Erythropoiesis- and thrombopoiesis-characterizing parameters in adenosine A3 receptor knock-out mice
Language English Country Czech Republic Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
23489188
DOI
10.33549/physiolres.932489
PII: 932489
Knihovny.cz E-resources
- MeSH
- Erythrocytes cytology physiology MeSH
- Erythropoiesis physiology MeSH
- Mesenchymal Stem Cells cytology physiology MeSH
- Mice, Inbred C57BL MeSH
- Mice, Knockout MeSH
- Mice MeSH
- Receptor, Adenosine A3 genetics metabolism MeSH
- Signal Transduction physiology MeSH
- Blood Platelets cytology physiology MeSH
- Thrombopoiesis physiology MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Mice MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Receptor, Adenosine A3 MeSH
Influence of the regulatory system mediated by adenosine A(3) receptors on the functioning of erythropoiesis and thrombopoiesis was studied by means of evaluation of the numbers and attributes of peripheral blood erythrocytes and platelets, as well as of erythroid bone marrow progenitor cells in adenosine A(3) receptor knock-out (Adora3(tm1Jbsn)/Adora3(tm1Jbsn), A(3)AR((-/-))) mice and their wild-type C57BL/6 counterparts, both males and females. Minor but statistically significant disturbances in the properties of erythrocytes, namely in the parameters of mean erythrocyte volume and mean erythrocyte hemoglobin were observed in A(3)AR((-/-)) mice. In addition, adenosine A(3) receptor knock-out mice were found to exhibit an expressive, statistically significant decrease of their blood platelet count, amounting to 17 % and 21 % in males and females, respectively. This decrease in platelet levels was accompanied by a significant 17 % decline in the plateletcrit in both sexes. The obtained data can help to define therapeutic applications based on the principle of adenosine receptor signaling.
References provided by Crossref.org
Lack of adenosine A3 receptors causes defects in mouse peripheral blood parameters
