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• W2021072536 abstract "Background. We postulated that the response of vascular smooth muscle cells (SMCs) to oxidized low-density lipoprotein (LDL) may be modulated through calcium and 3′, 5′ cyclic adenosine monophosphate (Ca+2-cAMP) second-messenger activity. Methods. Changes in cytosolic calcium [Ca+2]i in aortic SMCs exposed to native (N-) and oxidized (Ox-) LDL were measured with a Fura 2-AM indicator. The influence of cAMP on this response was determined by incubating the cells with either forskolin or 8-bromo-cAMP (stimulatory) or galanin (inhibitory). The cells were then activated by an initial preincubation with N- or Ox-LDL, and the subsequent cellular oxidation of N-LDL was measured. The effect of cAMP mediators alone or in conjunction with calcium antagonism was studied. Results. Exposure of SMCs to Ox-LDL resulted in a marked elevation of [Ca+2]i(306±12 nmol/L) compared with that in the control group (192±15 nmol/Liter; p<10−6). This response was augmented by cAMP stimulation (406±8 nmol/L; p<10−6) but reduced by cAMP inhibition (247±8 nmol/L; p<10−6). The activation of intracellular signaling by initial Ox-LDL priming increased the subsequent oxidation of N-LDL (0.40±0.02 nmol malondialdehyde versus 0.24±0.02 nmol MDA control; p<10−4). This response was enhanced by cAMP (0.45±0.03 nmol MDA; p<10−4) and inhibited by galanin (0.26±0.02; p<10−4). The cAMP effect was reversed by the blockade of calcium mobilization via membrane channels and reticular release. Conclusions. Oxidized LDL-induced Ca+2-cAMP signaling modulates the cellular oxidation of N-LDL. This finding suggests a mechanism through which the scavenger uptake of modified LDL may potentially be regulated. Background. We postulated that the response of vascular smooth muscle cells (SMCs) to oxidized low-density lipoprotein (LDL) may be modulated through calcium and 3′, 5′ cyclic adenosine monophosphate (Ca+2-cAMP) second-messenger activity. Methods. Changes in cytosolic calcium [Ca+2]i in aortic SMCs exposed to native (N-) and oxidized (Ox-) LDL were measured with a Fura 2-AM indicator. The influence of cAMP on this response was determined by incubating the cells with either forskolin or 8-bromo-cAMP (stimulatory) or galanin (inhibitory). The cells were then activated by an initial preincubation with N- or Ox-LDL, and the subsequent cellular oxidation of N-LDL was measured. The effect of cAMP mediators alone or in conjunction with calcium antagonism was studied. Results. Exposure of SMCs to Ox-LDL resulted in a marked elevation of [Ca+2]i(306±12 nmol/L) compared with that in the control group (192±15 nmol/Liter; p<10−6). This response was augmented by cAMP stimulation (406±8 nmol/L; p<10−6) but reduced by cAMP inhibition (247±8 nmol/L; p<10−6). The activation of intracellular signaling by initial Ox-LDL priming increased the subsequent oxidation of N-LDL (0.40±0.02 nmol malondialdehyde versus 0.24±0.02 nmol MDA control; p<10−4). This response was enhanced by cAMP (0.45±0.03 nmol MDA; p<10−4) and inhibited by galanin (0.26±0.02; p<10−4). The cAMP effect was reversed by the blockade of calcium mobilization via membrane channels and reticular release. Conclusions. Oxidized LDL-induced Ca+2-cAMP signaling modulates the cellular oxidation of N-LDL. This finding suggests a mechanism through which the scavenger uptake of modified LDL may potentially be regulated." @default.
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• W2021072536 title "Calcium-dependent second-messenger regulation of low-density lipoprotein oxidation by human aortic smooth muscle cells" @default.
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• W2021072536 doi "https://doi.org/10.1016/s0039-6060(96)80307-2" @default.
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