Browsing by Subject "extracellular matrix protein (ECM)"

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    EFFECTS OF TYPE VI COLLAGEN ON MACROPHAGES
    (Office of the Vice Chancellor for Research, 2011-04-08) Voiles, Larry; Han, Ling; Lupov, Ivan P.; Anderson, Bailey; Melnikov, Lonya; Pottratz, Sarah Marie; Chang, Hua-Chen
    Emphysema is an abnormal inflammatory response of the alveoli that lose their elasticity due to destruction of alveolar septi. Collagen, an extracellular matrix protein (ECM), is expressed in the lung, which is important in maintaining the integrity of the tissue. Destruction of the ECM components in the alveolar structure contributes to the development of emphysema. We have found that the gene expression of type VI collagen (COL6A1) is higher in the lungs of emphysema patients as compared to that from normal controls. Type VI collagen (COL6) is found in the pulmonary interstitial compartment where massive macrophages are infiltrated in the inflammatory environment. The hypothesis is that excessive COL6 activates macrophages to mediate inflammatory responses, which may contribute to the pathogenesis of emphysema. The goal is to define the effects of type VI collagen on macrophages. Results from murine bone marrow derived macrophages showed a marked increase in the numbers of CD86-positive cells after soluble COL6 stimulation. To further support the stimulatory function of COL6, human THP-1 cells as well as primary monocytes produced inflammatory cytokines IL-12 and IFNγ following COL6 stimulation. Taken together, our data has demonstrated the stimulatory effects on macrophages by COL6 stimulation, which may mediate the inflammatory responses in the pathogenesis of emphysema.
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    TYPE VI COLLAGEN STIMULATES MACROPHAGES TO PROMOTE INFLAMMATION
    (Office of the Vice Chancellor for Research, 2012-04-13) Voiles, Larry; Han, Ling; Lupov, Ivan; Chang, Hua-Chen
    Collagen VI (COL6), an extracellular matrix protein (ECM), is important in maintaining the integrity of the tissue. Our recent findings have demonstrat-ed that excess COL6 is present in the lungs of comorbid patients with em-physema and adenocarcinoma. COL6 localized in the pulmonary interstitium is likely to interact with endothelial, epithelial and infiltrated pulmonary mac-rophages. The hypothesis is that excessive COL6 activates macrophages to promote inflammation, which may exacerbate pulmonary diseases. To test our hypothesis, bone marrow derived macrophages or macrophage cell lines were stimulated with soluble COL6 followed by analysis of activation markers and pro inflammatory cytokines. And results showed an increase in the number of CD86 positive cells and the levels of IL-12 and IFNγ production following stimulation. Taken together, our data have provided a link between increased amounts of COL6 and subsequent immune responses, which may play a role in the pathogenesis of pulmonary inflammatory diseases.