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Meltem C Arikan

Publications and source records attributed to Meltem C Arikan.

3 recordsLinked to original sources

Epithelial cell PPAR[gamma] contributes to normal lung maturation.

Peroxisome proliferator-activated receptor (PPAR)-gamma is a member of the nuclear hormone receptor superfamily that can promote cellular differentiation and organ development. PPARgamma expression has been reported in a number of pulmonary cell types, including inflammatory, mesenchymal, and epithelial cells. We find that PPARgamma is prominently expressed in the airway epithelium in the mouse lung. In an effort to define the physiological role of PPARgamma within the lung, we have ablated PPARgamma using a novel line of mice capable of specifically targeting the airway epithelium. Airway epithelial cell PPARgamma-targeted mice display enlarged airspaces resulting from insufficient postnatal lung maturation. The increase in airspace size is accompanied by alterations in lung physiology, including increased lung volumes and decreased tissue resistance. Genome-wide expression profiling reveals a reduction in structural extracellular matrix (ECM) gene expression in conditionally targeted mice, suggesting a disruption in epithelial-mesenchymal interactions necessary for the establishment of normal lung structure. Expression profiling of airway epithelial cells isolated from conditionally targeted mice indicates PPARgamma regulates genes encoding known PPARgamma targets, additional lipid metabolism enzymes, and markers of cellular differentiation. These data reveal airway epithelial cell PPARgamma is necessary for normal lung structure and function.

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Induction of macrophage elastase (MMP-12) gene expression by statins.

The statins (including mevastatin and lovastatin) are a widely prescribed class of serum-cholesterol lowering drugs that function by inhibiting 3-hydroxymethylglutaryl coenzyme A (HMG CoA) reductase activity and cellular sterol synthesis. Statins are also widely being appreciated for their inhibitory effects upon inflammation, primarily mediated through direct regulation of inflammatory gene expression. Here we report that statins are also capable of increasing the expression of macrophage elastase (MMP-12). The induction of MMP-12 in mouse macrophages by statins is specific for HMG CoA reductase inhibition, rescued by mevalonate and not observed after inhibition of subsequent steps in the cholesterol biosynthetic pathway. Modulation of cholesterol metabolism may lead to changes in MMP-12 expression and subsequent impacts during physiological and pathophysiological states. We conclude that statins, in addition to their previously described anti-inflammatory properties, may promote the production of some proteinases from activated macrophages.

Animals↗