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    Angiotensin-(1-7)/Mas receptor as an antinociceptive agent in cancer-induced bone pain

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    Author
    Forte, Brittany L.
    Slosky, Lauren M.
    Zhang, Hong
    Arnold, Moriah R.
    Staatz, William D.
    Hay, Meredith
    Largent-Milnes, Tally M.
    Vanderah, Todd W.
    Affiliation
    Univ Arizona, Coll Med, Dept Pharmacol
    Univ Arizona, Coll Med, Dept Physiol, Evelyn McKnight Brain Inst
    Issue Date
    2016-12
    Keywords
    Angiotensin 1-7
    MasR
    Breast
    Cancer
    Pain
    Chronic
    
    Metadata
    Show full item record
    Publisher
    LIPPINCOTT WILLIAMS & WILKINS
    Citation
    Angiotensin-(1-7)/Mas receptor as an antinociceptive agent in cancer-induced bone pain 2016, 157 (12):2709 PAIN
    Journal
    PAIN
    Rights
    This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License 4.0 (CC BY-NC-ND), which permits downloading and sharing the work provided it is properly cited. The work cannot be changed in any way or used commercially.
    Collection Information
    This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.
    Abstract
    Many cancerous solid tumors metastasize to the bone and induce pain (cancer-induced bone pain [CIBP]). Cancer-induced bone pain is often severe because of enhanced inflammation, rapid bone degradation, and disease progression. Opioids are prescribed to manage this pain, but they may enhance bone loss and increase tumor proliferation, further compromising patient quality of life. Angiotensin-(1-7) (Ang-(1-7)) binds and activates the Mas receptor (MasR). Angiotensin-(1-7)/MasR activation modulates inflammatory signaling after acute tissue insult, yet no studies have investigated whether Ang-(1-7)/MasR play a role in CIBP. We hypothesized that Ang-(1-7) inhibits CIBP by targeting MasR in a murine model of breast CIBP. 66.1 breast cancer cells were implanted into the femur of BALB/cAnNHsd mice as a model of CIBP. Spontaneous and evoked pain behaviors were assessed before and after acute and chronic administration of Ang-(1-7). Tissues were collected from animals for ex vivo analyses of MasR expression, tumor burden, and bone integrity. Cancer inoculation increased spontaneous pain behaviors by day 7 that were significantly reduced after a single injection of Ang-(1-7) and after sustained administration. Preadministration of A-779 a selective MasR antagonist prevented this reduction, whereas pretreatment with the AT(2) antagonist had no effect; an AT(1) antagonist enhanced the antinociceptive activity of Ang-(1-7) in CIBP. Repeated Ang-(1-7) administration did not significantly change tumor burden or bone remodeling. Data here suggest that Ang-(1-7)/MasR activation significantly attenuates CIBP, while lacking many side effects seen with opioids. Thus, Ang-(1-7) may be an alternative therapeutic strategy for the nearly 90% of patients with advanced-stage cancer who experience excruciating pain.
    Note
    Open access article.
    ISSN
    0304-3959
    PubMed ID
    27541850
    DOI
    10.1097/j.pain.0000000000000690
    Version
    Final published version
    Sponsors
    College of Medicine at the University of Arizona; NIH- NCI [R01 CA142115-01]
    Additional Links
    http://content.wkhealth.com/linkback/openurl?sid=WKPTLP:landingpage&an=00006396-201612000-00011
    ae974a485f413a2113503eed53cd6c53
    10.1097/j.pain.0000000000000690
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