3 research outputs found
Platelet and red blood cell interactions and their role in rheumatoid arthritis
Cytokines, lymphocytes, platelets and several
biomolecules have long been implicated in the pathology
of rheumatoid arthritis (RA), and the influences of antibody
production and tagging, and cytokine, chemokine
and enzyme production at specific rheumatoid joints were
thought to be exclusive to the advancement of disease
parameters. Another role player in RA is red blood cells
(RBCs) which, of late, have been found to be involved in
RA pathobiology, as there is a positive correlation between
RBC counts and joint pathology, as well as with inflammatory
biomarkers in the disease. There is also an association
between RBC distribution width and the incidence of
myocardial infarction amongst RA patients, and there is a
change in the lipid distribution within RBC membranes.
Of late, certain RBC-associated factors with previously
obscure roles and cell-derived particles thought to be inconsequential
to the other constituents of plasma were found
to be active biomolecular players. Several of these have
been discovered to be present in or originating from RBCs.
Their influences have been shown to involve in membrane
dynamics that cause structural and functional changes
in both platelets and RBCs. RBC-derived microparticles
are emerging entities found to play direct roles in immunomodulation
via interactions with other plasma cells.
These correlations highlight the direct influences of RBCs
on exacerbating RA pathology. This review will attempt
to shed more light on how RBCs, in the true inflammatory milieu of RA, are playing an even greater role than previously
assumed.http://link.springer.com/journal/2962016-12-30hb201
Characterizing pathology in erythrocytes using morphological and biophysical membrane properties : relation to impaired hemorheology and cardiovascular function in rheumatoid arthritis
The inflammatory burden of the complex rheumatoid arthritis (RA) disease affects several organ-systems, including rheological properties of blood and its formed elements. Red blood cells (RBCs) are constantly exposed to circulating dysregulated inflammatory molecules that are co-transported within the vasculature; and their membranes may be particularly vulnerable to the accompanying oxidative stress. In the current study, we investigate biophysical and ultrastructural characteristics of RBCs obtained from a cohort of patients using atomic force microscopy (AFM), scanning electron microscopy (SEM) and confocal microscopy (CM). Statistical analyses of AFM data showed that RA RBCs possessed significantly reduced membrane elasticity relative to that of RBCs from healthy individuals (P-value < 0.0001). SEM imaging of RA RBCs revealed increased anisocytes and poikilocytes. Poikilocytes included knizocytes, stomatocytes, dacryocytes, irregularly contracted cells, and knot cells. CM imaging of several RA RBCs, spectrin, and band 3 protein networks portrayed the similar morphological profiles. Analyses of CM images confirmed changes to distribution of band-3 skeletal protein, a protein critical for gaseous exchange functions of the RBC and preventing membrane surface loss. Decreased membrane deformability impairs the RBC's capacity to adequately adapt its shape to navigate blood vessels, especially microvasculature, and this decrease is also reflected in the cell's morphology. Changes to morphology and deformability may also indicate loss of functional domains and/or pathological protein and lipid associations. These findings suggest that RA disease and/or its concomitant factors impact on the RBC and its membrane integrity with potential for exacerbating pathological cellular function, hemorheology, and cardiovascular function.Medical Research Council: E Pretorius (fund number A0X331) and National Research Foundation: E Pretorius (fund number: N00345).http://:www.elsevier.com/locate/bbamem2018-12-15hj2018Anatomy and PhysiologyPhysiologyStatistic