ArticleJournal of physiology and biochemistry2013
Hypercalcemia induces a proinflammatory phenotype in rat leukocytes and endothelial cells.
Article in Journal of physiology and biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Posterior reversible encephalopathy syndrome and parkinsonism as the first manifestation of primary hyperparathyroidism - a report of two cases.Endocrine · 2024Article
- Genetic insights into the effect of trace elements on cardiovascular diseases: multi-omics Mendelian randomization combined with linkage disequilibrium score regression analysis.Frontiers in immunology · 2024Article
- Reversible cerebral vasoconstriction syndrome (RCVS) caused by over-the-counter calcium supplement ingestion.BMJ case reports · 2021Article
- Primary Hyperparathyroidism Presenting as Posterior Reversible Encephalopathy Syndrome: A Report of Two CasesJournal of clinical research in pediatric endocrinology · 2020Article
- Paraneoplastic PRES from lymphoma induced hypercalcemia: Case report and review of the literature.eNeurologicalSci · 2018Article
- Hyperbaric environment up-regulates CD15s expression on leukocytes, down-regulates CD77 expression on renal cells and up-regulates CD34 expression on pulmonary and cardiac cells in rat.Iranian journal of basic medical sciences · 2016Article
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Authors and funding
6 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Endothelial plasma membrane lipid microdomains, so called lipid rafts/caveolae, are rich in neutral glycosphingolipid, globotriaosylceramide, Gb3Cer, or CD77. Several plasma membrane Ca(2+) channels and pumps are located in lipid rafts/caveolae. Increased Ca(2+) influx could cause the development of an endothelial proinflammatory phenotype. Therefore, the aim of this study was to estimate the effects of hypercalcemia in rats by determination of CD77 expression on CD34+ endothelial cells in the heart, kidney, and vena cava. In addition, potential proinflammatory calcium effect was estimated by CD11b and CD15s expression on leukocytes. To achieve hypercalcemia, Sprague-Dawley male rats were given CaCl2 solution with a concentration of 1.5 % elemental calcium during 14 days. CD77 expression on CD34+ endothelial cells in cell suspensions of the heart, kidney, and vena cava, as well as leukocyte expression of CD11b and CD15s in hypercalcemic and control rats were determined by flow cytometry. Ionized calcium concentration in plasma was 1.37 ± 0.01 mM in hypercalcemic vs. 1.19 ± 0.03 mM in control rats. Hypercalcemic group showed statistically significantly decreased proportion of endothelial CD34+ CD77- cells in the kidney and vena cava in parallel with increase of CD11b and CD15s leukocyte proinflammatory markers. In conclusion, it is tempting to speculate that plasma membranes of glycosphingolipid CD77- endothelial cells are poorer in caveolae lipid microdomains and therefore weaker in controlling of Ca(2+) influx. The percentage of CD11b+ CD15s+ leukocytes could be a measure of proinflammatory effects of mild hypercalcemia.
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