PittsburghV1, Main, Exploration, bibRecord, 001693

Regulation of Intrinsic Axon Growth Ability at Retinal Ganglion Cell Growth Cones

Identifieur interne : 001693 ( Main/Exploration ); précédent : 001692; suivant : 001694

Regulation of Intrinsic Axon Growth Ability at Retinal Ganglion Cell Growth Cones

Auteurs : Michael B. Steketee [États-Unis] ; Carly Oboudiyat [États-Unis] ; Richard Daneman [États-Unis] ; Ephraim Trakhtenberg [États-Unis] ; Philip Lamoureux [États-Unis] ; Jessica E. Weinstein [États-Unis] ; Steve Heidemann [États-Unis] ; Ben A. Barres [États-Unis] ; Jeffrey L. Goldberg [États-Unis]

Source :

Investigative Ophthalmology & Visual Science [ 0146-0404 ] ; 2014.

RBID : PMC:4102390

Descripteurs français

KwdFr :
- Animaux, Animaux nouveau-nés, Axones (métabolisme), Cellules ganglionnaires rétiniennes (anatomopathologie), Cellules ganglionnaires rétiniennes (métabolisme), Contrainte mécanique, Cônes de croissance (métabolisme), Femelle, Modèles animaux de maladie humaine, Mâle, Nerf optique (anatomopathologie), Nerf optique (croissance et développement), Nerf optique (métabolisme), Neurones (anatomopathologie), Neurones (métabolisme), Prolifération cellulaire, Rat Sprague-Dawley, Rats, Régénération nerveuse, Rétinopathies (anatomopathologie), Rétinopathies (métabolisme).
MESH :
- anatomopathologie : Cellules ganglionnaires rétiniennes, Nerf optique, Neurones, Rétinopathies.
- croissance et développement : Nerf optique.
- métabolisme : Axones, Cellules ganglionnaires rétiniennes, Cônes de croissance, Nerf optique, Neurones, Rétinopathies.
- Animaux, Animaux nouveau-nés, Contrainte mécanique, Femelle, Modèles animaux de maladie humaine, Mâle, Prolifération cellulaire, Rat Sprague-Dawley, Rats, Régénération nerveuse.

English descriptors

KwdEn :
- Animals, Animals, Newborn, Axons (metabolism), Cell Proliferation, Disease Models, Animal, Female, Growth Cones (metabolism), Male, Nerve Regeneration, Neurons (metabolism), Neurons (pathology), Optic Nerve (growth & development), Optic Nerve (metabolism), Optic Nerve (pathology), Rats, Rats, Sprague-Dawley, Retinal Diseases (metabolism), Retinal Diseases (pathology), Retinal Ganglion Cells (metabolism), Retinal Ganglion Cells (pathology), Stress, Mechanical.
MESH :
- growth & development : Optic Nerve.
- metabolism : Axons, Growth Cones, Neurons, Optic Nerve, Retinal Diseases, Retinal Ganglion Cells.
- pathology : Neurons, Optic Nerve, Retinal Diseases, Retinal Ganglion Cells.
- Animals, Animals, Newborn, Cell Proliferation, Disease Models, Animal, Female, Male, Nerve Regeneration, Rats, Rats, Sprague-Dawley, Stress, Mechanical.

Abstract

Purpose.

Mammalian central nervous system neurons fail to regenerate after injury or disease, in part due to a progressive loss in intrinsic axon growth ability after birth. Whether lost axon growth ability is due to limited growth resources or to changes in the axonal growth cone is unknown.

Methods.

Static and time-lapse images of purified retinal ganglion cells (RGCs) were analyzed for axon growth rate and growth cone morphology and dynamics without treatment and after manipulating Kruppel-like transcription factor (KLF) expression or applying mechanical tension.

Results.

Retinal ganglion cells undergo a developmental switch in growth cone dynamics that mirrors the decline in postnatal axon growth rates, with increased filopodial adhesion and decreased lamellar protrusion area in postnatal axonal growth cones. Moreover, expressing growth-suppressive KLF4 or growth-enhancing KLF6 transcription factors elicits similar changes in postnatal growth cones that correlate with axon growth rates. Postnatal RGC axon growth rate is not limited by an inability to achieve axon growth rates similar to embryonic RGCs; indeed, postnatal axons support elongation rates up to 100-fold faster than postnatal axonal growth rates. Rather, the intrinsic capacity for rapid axon growth is due to both growth cone pausing and retraction, as well as to a slightly decreased ability to achieve rapid instantaneous rates of forward progression. Finally, we observed that RGC axon and dendrite growth are regulated independently in vitro.

Conclusions.

Together, these data support the hypothesis that intrinsic axon growth rate is regulated by an axon-specific growth program that differentially regulates growth cone motility.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4102390

DOI: 10.1167/iovs.14-13882
PubMed: 24906860
PubMed Central: 4102390

Affiliations:

Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term>
<term>Animals, Newborn</term>
<term>Axons (metabolism)</term>
<term>Cell Proliferation</term>
<term>Disease Models, Animal</term>
<term>Female</term>
<term>Growth Cones (metabolism)</term>
<term>Male</term>
<term>Nerve Regeneration</term>
<term>Neurons (metabolism)</term>
<term>Neurons (pathology)</term>
<term>Optic Nerve (growth & development)</term>
<term>Optic Nerve (metabolism)</term>
<term>Optic Nerve (pathology)</term>
<term>Rats</term>
<term>Rats, Sprague-Dawley</term>
<term>Retinal Diseases (metabolism)</term>
<term>Retinal Diseases (pathology)</term>
<term>Retinal Ganglion Cells (metabolism)</term>
<term>Retinal Ganglion Cells (pathology)</term>
<term>Stress, Mechanical</term>
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<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Animaux nouveau-nés</term>
<term>Axones (métabolisme)</term>
<term>Cellules ganglionnaires rétiniennes (anatomopathologie)</term>
<term>Cellules ganglionnaires rétiniennes (métabolisme)</term>
<term>Contrainte mécanique</term>
<term>Cônes de croissance (métabolisme)</term>
<term>Femelle</term>
<term>Modèles animaux de maladie humaine</term>
<term>Mâle</term>
<term>Nerf optique (anatomopathologie)</term>
<term>Nerf optique (croissance et développement)</term>
<term>Nerf optique (métabolisme)</term>
<term>Neurones (anatomopathologie)</term>
<term>Neurones (métabolisme)</term>
<term>Prolifération cellulaire</term>
<term>Rat Sprague-Dawley</term>
<term>Rats</term>
<term>Régénération nerveuse</term>
<term>Rétinopathies (anatomopathologie)</term>
<term>Rétinopathies (métabolisme)</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Cellules ganglionnaires rétiniennes</term>
<term>Nerf optique</term>
<term>Neurones</term>
<term>Rétinopathies</term>
</keywords>
<keywords scheme="MESH" qualifier="croissance et développement" xml:lang="fr"><term>Nerf optique</term>
</keywords>
<keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>Optic Nerve</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Axons</term>
<term>Growth Cones</term>
<term>Neurons</term>
<term>Optic Nerve</term>
<term>Retinal Diseases</term>
<term>Retinal Ganglion Cells</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Axones</term>
<term>Cellules ganglionnaires rétiniennes</term>
<term>Cônes de croissance</term>
<term>Nerf optique</term>
<term>Neurones</term>
<term>Rétinopathies</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Neurons</term>
<term>Optic Nerve</term>
<term>Retinal Diseases</term>
<term>Retinal Ganglion Cells</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Animals, Newborn</term>
<term>Cell Proliferation</term>
<term>Disease Models, Animal</term>
<term>Female</term>
<term>Male</term>
<term>Nerve Regeneration</term>
<term>Rats</term>
<term>Rats, Sprague-Dawley</term>
<term>Stress, Mechanical</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Animaux nouveau-nés</term>
<term>Contrainte mécanique</term>
<term>Femelle</term>
<term>Modèles animaux de maladie humaine</term>
<term>Mâle</term>
<term>Prolifération cellulaire</term>
<term>Rat Sprague-Dawley</term>
<term>Rats</term>
<term>Régénération nerveuse</term>
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<front><div type="abstract" xml:lang="en"><sec id="st1"><title>Purpose.</title>
<p>Mammalian central nervous system neurons fail to regenerate after injury or disease, in part due to a progressive loss in intrinsic axon growth ability after birth. Whether lost axon growth ability is due to limited growth resources or to changes in the axonal growth cone is unknown.</p>
</sec>
<sec id="st2"><title>Methods.</title>
<p>Static and time-lapse images of purified retinal ganglion cells (RGCs) were analyzed for axon growth rate and growth cone morphology and dynamics without treatment and after manipulating Kruppel-like transcription factor (KLF) expression or applying mechanical tension.</p>
</sec>
<sec id="st3"><title>Results.</title>
<p>Retinal ganglion cells undergo a developmental switch in growth cone dynamics that mirrors the decline in postnatal axon growth rates, with increased filopodial adhesion and decreased lamellar protrusion area in postnatal axonal growth cones. Moreover, expressing growth-suppressive KLF4 or growth-enhancing KLF6 transcription factors elicits similar changes in postnatal growth cones that correlate with axon growth rates. Postnatal RGC axon growth rate is not limited by an inability to achieve axon growth rates similar to embryonic RGCs; indeed, postnatal axons support elongation rates up to 100-fold faster than postnatal axonal growth rates. Rather, the intrinsic capacity for rapid axon growth is due to both growth cone pausing and retraction, as well as to a slightly decreased ability to achieve rapid instantaneous rates of forward progression. Finally, we observed that RGC axon and dendrite growth are regulated independently in vitro.</p>
</sec>
<sec id="st4"><title>Conclusions.</title>
<p>Together, these data support the hypothesis that intrinsic axon growth rate is regulated by an axon-specific growth program that differentially regulates growth cone motility.</p>
</sec>
</div>
</front>
</TEI>
<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Californie</li>
<li>Floride</li>
<li>Michigan</li>
<li>Pennsylvanie</li>
</region>
<settlement><li>East Lansing</li>
<li>Pittsburgh</li>
</settlement>
<orgName><li>Université d'État du Michigan</li>
<li>Université de Pittsburgh</li>
</orgName>
</list>
<tree><country name="États-Unis"><region name="Floride"><name sortKey="Steketee, Michael B" sort="Steketee, Michael B" uniqKey="Steketee M" first="Michael B." last="Steketee">Michael B. Steketee</name>
</region>
<name sortKey="Barres, Ben A" sort="Barres, Ben A" uniqKey="Barres B" first="Ben A." last="Barres">Ben A. Barres</name>
<name sortKey="Daneman, Richard" sort="Daneman, Richard" uniqKey="Daneman R" first="Richard" last="Daneman">Richard Daneman</name>
<name sortKey="Goldberg, Jeffrey L" sort="Goldberg, Jeffrey L" uniqKey="Goldberg J" first="Jeffrey L." last="Goldberg">Jeffrey L. Goldberg</name>
<name sortKey="Goldberg, Jeffrey L" sort="Goldberg, Jeffrey L" uniqKey="Goldberg J" first="Jeffrey L." last="Goldberg">Jeffrey L. Goldberg</name>
<name sortKey="Heidemann, Steve" sort="Heidemann, Steve" uniqKey="Heidemann S" first="Steve" last="Heidemann">Steve Heidemann</name>
<name sortKey="Lamoureux, Philip" sort="Lamoureux, Philip" uniqKey="Lamoureux P" first="Philip" last="Lamoureux">Philip Lamoureux</name>
<name sortKey="Oboudiyat, Carly" sort="Oboudiyat, Carly" uniqKey="Oboudiyat C" first="Carly" last="Oboudiyat">Carly Oboudiyat</name>
<name sortKey="Steketee, Michael B" sort="Steketee, Michael B" uniqKey="Steketee M" first="Michael B." last="Steketee">Michael B. Steketee</name>
<name sortKey="Trakhtenberg, Ephraim" sort="Trakhtenberg, Ephraim" uniqKey="Trakhtenberg E" first="Ephraim" last="Trakhtenberg">Ephraim Trakhtenberg</name>
<name sortKey="Weinstein, Jessica E" sort="Weinstein, Jessica E" uniqKey="Weinstein J" first="Jessica E." last="Weinstein">Jessica E. Weinstein</name>
</country>
</tree>
</affiliations>
</record>

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Regulation of Intrinsic Axon Growth Ability at Retinal Ganglion Cell Growth Cones

Regulation of Intrinsic Axon Growth Ability at Retinal Ganglion Cell Growth Cones

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