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Thread: New clues to why nerve cells fail to grow in scar tissue

  1. #1

    New clues to why nerve cells fail to grow in scar tissue

    New clues to why nerve cells fail to grow in scar tissue

    4 April 2011

    A new study led by researchers at the Wellcome Trust Centre for Human Genetics, University of Oxford, has shown how the battle between two competing molecules can determine whether nerve cells grow and migrate or whether, in the case of scar tissue, they are inhibited, severely limiting recovery from damage to the central nervous system.

    The regeneration of nerve cells within and across scar tissue is inhibited by a molecule known as chondroitin sulphate proteoglycan (CSPG), which is produced in large amounts in scar tissue after damage to the nervous system. Previous work has shown that this molecule interacts with a protein found on the surface of the nerve cells, essentially switching cell movement 'off' (1).
    In a new study, published online in the journal 'Science', researchers have shown that a closely related family of molecules, the heparan sulphate proteoglycans (HSPGs), typically promote nerve growth by acting on this same protein switch to turn 'on' cell growth (2). In fact, both types of molecule act on the same component of the switch, known as a receptor, as revealed by high-resolution structural work performed at the UK synchrotron facility, the Diamond Light Source.
    "These two molecules target exactly the same site on this protein switch, which poses the question: how can they produce opposing effects on the growth of nerve cells?" says Dr Radu Aricescu.
    The new research suggests that HSPGs are able to bind together multiple copies of the receptor, creating clusters of the protein on the surface of the nerve cell. This allows signalling to other proteins inside the cells responsible for cell movement. Without this signal, the nerve cells are unable to move into the damaged tissue.
    "Earlier work suggested that drugs blocking the interaction of CSPG with the protein switch would be beneficial to nerve regeneration," says Dr Charlotte Coles, first author of the study and a Wellcome Trust PhD student at the time of the research. "Our work has added an unexpected twist to the story, however: such molecules would also block the positive effect of HSPGs, so the benefits would be minimal, if any."
    The researchers believe that drugs that promote the clustering activity - thus mimicking the action of HSPGs rather than simply blocking CSPG interactions - are likely to prove beneficial in aiding nerve regeneration after nervous system injury.
    The research was carried out in collaboration with scientists at the University of Manchester, Harvard Medical School and Columbia University.


    http://www.wellcome.ac.uk/News/2011/News/WTVM050762.htm


  2. #2
    Senior Member JEAPOW's Avatar
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    so why can't they come with anything to promote nerve cell growth?

    thread very interesting seems like such a slow process to try to heal. I alm L1 frac inc and so much of my nerve growth depends on my pain, my neuropothy, and my walking guess I am venting,I know we all want to get better so I pray they find more cures.

    thanks..
    JeAnNE L1Burst Fracture inc. 11/5/10

    Live Well--Laugh often

  3. #3
    This is a very interesting finding I think.
    I am curious to hear what all the "fans" of chondritinase has to say about that.

    Paolo
    In God we trust; all others bring data. - Edwards Deming

  4. #4
    Wow, very interesting.

    Agree with you Paolo, it would be great to hear from the Chondroitinase and Decorin guys about this.

  5. #5
    It seems to me that breaking down chondroitin-6-sulfate-proteoglycan by chondroitinase is still a good way to block the inhibitory effects of this molecule. Let me read the article and comment more later. Wise.

    Quote Originally Posted by KofQ View Post
    New clues to why nerve cells fail to grow in scar tissue

    4 April 2011

    A new study led by researchers at the Wellcome Trust Centre for Human Genetics, University of Oxford, has shown how the battle between two competing molecules can determine whether nerve cells grow and migrate or whether, in the case of scar tissue, they are inhibited, severely limiting recovery from damage to the central nervous system.

    The regeneration of nerve cells within and across scar tissue is inhibited by a molecule known as chondroitin sulphate proteoglycan (CSPG), which is produced in large amounts in scar tissue after damage to the nervous system. Previous work has shown that this molecule interacts with a protein found on the surface of the nerve cells, essentially switching cell movement 'off' (1).
    In a new study, published online in the journal 'Science', researchers have shown that a closely related family of molecules, the heparan sulphate proteoglycans (HSPGs), typically promote nerve growth by acting on this same protein switch to turn 'on' cell growth (2). In fact, both types of molecule act on the same component of the switch, known as a receptor, as revealed by high-resolution structural work performed at the UK synchrotron facility, the Diamond Light Source.
    "These two molecules target exactly the same site on this protein switch, which poses the question: how can they produce opposing effects on the growth of nerve cells?" says Dr Radu Aricescu.
    The new research suggests that HSPGs are able to bind together multiple copies of the receptor, creating clusters of the protein on the surface of the nerve cell. This allows signalling to other proteins inside the cells responsible for cell movement. Without this signal, the nerve cells are unable to move into the damaged tissue.
    "Earlier work suggested that drugs blocking the interaction of CSPG with the protein switch would be beneficial to nerve regeneration," says Dr Charlotte Coles, first author of the study and a Wellcome Trust PhD student at the time of the research. "Our work has added an unexpected twist to the story, however: such molecules would also block the positive effect of HSPGs, so the benefits would be minimal, if any."
    The researchers believe that drugs that promote the clustering activity - thus mimicking the action of HSPGs rather than simply blocking CSPG interactions - are likely to prove beneficial in aiding nerve regeneration after nervous system injury.
    The research was carried out in collaboration with scientists at the University of Manchester, Harvard Medical School and Columbia University.


    http://www.wellcome.ac.uk/News/2011/News/WTVM050762.htm


  6. #6
    come on guys sounds to me that if we make an all out push in research and attack in this area we might be looking at [may i be bold enough to say it] a possible CURE. at the least prove it not to be the case. i say all out attack on this BUT after all i am simply a layman. poobear

  7. #7
    Poobear, we're all laymen,but have the same desires that you do. I can tell you that your posts and persistence are well accepted and give us all hope to the end you've described. Gerons will presenting their findings for the first spinal pateint to recieve thier therapy of embryonic stem cells. This annoucnement will be made in June as I see it. I hope it will present a first in successful therapy. In the meantime, anything we can find of new therapies that are being conducted is what we all need.

    keeping on

  8. #8
    Senior Member Imight's Avatar
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    interesting.

    marked.

  9. #9
    Quote Originally Posted by Wise Young View Post
    It seems to me that breaking down chondroitin-6-sulfate-proteoglycan by chondroitinase is still a good way to block the inhibitory effects of this molecule. Let me read the article and comment more later. Wise.
    Wise,
    I hope we'll have some time to talk about that in Brescia. I am more confused then ever about chondroitinase.
    I also hope we'll have some fun too :-)

    Paolo
    In God we trust; all others bring data. - Edwards Deming

  10. #10
    Quote Originally Posted by paolocipolla View Post
    Wise,
    I hope we'll have some time to talk about that in Brescia. I am more confused then ever about chondroitinase.
    I also hope we'll have some fun too :-)

    Paolo
    There are several ways to overcome inhibitory extracellular matrix molecules, such as chondroitin-6-sulfate-proteoglycan (CSPG). One way is to break down CSPG with chondroitinase. This has been used successfully by many dozens of laboratories. Although a single injection of chondroitinase into a contused spinal cord will clear most CSPG from 2 cm around the injection site for several weeks and it will return only as more CSPG is made and secrete by astrocytes in the area.

    Chondroitinase, however, has several weaknesses as a therapy. First, it is an enzyme that is relatively unstable at body temperatures. Therefore, if one wants to keep the tissue free of CSPG for a long time, one has to give repeated injections of the enzyme. Recently, a more stable version of the enzyme was reported. Second, it is a enzyme made by a common bacteria and many people may have antibodies against this enzyme. Third, there may be other growth inhibitors. Fourth, CSPG does play an important role in restricting cell migration and growth.

    Nevertheless, I think that it is a very useful enzyme that can be used create a several-week long "window" for axons to cross the injury site. Used in combination with a cellular bridge and other blockers of axonal growth inhibitors, it may well work. Note that it is possible to get axons to ignore CSPG by increase cAMP levels inside the axons. Likewise, lithium is known to stimulate axons to grow across areas of CSPG.

    Wise.

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