6 research outputs found
Cardiac protein expression patterns are associated with distinct inborn exercise capacity in non-selectively bred rats
Accelerated apoptotic death and <i>in vivo</i> turnover of erythrocytes in mice lacking functional mitogen- and stress-activated kinase MSK1/2
The mitogen- and stress-activated kinase MSK1/2 plays a decisive role in
apoptosis. In analogy to apoptosis of nucleated cells, suicidal erythrocyte
death called eryptosis is characterized by cell shrinkage and cell membrane
scrambling leading to phosphatidylserine (PS) externalization. Here, we
explored whether MSK1/2 participates in the regulation of eryptosis. To this
end, erythrocytes were isolated from mice lacking functional MSK1/2 (mskâ/â)
and corresponding wild-type mice (msk+/+). Blood count, hematocrit, hemoglobin
concentration and mean erythrocyte volume were similar in both mskâ/â and
msk+/+ mice, but reticulocyte count was significantly increased in mskâ/â
mice. Cell membrane PS exposure was similar in untreated mskâ/â and msk+/+
erythrocytes, but was enhanced by pathophysiological cell stressors ex vivo
such as hyperosmotic shock or energy depletion to significantly higher levels
in mskâ/â erythrocytes than in msk+/+ erythrocytes. Cell shrinkage following
hyperosmotic shock and energy depletion, as well as hemolysis following
decrease of extracellular osmolarity was more pronounced in mskâ/â
erythrocytes. The in vivo clearance of autologously-infused CFSE-labeled
erythrocytes from circulating blood was faster in mskâ/â mice. The spleens
from mskâ/â mice contained a significantly greater number of PS-exposing
erythrocytes than spleens from msk+/+ mice. The present observations point to
accelerated eryptosis and subsequent clearance of erythrocytes leading to
enhanced erythrocyte turnover in MSK1/2-deficient mice