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Biology subjects

Ekstrom, L.

Publications and source records attributed to Ekstrom, L..

3 recordsLinked to original sources

Cartilage canals in sharks and rays show that blood vessels can exist in mature cartilage without triggering endochondral bone formation

Although cartilage in tetrapod skeletons is typically said to lack blood vessels, this is only true for adult cartilage. In young bird and mammal cartilage, a dense network of vasculature-containing tunnels --cartilage canals-- perforate the growing skeleton, helping nourish the cartilage and develop the ossification centers that will later form the skeletons epiphyseal bone. As the canals and their rich vascular network typically recede as animals age, the healthy cartilage of adult animals is typically known to be avascular. Here, however, we use a range of tissue characterization and visualization techniques --including light/electron microscopy and microCT-- to show that the skeletons of rays and sharks (elasmobranch fishes) not only possess cartilage canals, but that these structures persist in the adult skeleton. The morphology and tissue composition of elasmobranch cartilage canals argues homology with mammalian cartilage canals and an ancient invasion of the vascular system into cartilage. However, the anatomical location of canals --extending away from mineralized tissue not toward it-- and the lack of endochondral ossification in ray and shark cartilage suggest that cartilage canals developed early in vertebrates as a transport system for nutrients and mesenchymal cells into the growing skeleton. We describe distinctive features and variation in elasmobranch cartilage canals, discuss their possible roles and their potential for tissue mineralization, and the biomedical implications for their presence in a clade of animals with continuously growing cartilaginous skeletons.

evolutionary biology↗

Erythropoietin and miRNA profiles during the menstrual cycle in relation to hematological and lipid biomarkers

BackgroundCirculatory micro RNAs (miRNA) have been discussed as complementary diagnostic markers in cardiovascular diseases, and in anti-doping testing. MiR-144 and miR-486 have been associated with cholesterol homeostasis and hematopoiesis, respectively. In addition, they have been suggested as putative biomarkers for autologous blood transfusion and erythropoietin (EPO) doping. The aim of the present study was to assess the variability of miR-144-3p/5p, miR-486-5p/3p and EPO during the menstrual cycle. Secondary aim was to study the correlations between miRNAs, EPO and hematological parameters and lipids. Methods13 healthy women with regular menses were followed with weekly blood sampling during two whole menstrual cycles. MiRNAs were analyzed using TaqMan and PCR followed by calculation of the relative expression for each miRNA using ddCT approach. ResultsThere was no menstrual cycle variability in miRNAs and EPO. MiRNA-144-3p was associated with HDL-C (rs=-0.34, p=0.036) and miRNA-486-5p with Hb (rs=0.32, p=0.046). EPO concentrations correlated to lymphocytes (rs=-0.062, p=0.0002)), Hb (rs= -0.42, p=0.0091), HDL-C (rs=0.36, p=0.030) and triglycerides (rs=-0.54, p=0.0006). ConclusionsThe results of this study may increase the understanding of how miR486-5p and miR144-3p as well as EPO correlate to hematopoietic and lipid biomarkers.

physiology↗

Integrated K+ channel and K+-Cl- cotransporter functions regulate fin proportionality in zebrafish

The coordination of growth during development establishes proportionality within and among the different anatomic structures of organisms. Innate memory of this proportionality is preserved, as shown in the ability of regenerating structures to return to their original size. Although the regulation of this coordination is incompletely understood, mutant analyses of zebrafish with long-finned phenotypes have uncovered important roles for bioelectric signaling in modulating growth and size of the fins and barbs. To date, long-finned mutants identified are caused by hypermorphic mutations, leaving unresolved whether such signaling is required for normal development. We isolated a new zebrafish mutant, schleier, with proportional overgrowth phenotypes caused by a missense mutation and loss of function in the K+-Cl- cotransporter Kcc4a. Genetic depletion of Kcc4a in wild-type fish leads to a dose-dependent loss of growth restriction in fins and barbs, supporting a requirement for Kcc4a in regulation of proportion. Epistasis experiments suggest that Kcc4a and the two-pore potassium channel Kcnk5b both contribute to a common bioelectrical signaling response in the fin. These data suggest that an integrated bioelectric signaling pathway is required for the coordination of size and proportion during development.\n\nGraphical Abstract\n\nO_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=145 SRC=\"FIGDIR/small/621243v1_ufig1.gif\" ALT=\"Figure 1\">\nView larger version (26K):\norg.highwire.dtl.DTLVardef@2ba7b0org.highwire.dtl.DTLVardef@e3df5org.highwire.dtl.DTLVardef@105b878org.highwire.dtl.DTLVardef@920b54_HPS_FORMAT_FIGEXP M_FIG C_FIG

genetics↗