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Effect of β3 subunit deletion on L‐type calcium channels in mouse small mesenteric arteries
Author(s) -
Kharade Sujay V,
Rusch Nancy J
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.576.2
Subject(s) - protein subunit , vascular smooth muscle , mesenteric arteries , cav1.2 , western blot , microbiology and biotechnology , heterologous expression , cell type , biology , l type calcium channel , chemistry , voltage dependent calcium channel , cell , medicine , endocrinology , gene , calcium , smooth muscle , biochemistry , artery , recombinant dna
The L‐type Ca 2+ channels in vascular smooth muscle cells (VSMCs) are presumed to be heteromeric complexes composed of pore‐forming α 1C subunits and regulatory β and α 2 δ subunits. The β subunits emanate from four gene families (β1, β2, β3, β4) and are thought to promote the expression of α 1C and uniquely regulate its properties in a subunit–specific manner. Based on studies in aortic VSMCs, it is presumed that the β2 and β3 subunits complex with α 1C in VSMCs. The present study used β3 KO mice to define the effect of β3 deletion on the expression and properties of Ca 2+ channels in mouse small mesenteric arteries (MA). Western blots showed a 30% loss of α 1C expression in MA from β3 KO mice compared to WT mice, presumably reflecting the deletion of α 1C ‐β3 channel complexes. Single channel recordings of Ba 2+ currents in cell‐attached patches of mesenteric VSMCs revealed the persistence of functional Ca 2+ channels after β3 deletion. We hypothesize that these currents emanate from α 1C ‐β2 channel complexes since we failed to detect other known β subunits (β1, β4) on Western blot. In this regard, the β3 KO mouse may provide a unique opportunity to study the properties and regulation of relatively pure populations of vascular α 1C ‐β2 channels. The β2 subunit is reported to confer novel properties to Ca 2+ channel complexes in heterologous expression systems and nonvascular cell types that may affect Ca 2+ signaling in the vasculature.