Reading PAGE

Peer Evaluation activity

Downloads 3
Followed by 1
Following... 1

Total impact ?

    Send a

    Werner has...

    Trusted 0
    Reviewed 0
    Emailed 0
    Shared/re-used 0
    Discussed 0
    Invited 0
    Collected 0

     

    This was brought to you by:

    block this user Werner Muller

    Professor

    Faculty of Life Science, University of Manchester, Manchester

    Preconditioning-induced protection of photoreceptors requires activation of the signal-transducing receptor gp130 in photoreceptors

    Export to Mendeley

    Retinal degenerations are a class of neurodegenerative disorders that ultimately lead to blindness due to the death of retinal photoreceptors. In most cases, death is the result of long-term exposure to environmental, inflammatory, and genetic insults. In age-related macular degeneration, significant vision loss may take up to 70-80 years to develop. The protracted time to develop blindness suggests that retinal neurons have an endogenous mechanism for protection from chronic injury. Previous studies have shown that endogenous protective mechanisms can be induced by preconditioning animals with sublethal bright cyclic light. Such preconditioning can protect photoreceptors from a subsequent damaging insult and is thought to be accomplished through induced expression of protective factors. Some of the factors shown to be associated with protection bind and activate the signal transducing receptor gp130. To determine whether stress-induced endogenous protection of photoreceptors requires gp130, we generated conditional gp130 knockout (KO) mice with the Cre/lox system and used light-preconditioning to induce neuroprotection in these mice. Functional and morphological analyses demonstrated that the retina-specific gp130 KO impaired preconditioning-induced endogenous protection. Photoreceptor-specific gp130 KO mice had reduced protection, although the Müller cell KO mice did not, thus gp130-induced protection was restricted to photoreceptors. Using an animal model of retinitis pigmentosa, we found that the photoreceptor-specific gp130 KO increased sensitivity to genetically induced photoreceptor cell death, demonstrating that gp130 activation in photoreceptors had a general protective role independent of whether stress was caused by light or genetic mutations.

    Oh la laClose

    Your session has expired but don’t worry, your message
    has been saved.Please log in and we’ll bring you back
    to this page. You’ll just need to click “Send”.

    Your evaluation is of great value to our authors and readers. Many thanks for your time.

    Review Close

    Short review
    Select a comment
    Select a grade
    You and the author
    Anonymity My review is anonymous( Log in  or  Register )
    publish
    Close

    When you're done, click "publish"

    Only blue fields are mandatory.

    Relation to the author*
    Overall Comment*
    Anonymity* My review is anonymous( Log in  or  Register )
     

    Focus & Objectives*

    Have the objectives and the central topic been clearly introduced?

    Novelty & Originality*

    Do you consider this work to be an interesting contribution to knowledge?

    Arrangement, Transition and Logic

    Are the different sections of this work well arranged and distributed?

    Methodology & Results

    Is the author's methodology relevant to both the objectives and the results?

    Data Settings & Figures

    Were tables and figures appropriate and well conceived?

    References and bibliography

    Is this work well documented and has the bibliography been properly established?

    Writing

    Is this work well written, checked and edited?

    Write Your Review (you can paste text as well)
    Please be civil and constructive. Thank you.


    Grade (optional, N/A by default)

    N/A 1 1.5 2 2.5 3 3.5 4 4.5 5 5.5 6 6.5 7 7.5 8 8.5 9 9.5 10
    Close

    Your mailing list is currently empty.
    It will build up as you send messages
    and links to your peers.

     No one besides you has access to this list.
    Close
    Enter the e-mail addresses of your recipients in the box below.  Note: Peer Evaluation will NOT store these email addresses   log in
    Your recipients

    Your message:

    Your email : Your email address will not be stored or shared with others.

    Your message has been sent.

    Description

    Title : Preconditioning-induced protection of photoreceptors requires activation of the signal-transducing receptor gp130 in photoreceptors
    Author(s) : Y. Ueki, Y.-Z. Le, S. Chollangi, W. Muller, J. D. Ash
    Abstract : Retinal degenerations are a class of neurodegenerative disorders that ultimately lead to blindness due to the death of retinal photoreceptors. In most cases, death is the result of long-term exposure to environmental, inflammatory, and genetic insults. In age-related macular degeneration, significant vision loss may take up to 70-80 years to develop. The protracted time to develop blindness suggests that retinal neurons have an endogenous mechanism for protection from chronic injury. Previous studies have shown that endogenous protective mechanisms can be induced by preconditioning animals with sublethal bright cyclic light. Such preconditioning can protect photoreceptors from a subsequent damaging insult and is thought to be accomplished through induced expression of protective factors. Some of the factors shown to be associated with protection bind and activate the signal transducing receptor gp130. To determine whether stress-induced endogenous protection of photoreceptors requires gp130, we generated conditional gp130 knockout (KO) mice with the Cre/lox system and used light-preconditioning to induce neuroprotection in these mice. Functional and morphological analyses demonstrated that the retina-specific gp130 KO impaired preconditioning-induced endogenous protection. Photoreceptor-specific gp130 KO mice had reduced protection, although the Müller cell KO mice did not, thus gp130-induced protection was restricted to photoreceptors. Using an animal model of retinitis pigmentosa, we found that the photoreceptor-specific gp130 KO increased sensitivity to genetically induced photoreceptor cell death, demonstrating that gp130 activation in photoreceptors had a general protective role independent of whether stress was caused by light or genetic mutations.
    Keywords : il6 signal transducing receptor, neuroprotection, conditional gp130 knockout, inherited retinal degeneration, light damage

    Subject : unspecified
    Area : Other
    Language : English
    Year : 2009

    Affiliations Faculty of Life Science, University of Manchester, Manchester
    Journal : Proceedings of the National Academy of Sciences
    Volume : 106
    Issue : 50
    Publisher : National Academy of Sciences
    Pages : 21389 - 21394
    Url : http://www.pnas.org/cgi/doi/10.1073/pnas.0906156106
    Doi : 10.1073/pnas.0906156106

    Leave a comment

    This contribution has not been reviewed yet. review?

    You may receive the Trusted member label after :

    • Reviewing 10 uploads, whatever the media type.
    • Being trusted by 10 peers.
    • If you are blocked by 10 peers the "Trust label" will be suspended from your page. We encourage you to contact the administrator to contest the suspension.

    Does this seem fair to you? Please make your suggestions.

    Please select an affiliation to sign your evaluation:

    Cancel Evaluation Save

    Please select an affiliation:

    Cancel   Save

    Werner's Peer Evaluation activity

    Downloads 3
    Followed by 1
    • Mahendra Kumar Trivedi, Independent researcher, Las Vegas Naveda, Trivedi Global Inc., Trivedi Science Research Laboratory Pvt. Ltd.
    Following... 1

    Werner has...

    Trusted 0
    Reviewed 0
    Emailed 0
    Shared/re-used 0
    Discussed 0
    Invited 0
    Collected 0
    Invite this peer to...
    Title
    Start date (dd/mm/aaaa)
    Location
    URL
    Message
    send
    Close

    Full Text request

    Your request will be sent.

    Please enter your email address to be notified
    when this article becomes available

    Your email


     
    Your email address will not be shared or spammed.