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Increased hyaluronan fragmentation during pulmonary ischemia.

Lindsey Eldridge1, Aigul Moldobaeva, Elizabeth M Wagner

  • 1Department of Medicine, Johns Hopkins University, Baltimore, Maryland, USA.

American Journal of Physiology. Lung Cellular and Molecular Physiology
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Lung ischemia causes hyaluronan (HA) fragmentation and increased synthesis, leading to low-molecular-weight HA fragments. These fragments promote angiogenesis, stimulating new blood vessel growth in response to ischemic injury.

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Area of Science:

  • Pulmonary Medicine
  • Biochemistry
  • Extracellular Matrix Biology

Background:

  • Hyaluronan (HA) is a key component of the lung extracellular matrix.
  • Injurious stimuli can cause HA to fragment into low-molecular-weight (LMW) forms.
  • The role of HA changes in lung ischemia and their effect on angiogenesis is not well understood.

Purpose of the Study:

  • To investigate changes in lung hyaluronan during ischemia.
  • To determine the effect of these HA changes on subsequent angiogenesis.

Main Methods:

  • Mice underwent left pulmonary artery ligation (LPAL) to induce lung ischemia.
  • Lung homogenates were analyzed for HA levels, size distribution, hyaluronidase activity, and HA synthase (HAS) gene expression (HAS1, HAS2, HAS3) via RT-PCR.
  • Angiogenesis was assessed using in vitro tube formation assays and in vivo models.

Main Results:

  • Total lung HA increased by 50% within 16 hours of ischemia and remained elevated for 7 days.
  • A fourfold increase in LMW HA fragments was observed by 4 hours post-LPAL.
  • Increased expression of HAS1 and HAS2 was noted, while hyaluronidase activity remained unchanged.
  • LMW HA fragments promoted angiogenesis both in vitro and in vivo.

Conclusions:

  • Lung ischemia leads to both HA fragmentation and increased HA synthesis.
  • These changes result in elevated levels of LMW HA fragments.
  • LMW HA fragments stimulate neovascularization, suggesting a role in the response to ischemic injury.