Mechanism of impaired local hyaluronan turnover in bleomycin-induced lung injury in rat.

@article{Teder1997MechanismOI,
  title={Mechanism of impaired local hyaluronan turnover in bleomycin-induced lung injury in rat.},
  author={Priit Teder and Paraskevi Heldin},
  journal={American journal of respiratory cell and molecular biology},
  year={1997},
  volume={17 3},
  pages={
          376-85
        }
}
  • P. Teder, P. Heldin
  • Published 1 September 1997
  • Biology, Chemistry
  • American journal of respiratory cell and molecular biology
Hyaluronan, a linear polysaccharide, is accumulated in lung interstitium during different pathological conditions, causing interstitial edema and thereby impaired lung function. We investigated the mechanism of local hyaluronan turnover during the early phase of bleomycin-induced fibrotic lung injury in rats. The binding of [3H]hyaluronan to alveolar macrophages (AM) established from bleomycin-treated rats 1 and 5 days after induction of injury was decreased 8- and 15-fold, respectively… 
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A role for hyaluronan in macrophage accumulation and collagen deposition after bleomycin-induced lung injury.
TLDR
A model in which HA plays a critical role in the inflammatory response and fibrotic consequences of acute lung injury is proposed, in which systemic administration of HA-binding peptide to rats before injury not only decreased alveolar macrophage motility and accumulation in the lung, but also reduced lung collagen alpha (I) messenger RNA and hydroxyproline contents.
Expression and role of the hyaluronan receptor RHAMM in inflammation after bleomycin injury.
  • A. Zaman, Z. Cui, +4 authors R. Savani
  • Biology, Medicine
    American journal of respiratory cell and molecular biology
  • 2005
TLDR
It is concluded that the interaction of RHAMM with HA is a critical component of the recruitment of inflammatory cells to the lung after injury and the inhibitory effects of HA-binding peptide on inflammation and fibrosis are shown.
The Receptor for Hyaluronan-Mediated Motility (CD168) promotes inflammation and fibrosis after acute lung injury
  • Z. Cui, J. Liao, +4 authors R. Savani
  • Biology, Medicine
    Matrix biology : journal of the International Society for Matrix Biology
  • 2019
Chapter 11 – Hyaluronan in the Pulmonary Alveolus and Interstitium
Irradiation-induced expression of hyaluronan (HA) synthase 2 and hyaluronidase 2 genes in rat lung tissue accompanies active turnover of HA and induction of types I and III collagen gene expression.
TLDR
The results indicate that rHAS2 and rHYAL2 are involved in the turnover of HA during the early phase of lung injury and that rRHAS 2 and rHyAL2 as well as HA fragments may play important roles in the pathogenesis of lung fibrosis.
Role of hyaluronan and hyaluronan-binding proteins in lung pathobiology.
TLDR
Recent research indicates that exogenous administration of high-molecular-weight HA can serve as a novel therapeutic intervention for lung diseases, including lipopolysaccharide (LPS)-induced acute lung injury, sepsis/ventilator-induced lung injury and airway hyperreactivity.
Lack of hyaluronidases exacerbates renal post-ischemic injury, inflammation, and fibrosis.
TLDR
Both HA-degrading enzymes seem to be protective against IRI most likely by reducing HA accumulation in the post-ischemic kidney and decreasing the inflammatory processes.
Acute Lung Injury Regulation by Hyaluronan.
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The dichotomous role of HA to both promote and inhibit ALI based on its size and the HA binding proteins present is focused on.
Hyaluronan Regulation of Acute Lung Injury
TLDR
The role of HA to both promote and inhibit ALI based on its size and the HA binding proteins present is focused on.
Hyaluronan-induced VEGF-C promotes fibrosis-induced lymphangiogenesis via Toll-like receptor 4-dependent signal pathway.
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