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Versican/PG-M isoforms in vascular smooth muscle cells
J M Lemire1, K R Braun, P Maurel
1Department of Pathology, University of Washington, Seattle, WA, USA. joanlemi@u.washington.edu
Arteriosclerosis, Thrombosis, and Vascular Biology
|July 9, 1999
Summary
Vascular smooth muscle cells (SMCs) express multiple versican splice variants, including V0, V1, and V3. A novel variant retaining an intron was identified, potentially altering protein structure in atherosclerosis.
Area of Science:
- Biochemistry
- Molecular Biology
- Cardiovascular Research
Background:
- Proteoglycans, like versican, in the extracellular matrix are implicated in vascular stenosis and lipid retention.
- Versican is synthesized by vascular smooth muscle cells (SMCs), accumulates in atherosclerosis, and binds LDLs.
Purpose of the Study:
- To characterize versican RNA splice variants expressed by rat SMCs.
- To identify novel versican splice variants and their structural implications.
Main Methods:
- Cloning, sequencing, and hybridization with domain-specific probes to analyze versican RNAs.
- RT-PCR and Northern blot analysis to confirm the presence of specific isoforms.
- PCR amplification to identify novel splice variants.
Main Results:
- The V0, V1, and V3 versican isoforms were confirmed in vascular SMCs.
- A novel, incompletely spliced variant retaining an intron was identified in both rat and human SMCs.
- This novel variant's predicted translation product has a distinct carboxy-terminus.
Conclusions:
- Vascular SMCs express a complex repertoire of versican splice variants.
- The novel intron-retaining variant represents a new isoform with potential functional consequences.
- Understanding versican heterogeneity is crucial for studying vascular diseases like atherosclerosis.