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*
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205;
Department of Medicine, Washington University School of Medicine at Barnes-Jewish Hospital, St. Louis, MO 63110; and
Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, and the Veterans Affairs Connecticut Healthcare System, West Haven, CT 06516
Although the metalloproteinase murine metalloelastase (MME) has
been implicated in lung disorders such as emphysema and pulmonary
fibrosis, the mechanisms regulating MME expression are unclear. Low
m.w. fragments of the extracellular matrix component hyaluronan (HA)
that accumulate at sites of lung inflammation are capable of inducing
inflammatory gene expression in macrophages (M
). The purpose of this
study was to examine the effect of HA fragments on the expression of
MME in alveolar M. The mouse alveolar M cell line MH-S was
stimulated with HA fragments over time, total RNA was isolated, and
Northern blot analysis was performed. HA fragments induced MME mRNA in
a time-dependent fashion, with maximal levels at 6 h. HA
fragments also induced MME protein expression as well as enzyme
activity. The induction of MME gene expression was specific for low
m.w. HA fragments and dependent upon new protein synthesis; it occurred
at the level of gene transcription. We also examined the effect
of HA fragments on MME expression in inflammatory alveolar M from
bleomycin-injured rat lungs. Although normal rat alveolar M did not
express MME mRNA in response to HA fragments, alveolar M from the
bleomycin-treated rats responded to HA fragment stimulation by
increasing MME mRNA levels. Furthermore, baseline and HA
fragment-induced MME gene expression in alveolar M from
bleomycin-treated rats was inhibited by IFN-
. These data suggest
that HA fragments may be an important mechanism for the expression of
MME by M in inflammatory lung disorders.
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