Key result
Cerebral arteries express approximately 20 times more total alpha-BKCa protein at the cell membrane compared to cremaster arteries, despite higher STREX mRNA expression in cremaster vessels.
Cerebral-peripheral BKCa differences warrant caution extrapolating systemic data; extends vascular heterogeneity research but leaves open functional relevance.
Previous studies report functional differences in large conductance Ca2+ activated-K+ channels (BKCa) of smooth muscle cells (VSMC) from rat cerebral and cremaster muscle resistance arteries. The present studies aimed to determine if this complexity in BKCa activity may, in part, be due to splice variants in the pore-forming α-subunit. BKCa variants in the intracellular C terminus of the α-subunit, and their relative expression to total α-subunit, were examined by qPCR. Sequencing of RT-PCR products showed two α-subunit variants, ZERO and STREX, to be identical in cremaster and cerebral arteries. Levels of STREX mRNA expression were, however, significantly higher in cremaster VSMCs (28.9±4.2% of total α-BKCa) compared with cerebral vessels (16.5±0.9%). Further, a low level of BKCa SS4 α-subunit variant was seen in cerebral arteries, while undetectable in cremaster arteries. Protein biotinylation assays, in expression systems and arterial preparations, were used to determine whether differences in splice variant mRNA expression affect surface membrane/cytosolic location of the channel. In AD-293 and CHO-K1 cells, rat STREX was more likely to be located at the plasma membrane compared to ZERO, although the great majority of channel protein was in the membrane in both cases. Co-expression of β1-BKCa subunit with STREX or ZERO did not influence the dominant membrane expression of α-BKCa subunits, whereas in the absence of α-BKCa, a significant proportion of β1-subunit remained cytosolic. Biotinylation assays of cremaster and cerebral arteries showed that differences in STREX/ZERO expression do not alter membrane/cytosolic distribution of the channel under basal conditions. These data, however, revealed that the amount of α-BKCa in cerebral arteries is approximately 20X higher than in cremaster vessels. Thus, the data support the major functional differences in BKCa activity in cremaster, as compared to cerebral VSMCs, being related to total α-BKCa expression, regardless of differences in splice variant expression.
No takes yet. Share an insight, caveat, or question.
Nourian et al. (2014) studied Healthy (preclinical animal model). Cremaster vs Cerebral arteries vs. Cerebral arteries was evaluated on STREX mRNA expression (% of total alpha-BKCa) (p=<0.05). Cerebral arteries express approximately 20 times more total alpha-BKCa protein at the cell membrane compared to cremaster arteries, despite higher STREX mRNA expression in cremaster vessels.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: