Abstract
We determined the presence of Ca2+/calmodulin-dependent protein kinases (CaMKs), a family of multifunctional proteins engaged in Ca2+-linked signaling, in carotid body chemoreceptor cells which are critical for the hypoxia-sensing. Carotid bodies were dissected from anesthetized normoxic adult Wistar rats and were double stained for individual CaMKs and for tyrosine hydroxylase (TH), a marker of chemoreceptor cells. Immunofluorescence was examined by confocal laser scanning microscopy. We found that CaMKI and CaMKII were expressed in chemoreceptor cells, but their distribution and intensity varied. CaMKI immunoreactivity was distributed throughout the cytoplasm, whereas that of CaMKII was localized in the cytoplasmic periphery of chemoreceptor cells. An overlap of CaMKI or CaMKII fluorescent probes with TH affirmed the presence of either protein in the chemoreceptor cells. CaMKIV could not be conclusively visualized by the used method. The study shows the expressions of CaMKI and CaMKII in chemoreceptor cells, which raises the plausibility of CaMKs` role in carotid body function.
Highlights
Ca2+/calmodulin (CaM)-dependent protein kinases (CaMKs): CaMKI, CaMKII, and CaMKIV are a family of proteins which, through phosphorylation of intracellular substrates, mediate a host of neural functions, including neurotransmitter metabolism, long-term facilitation, and gene transcription
We found that CaMKI and CaMKII, but not CaMKIV, were expressed in carotid chemoreceptor cells
Representative examples of the expression pattern of CaMKI are displayed in Figure 1 and of CaMKII in Figures 2 & 3
Summary
Ca2+/calmodulin (CaM)-dependent protein kinases (CaMKs): CaMKI, CaMKII, and CaMKIV are a family of proteins which, through phosphorylation of intracellular substrates, mediate a host of neural functions, including neurotransmitter metabolism, long-term facilitation, and gene transcription. CaMKs are foremost the key regulators of cellular responses to Ca2+/calmodulin mobilizing stimuli (Hook & Means 2001). Hypoxic hypoxia unleashes pulmonary hyperventilation, a primary reflex defense reaction, aimed at sustaining delivery of O2 to tissues. The reaction is explicitly generated by the carotid body chemoreceptor cells which detect the deficit of O2 and transduce that extracellular signal into the intracellular Ca2+ rise (Pokorski et al 2012), followed by neurotransmitter release and a signaling cascade leading eventually to cell excitation and increased neural discharge rate from the organ
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