Abstract:
BACKGROUND:Transient Receptor Potential Canonical 1 (TRPC1) is a widely-expressed mammalian cationic channel with functional effects that include stimulation of cardiovascular remodelling. The initial aim of this study was to investigate variation in TRPC1-encoding gene transcripts. RESULTS:Extensive TRPC1 transcript alternative splicing was observed, with exons 2, 3 and 5-9 frequently omitted, leading to variants containing premature termination codons. Consistent with the predicted sensitivity of such variants to nonsense-mediated decay (NMD) the variants were increased by cycloheximide. However it was notable that control of the variants by NMD was prominent in human embryonic kidney 293 cells but not human vascular smooth muscle cells. The cellular difference was attributed in part to a critical protein in NMD, up-frameshift-1 (UPF1), which was found to have low abundance in the vascular cells. Rescue of UPF1 by expression of exogenous UPF1 was found to suppress vascular smooth muscle cell proliferation. CONCLUSIONS:The data suggest: (i) extensive NMD-sensitive transcripts of TRPC1; (ii) inefficient clearance of aberrant transcripts and enhanced proliferation of vascular smooth muscle cells in part because of low UPF1 expression.
journal_name
BMC Mol Bioljournal_title
BMC molecular biologyauthors
Dedman AM,Majeed Y,Tumova S,Zeng F,Kumar B,Munsch C,Bateson AN,Wittmann J,Jäck HM,Porter KE,Beech DJdoi
10.1186/1471-2199-12-30subject
Has Abstractpub_date
2011-07-12 00:00:00pages
30issn
1471-2199pii
1471-2199-12-30journal_volume
12pub_type
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