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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Single pericytes and pericytes in suspension are stimulated in a similar way by low-density lipoprotein.

BACKGROUND: Pericytes are regarded as the microvascular counterpart of smooth muscle cells and implicated in the regulation of blood pressure at the microvascular level. Ca2+ plays an important role in biochemical processes involved in blood pressure regulation and can be activated by low-density lipoprotein (LDL) cholesterol. OBJECTIVE: To determine whether stimulation either of single cells or of cells in suspension by LDL would produce any difference in the increase in cytosolic free calcium levels ([Ca2+]i). DESIGN AND METHODS: Single pericytes were loaded with 2 micromol/l of the Ca2+-sensitive dye Indo-1/AM. The Indo-1 fluorescence was recorded at 405 nm (Ca2+-bound) and 485 nm (Ca2+-free) after stimulation with LDL. Pericytes in suspension were loaded with 2 micromol/l of the Ca2+-sensitive dye FURA-2/AM. The FURA-2 fluorescence kinetics were recorded at 340-380 nm. Ratios of fluorescence at the two wavelengths were transformed to [Ca2+]i. RESULTS: Basal [Ca2+] levels appeared to be higher in single cells (148+/-13 nmol/l, n = 20) than they were in cells in suspension (128+/-8 nmol/l, n = 25; P= 0.0078). After stimulation with LDL the increase in [Ca2+]i in both systems was about 220% above baseline. A clear dose dependency was seen for both systems. CONCLUSIONS: Single pericytes and pericytes in suspension increase their [Ca2+]i after stimulation with LDL dose-dependently. Even though single-cell measurements revealed some technical limitations, their responses were comparable to those obtained in a cell suspension. In analogy to aortic smooth muscle cells, our results indicate that LDL might also play a blood-pressure-regulatory role in the microvasculature.[1]

References

  1. Single pericytes and pericytes in suspension are stimulated in a similar way by low-density lipoprotein. Skinner, S., Niederer, E., Locher, R., Vetter, W. J. Hypertens. (1998) [Pubmed]
 
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