rdf-syntax-grammar
mods:
  schema location: http://www.loc.gov/mods/v3 http://www.loc.gov/standards/mods/v3/mods-3-2.xsd
  title info:
    title: MicroRNA-223 Regulates Macrophage Polarization and Diet-induced Insulin Resistance
  name:
    name part: Meng, Cong
    role:
      role term: creator
    role:
      role term: author.
  name:
    name part: Zhou, Beiyan
    role:
      role term: thesis advisor.
  name:
    name part: Texas A & M University
    role:
      role term: degree granting institution.
  type of resource: text
  genre: bibliography
  origin info:
    place:
      place term: txu
    date issued: 2013
    issuance: monographic
  language:
    language term: eng
  physical description:
    form: remote
    extent: 1 online resource.
  abstract: Macrophage activation plays a crucial role in regulating adipose tissue inflammation and is a major contributor to the pathogenesis of obesity-associated cardiovascular diseases. On various types of stimuli, macrophages respond with either classic (M1) or alternative (M2) activation. M1- and M2-mediated signaling pathways and corresponding cytokine production profiles are not completely understood. The discovery of microRNAs provides a new opportunity to understand this complicated but crucial network for macrophage activation and adipose tissue function. We have examined the activity of microRNA-223 (miR-223) and its role in controlling macrophage functions in adipose tissue inflammation and systemic insulinresistance. miR-223-/- mice on a high-fat diet exhibited an increased severity of systemic insulin resistance compared with wild-type mice that was accompanied by a marked increase in adipose tissue inflammation. The specific regulatory effects of miR-223 in myeloid cell-mediated regulation of adipose tissue inflammation and insulin resistance were then confirmed by transplantation analysis. Moreover, using bone marrow-derived macrophages, we demonstrated that miR-223 is a novel regulator of macrophage polarization, which suppresses classic pro-inflammatory pathways and enhances the alternative anti-inflammatory responses. In addition, we identified Pknox1 as a genuine miR-223 target gene and an essential regulator for macrophage polarization. For the first time, this study demonstrates that miR-223 acts to inhibit Pknox 1,suppressing pro-inflammatory activation of macrophages; thus, it is a crucial regulator of macrophage polarization and protects against diet-induced adipose tissue inflammatory response and systemic insulin resistance. The electronic version of this dissertation is accessible from http://hdl.handle.net/1969.1/149464
  note: by Cong Meng.
  note: "Major Subject: Biomedical Sciences"
  note: Includes vita.
  note: Master of Science Texas A & M University 2013 http://hdl.handle.net/1969.1/149464
  note: Includes bibliographical references.
  note: Text (Thesis)
  subject:
    topic: Major Biomedical Sciences
  subject:
    topic: MicroRNAs
  subject:
    topic: Macrophages
  subject:
    topic: Adipose tissue inflammation
  identifier: http://hdl.handle.net/1969.1/149464
  record info:
    record content source: TXA
    record creation date: 140116
    record change date: 20151206091153.0
    record identifier: in00003431058
    language of cataloging:
      language term: eng