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- W1987804524 abstract "We used an antisense oligonucleotide (ODN) to inhibit laminin (LM) β 1 chain synthesis in mouse embryonic lung explants and cell cultures. The ODN spanned 17 bases located 13 bases downstream the initiation codon and contained phosphorothioate and C-5 propynyl pyrimidine modifications. Penetration of the ODN into the lung explants was confirmed by fluorescein isothiocyanate (FITC) tagging. 50 μM of antisense ODN decreased LM β 1 chain synthesis by 82±6.9% with no significant changes in the synthesis of other LM chains. The same antisense probe but without C-5 propynyl pyrimidine modification, another 17-mer ODN complementary to the LM β 1 initiation codon, and a 17-mer ODN complementary to the LM α 1 initiation codon had no antisense activity. Lung explants exposed to the active LM β 1 antisense ODN showed decreased LM-1 and collagen type IV deposition at the epithelial–mesenchymal interface and an arrest in bronchial smooth muscle (SM) development. Histological examination and cell motility assays suggested that this arrest was due to impaired spreading and migration of SM cell precursors over the defective basement membrane (BM). Our studies indicate that β 1-chain containing LMs play a role in bronchial myogenesis." @default.
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- W1987804524 date "1999-12-01" @default.
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- W1987804524 title "Bronchial smooth muscle hypoplasia in mouse embryonic lungs exposed to a laminin β1 chain antisense oligonucleotide" @default.
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- W1987804524 doi "https://doi.org/10.1016/s0925-4773(99)00198-7" @default.
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