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Nuclear localization of active matrix metalloproteinase-2 in cigarette smoke-exposed apoptotic endothelial cells

Ruta Aldonyte1, Aldonyte Ruta, Mark Brantly

  • 1Department of Medicine, Division of Pulmonary Medicine, University of Florida, Gainesville, Florida 32610, USA. aldonyte.ruta@gmail.com

Experimental Lung Research
|February 5, 2009
PubMed

Insights

Cigarette smoke triggers matrix metalloproteinases (MMPs) in lung cells, leading to apoptosis. MMP-2 activation in the nucleus contributes to cell death and nuclear matrix degradation.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Pulmonary Medicine

Background:

  • Cigarette smoke (CS) activates proteases, including matrix metalloproteinases (MMPs), contributing to lung damage.
  • MMPs are implicated in cell death and tissue destruction within the lungs.

Purpose of the Study:

  • To investigate MMP production in pulmonary artery endothelial cells (PAECs) upon CS exposure.
  • To determine the association between CS-induced MMP activation and apoptosis in PAECs.

Main Methods:

  • Cultured PAECs were exposed to CS.
  • Apoptosis was assessed using annexin V binding and cleaved poly-ADP-ribose-polymerase (PARP) assays.
  • MMP activity and levels were analyzed using Western blotting and in situ zymography.

Main Results:

  • CS exposure induced apoptosis in PAECs, evidenced by increased annexin V binding and PARP cleavage.
  • Gelatinolytic activity, a marker of MMP function, increased and correlated with apoptosis.
  • Levels of pro-MMP-2 and active MMP-2 were elevated in both cytosolic and nuclear fractions of CS-exposed cells.
  • MMP-2 was found in the nucleus of apoptotic cells, colocalizing with gelatinolytic activity.

Conclusions:

  • MMP-2 plays a significant role in CS-induced gelatinase activity within the nucleus.
  • CS-induced MMP-2 activation correlates with endothelial cell apoptosis.
  • MMP-2 may have a novel function in degrading the nuclear matrix during CS-induced endothelial apoptosis.

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