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Actions of Secreted Phosphoprotein 1 in the Bovine Corpus Luteum and the Role of Resident T Lymphocytes during Luteolysis

Poole, Daniel Heath
http://rave.ohiolink.edu/etdc/view?acc_num=osu1250361867

Abstract Details

2009, Doctor of Philosophy, Ohio State University, Animal Sciences.
Lymphocytes are present in the fully functional corpus luteum (CL) and have been shown to proliferate during luteal regression due to migration into, as well as proliferation within, the tissue. Secreted phosphoprotein 1 (SPP1) is a multifunctional extracellular matrix protein. It is hypothesized that bovine luteal cells synthesize SPP1, which acts as a paracrine regulator of immune and other cells of the parenchyma during luteal regression. Thus the objectives of the present study were to: 1) Identify SPP1 expression and its regulators throughout the bovine estrous cycle 2) investigate if removal of SPP1 inhibits lymphocyte migration and proliferation 3) determine if luteal function directs specialization of resident T lymphocyte (RTC) subsets, 4) investigate if the expression of proinflammatory and antiinflammatory cytokines of RTC change in response to prostaglandin (PG) F 2alpha . Corpora lutea (CL) were removed on days 4, 5, 10–12, and 18 of the estrous cycle, and at 0.5, 1, 4, 8 and 12 hours after a luteolytic injection of PGF 2alpha to evaluate the role of SPP1 in the CL. Additionally, peripheral and resident T lymphocytes from either functional or regressing CL (collected 8 hr after a luteolytic injection of PGF 2alpha were isolated from whole blood and from dissociated luteal cell suspensions immunomagnetically by positive selection for cell surface proteins (CD2 and gamma delta). Secreted phosphoprotein 1 is temporally regulated throughout the estrous cycle and stimulated in vitro by luteolytic stimulators, PGF 2alpha and TNF alpha . Additionally, these analyses revealed differences in the percentage of regulatory, pro- and antiinflammatory lymphocytes in the resident T lymphocyte population, depending on luteal status. It is concluded that when the CL is fully functional, resident T lymphocytes are predominately antiinflammatory and may serve as regulatory T lymphocytes to facilitate survival and differentiation of various specialized T lymphocyte subsets. However, upon the induction of luteolysis with PGF 2alpha , the proportion of proinflammatory lymphocytes increases and tolerance toward luteal proteins may be reduced. These data demonstrate a functional shift from antiinflammatory to proinflammatory phenotypes of T lymphocyte subsets isolated from the corpus luteum. Based on these data, it is proposed that lymphocytes encounter a novel means of lymphocyte regulation and/or differentiation within the CL.
Joy Pate, PhD (Committee Chair)
Michael Day, PhD (Committee Co-Chair)
John Sheridan, PhD (Committee Member)
Sandra Velleman, PhD (Committee Member)
251 p.
Agriculture; Animals; Immunology
Corpus Luteum; Secreted Phosphoprotein 1; Lymphocytes;

Recommended Citations

Citations

  • Poole, D. H. (2009). Actions of Secreted Phosphoprotein 1 in the Bovine Corpus Luteum and the Role of Resident T Lymphocytes during Luteolysis [Doctoral dissertation, Ohio State University]. OhioLINK Electronic Theses and Dissertations Center. http://rave.ohiolink.edu/etdc/view?acc_num=osu1250361867

    APA Style (7th edition)

  • Poole, Daniel. Actions of Secreted Phosphoprotein 1 in the Bovine Corpus Luteum and the Role of Resident T Lymphocytes during Luteolysis. 2009. Ohio State University, Doctoral dissertation. OhioLINK Electronic Theses and Dissertations Center, http://rave.ohiolink.edu/etdc/view?acc_num=osu1250361867.

    MLA Style (8th edition)

  • Poole, Daniel. "Actions of Secreted Phosphoprotein 1 in the Bovine Corpus Luteum and the Role of Resident T Lymphocytes during Luteolysis." Doctoral dissertation, Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1250361867

    Chicago Manual of Style (17th edition)

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© 2009, all rights reserved.
This open access ETD is published by The Ohio State University and OhioLINK.