole blood from hepa-rinized donor rats. Ventricles were then flushed with KHB, fixed in 2.5% glutaraldehyde and post-fixed in 1% osmium tetrox-ide in cacodylate buffer.Scanning and transmission electron microscopy showed that platelets adhered to exposed basal lamina, microfibrils and collagen but not to intact or damaged endothelial cells. However densely aggregated thrombi only farmed on regions of exposed connective tissue and never on basal lamina. Fibrin, leukocytes and red blood cells were associated with these platelet thrombi. Thus lactic acid and other ischaemic metabolites which could possibly diffuse in vivo from an infarct can contribute to endocardial damage which predisposes to mural thrombosis.

scholarly journals Effects of NAD+ in Caenorhabditis elegans Models of Neuronal Damage

Biomolecules ◽  
2020 ◽  
Vol 10 (7) ◽  
pp. 993
Author(s):  
Yuri Lee ◽  
Hyeseon Jeong ◽  
Kyung Hwan Park ◽  
Kyung Won Kim
Keyword(s):  
Caenorhabditis Elegans ◽  
Therapeutic Strategy ◽  
Axon Regeneration ◽  
Neuronal Damage ◽  
Biological Processes ◽  
Nematode Caenorhabditis Elegans ◽  
C Elegans ◽  
Neuronal Functions ◽  
Molecular Components

Nicotinamide adenine dinucleotide (NAD+) is an essential cofactor that mediates numerous biological processes in all living cells. Multiple NAD+ biosynthetic enzymes and NAD+-consuming enzymes are involved in neuroprotection and axon regeneration. The nematode Caenorhabditis elegans has served as a model to study the neuronal role of NAD+ because many molecular components regulating NAD+ are highly conserved. This review focuses on recent findings using C. elegans models of neuronal damage pertaining to the neuronal functions of NAD+ and its precursors, including a neuroprotective role against excitotoxicity and axon degeneration as well as an inhibitory role in axon regeneration. The regulation of NAD+ levels could be a promising therapeutic strategy to counter many neurodegenerative diseases, as well as neurotoxin-induced and traumatic neuronal damage.

Role of Basal Lamina in Tissue Interactions

1980 ◽  
Vol 3 (1-6) ◽  
pp. 193-204 ◽  
Author(s):  
Anna G. Brownell ◽  
Harold C. Slavkin
Keyword(s):  
Basal Lamina ◽  
Tissue Interactions

scholarly journals Autophagy induction stabilizes microtubules and promotes axon regeneration after spinal cord injury

2016 ◽  
Vol 113 (40) ◽  
pp. 11324-11329 ◽  
Author(s):  
Miao He ◽  
Yuetong Ding ◽  
Chen Chu ◽  
Jing Tang ◽  
Qi Xiao ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Cortical Neurons ◽  
Axon Regeneration ◽  
Neuronal Degeneration ◽  
Dorsal Column ◽  
Microtubule Assembly ◽  
Autophagy Induction ◽  
Cord Injury

Remodeling of cytoskeleton structures, such as microtubule assembly, is believed to be crucial for growth cone initiation and regrowth of injured axons. Autophagy plays important roles in maintaining cellular homoeostasis, and its dysfunction causes neuronal degeneration. The role of autophagy in axon regeneration after injury remains speculative. Here we demonstrate a role of autophagy in regulating microtubule dynamics and axon regeneration. We found that autophagy induction promoted neurite outgrowth, attenuated the inhibitory effects of nonpermissive substrate myelin, and decreased the formation of retraction bulbs following axonal injury in cultured cortical neurons. Interestingly, autophagy induction stabilized microtubules by degrading SCG10, a microtubule disassembly protein in neurons. In mice with spinal cord injury, local administration of a specific autophagy-inducing peptide, Tat-beclin1, to lesion sites markedly attenuated axonal retraction of spinal dorsal column axons and cortical spinal tract and promoted regeneration of descending axons following long-term observation. Finally, administration of Tat-beclin1 improved the recovery of motor behaviors of injured mice. These results show a promising effect of an autophagy-inducing reagent on injured axons, providing direct evidence supporting a beneficial role of autophagy in axon regeneration.

scholarly journals The role of neurotrophic factors in nerve regeneration

2009 ◽  
Vol 26 (2) ◽  
pp. E3 ◽  
Author(s):  
Tessa Gordon
Keyword(s):  
Electrical Stimulation ◽  
Growth Factors ◽  
Schwann Cells ◽  
Neurotrophic Factors ◽  
Axon Regeneration ◽  
Nerve Repair ◽  
Low Frequency ◽  
Nerve Stump ◽  
Distal Nerve

This review considers the 2 sources of neurotrophic factors in the peripheral nervous system (PNS), the neurons and the nonneuronal cells in the denervated distal nerve stumps, and their role in axon regeneration. Morphological assessment of regenerative success in response to administration of exogenous growth factors after nerve injury and repair has indicated a role of the endogenous neurotrophic factors from Schwann cells in the distal nerve stump. However, the increased number of axons may reflect more neurons regenerating their axons and/or increased numbers of axon sprouts from the same number of neurons. Using fluorescent dyes to count neurons that regenerated their axons across a suture site and into distal nerve stumps, brain-derived neurotrophic factor (BDNF) and glial cell–derived neurotrophic factor (GDNF) were found not to increase the number of neurons that regenerated their axons after immediate nerve repair. Nevertheless, the factors did reverse the deleterious effect of delayed nerve repair, indicating that the axons that regenerate into the distal nerve stump normally have access to sufficient levels of endogenous neurotrophic factors to sustain their regeneration, while neurons that do not have access to these factors require exogenous factors to sustain axon regeneration. Neurons upregulate neurotrophic factors after axotomy. The upregulation is normally slow, beginning after 7 days and occurring in association with a protracted period of axonal regeneration in which axons grow out from the proximal nerve stump across a suture site over a period of 1 month in rodents. This staggered axon regeneration across the suture site is accelerated by a 1-hour period of low-frequency electrical stimulation that simultaneously accelerates the expression of BDNF and its trkB receptor in the neurons. Elevation of the level of BDNF after 2 days to > 3 times that found in unstimulated neurons was accompanied by elevation of the level of cAMP and followed by accelerated upregulation of growth-associated genes, tubulin, actin, and GAP-43 and downregulation of neurofilament protein. Elevation of cAMP levels via rolipram inhibition of phosphodiesterase 4 mimicked the effect of the low-frequency electrical stimulation. In conclusion, the enhanced upregulation of neurotrophic factors in the electrically stimulated axotomized neurons accelerates axon outgrowth into the distal nerve stumps where endogenous sources of growth factors in the Schwann cells support the regeneration of the axons toward the denervated targets. The findings provide strong support for endogenous neurotrophic factors of axotomized neurons and of denervated Schwann cells playing a critical role in supporting axon regeneration in the PNS.

scholarly journals Basal lamina of embryonic salivary epithelia. Production by the epithelium and role in maintaining lobular morphology.

1977 ◽  
Vol 73 (2) ◽  
pp. 445-463 ◽  
Author(s):  
S D Banerjee ◽  
R H Cohn ◽  
M R Bernfield
Keyword(s):  
Basal Lamina ◽  
Free Medium ◽  
Normal Morphology ◽  
Selective Degradation ◽  
Cellular Architecture ◽  
Salivary Epithelia ◽  
Testicular Hyaluronidase ◽  
Chondroitin Sulfate A ◽  
Cellular Alterations

The role of the basal lamina in maintaining the normal morphology of mouse embryo submandibular epithelia was assessed by examining its production as well as the cellular and organ culture changes associated with its removal and replacement. The lamina was removed from epithelia isolated free of mesenchyme by brief treatment with testicular hyaluronidase in the absence of calcium. The treatment causes rounding-up of the cells, loss of cellular cohesion, appearance of microvilli, and changes in the organization of cytoskeletal structures. The lamina is not removed and the cellular alterations do not occur in the absence of hyaluronidase in calcium-free medium or when both enzyme and calcium are present, possibly because digestion of chondroitin sulfate, a component of the lamina, is inhibited by calcium. Within 2 h after treatment, in the absence of mesenchyme or biological substrata, the epithelia deposits a new lamina, which is identical by several criteria to the preexisting lamina, and reverses the cellular alterations. Epithelia treated with hyaluronidase lose lobular morphology during culture with mesenchyme. Delaying culture with mesenchyme, to allow restoration of the lamina and of normal cellular architecture, prevents the loss of lobular morphology. The results indicate that the basal lamina imposes morphologic stability on the epithelium, while the mesenchyme apparently affects processes involved in changes in morphology, possibly by selective degradation of the basal lamina.

Sign in / Sign up

Export Citation Format

Share Document