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Torres-Palsa Dissertation 2016.pdf (2.87 MB)

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ICAM-1 in Skeletal Muscle Disease and Regeneration

Torres-Palsa, Maria Jose
http://rave.ohiolink.edu/etdc/view?acc_num=toledo1461860958

Abstract Details

2016, Doctor of Philosophy, University of Toledo, Exercise Science.
Skeletal muscle tissue has the unique ability to restore its structure and function after sustaining trauma and disease. The primary purpose of this research dissertation is to gain insight into the interactions between skeletal muscle regeneration and ICAM-1, an important protein of the inflammatory process and primary ligand for myeloid cells. The present study uses two murine models to characterize the expression and localization of ICAM-1 in skeletal muscle disease and regeneration. First, the hypothesis that ICAM-1 is expressed by myofibers and myeloid cells in dystrophin-deficient mice was tested. In muscles from Duchenne muscular dystrophy (mdx) mice, western blot revealed increased expression of ICAM-1 compared to control. ICAM-1 was expressed on the membrane of necrotic, injured, and regenerating myofibers and by CD11b+ myeloid cells in mdx muscles during the degenerative and regenerative stages of the pathology. CD11b+ myeloid cells were closely associated with the membrane of ICAM-1 myofibers and within necrotic myofibers. These observations may indicate that myofiber expression of ICAM-1 serves as a mechanism by which myeloid cells attach to skeletal muscle and exacerbate the myopathy in mdx mice. Next, the hypotheses that ICAM-1 expression was elevated after skeletal muscle injury and that its expression contributes to muscle regeneration were tested. EDL muscles of wild type and ICAM-1-/- mice were injected with cardiotoxin to induce muscle injury and markers of regeneration (percentage of regenerating myofibers, eMHC expression, and CSA of regenerating myofibers) were measured at 5, 7, 10, and 14 days of recovery. Western blot revealed elevated expression of ICAM-1 in wild type muscles after injury compared to control. ICAM-1 was expressed on the membrane of normal and regenerating myofibers and by CD11b+ myeloid cells in wild type muscles after injury. At 10 days after injury, CSA of regenerating myofibers was significantly elevated in wild type muscles compared to ICAM-1-/-, but similar between strains 14 days after injury. The percentage of regenerating myofibers and the expression of eMHC after injury were similar between wild type and ICAM-1-/- injured muscles. These findings indicate that the absence of ICAM-1 does not impair regeneration but may delay the growth of regenerating myofibers after injury. Overall, the novel findings in this study characterize the expression and localization of ICAM-1 in skeletal muscle disease and regeneration, and provide us with a greater insight on potential mechanisms by which its expression may contribute to muscle regeneration.
Francis X. Pizza (Committee Chair)
Thomas J. McLoughlin (Committee Member)
Abraham D. Lee (Committee Member)
Michael A. Tevald (Committee Member)
87 p.
Biology; Kinesiology; Physiology
ICAM-1; skeletal muscle; regeneration; mdx; inflammatory response; adhesion molecule; muscle injury

Recommended Citations

Citations

  • Torres-Palsa, M. J. (2016). ICAM-1 in Skeletal Muscle Disease and Regeneration [Doctoral dissertation, University of Toledo]. OhioLINK Electronic Theses and Dissertations Center. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1461860958

    APA Style (7th edition)

  • Torres-Palsa, Maria Jose. ICAM-1 in Skeletal Muscle Disease and Regeneration. 2016. University of Toledo, Doctoral dissertation. OhioLINK Electronic Theses and Dissertations Center, http://rave.ohiolink.edu/etdc/view?acc_num=toledo1461860958.

    MLA Style (8th edition)

  • Torres-Palsa, Maria Jose. "ICAM-1 in Skeletal Muscle Disease and Regeneration." Doctoral dissertation, University of Toledo, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1461860958

    Chicago Manual of Style (17th edition)

toledo1461860958
425
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This open access ETD is published by University of Toledo and OhioLINK.