«Systems Biology and Physiology Reports:Issue #4»

Published on December 31, 2021

Systems Biology and Physiology Reports in 2021: a yearly report

Dear All,

I am happy to greet all readers, editors, reviewers, staff members and publishers of SBPR on the eve of year 2022. I thank all of you for your efforts in creating this journal and making it work despite all the challenges faced by a new independent journal in the age dominated by huge publishers, research societies and citation systems. Please accept my best wishes for the year 2022 in your professional and personal undertakings!

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First year of open-access scientific journal publishing: our mishaps, our expectations, our plans for the bright future

In silico methods have become a versatile and effective tool for the studies of the natural phenomenon at multiple levels. However, unlike such fields as economics and physics, biology and physiology have always been slightly reluctant in acceptance of the novel systemic approaches. Since scientific articles are among the key metrics for the modern scientific society, the number of scientific journals, devoted to some topic, can be a good marker to evaluate the impact of this topic for the society. Indeed, there are esteemed journals, such as PLOS Computational Biology or Journal of Theoretical Biology, but they focus mainly on a common biological phenomenon, while questions of physiology and pathophysiology are often overlooked. On the other hand, the amount of work on computational biology is steadily growing with ~12000 works published in 2010 and ~28000 in 2020 with the keyword “computational model”, according to PubMed. With all this being said and our great experience in the different aspects of the field of computational physiology, our team has decided that it would be a mistake to lose an opportunity to cover this niche. Likewise, we, as a group of fellow scientists, at the end of 2019 decided to create our own venture and to launch our own scientific journal – Systems Biology and Physiology Reports (SBPReports) [1]. This publisher's would be an attempt to underline our first hectic year of the open access scientific publishing.


On calcium fluorophore’s impact in platelet signaling studies

Observation of calcium signaling in platelets - blood cells designed to be involved in stopping bleeding and forming blood clots - is an important part of fundamental research in hemostasis. However, such a study is possible only with the use of calcium fluorophores - small molecules that penetrate the platelet membrane due to their hydrophobic -AM part, which is then hydrolyzed by cytosol esterases. In this work, we consider the phenomenon of inhomogeneous loading of calcium fluorophores into platelets.

We used platelets from healthy adult donors loaded with various fluorescent probes (CalBryte590, DiOC6 (3), Fura Red, Fluo-4 and CellTracker Violet BMQC) and immobilized on antibodies to CD31 in parallel plane flow chambers. Total internal reflection fluorescence (TIRF) microscopy was used for observations.

We demonstrated that all studied probes are loaded heterogeneously, with 30% platelets being loaded with a probe 2-6 times higher than the population median value. Using the CalBryte590 probe as an example, we have shown that a decrease in the incubation temperature, the addition of Pluronic 127 to the incubation medium, or membrane cholesterol depletion significantly reduces the heterogeneity of the probe distribution in the population. By looking at platelet activation from the surface, we have shown that the probability of experiencing strong activation, as measured by the intensity of calcium oscillations, correlates with the amount of probe in the platelet.

Thus, we conclude that the type of fluorophore used and the conditions of its loading into platelets can significantly affect the results of experiments on the observation of calcium signaling in platelets.

Overall scheme of the assay. First, whole pre-processed blood is perfused through the flow chamber for 2.5 minutes. Then Tyrode's buffer is perfused through the chamber for 5 minutes to wash away unattached cells. Then, depending on the protocol, the microscopy video is recorded for 5-10 minutes.
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#platelets#calcium fluorophores#membrane#fluorescent probes#intracellular signaling

Immune thrombocytopenia: what can the systems biology and systems physiology offer?

Immune thrombocytopenia (ITP) is an acquired bleeding disorder of autoimmune pathophysiology. The causes of ITP could be related to other pathology (viral, bacterial, or systemic), or ITP could develop without any apparent reason. While the immune system dysregulation mechanisms in ITP were described, its etiology remains unclear. Moreover, all existing treatment approaches are not specific for ITP, and its action is highly patient- specific. Here we describe recent findings in the origins and development of ITP and discuss novel experimental and theoretical approaches to diagnosing ITP and predicting therapy effects.

Schematic of immune thrombocytopenia mechanisms. The thrombocytopenia in patients could be caused by both T-cells cytotoxicity (CTLs are more active because T-regulatory cells and T-helpers provide dysregulated stimuli) and B-cells antibody production (plasma cells are producing antiplatelet antibodies of IgG and IgM classes; B-regulatory cells provide more activating signals to B-cells to produce antibodies). CTLs specifically attack platelets and induce their apoptosis. Antibodies from plasma cells opsonize platelets. Consecutively, opsonized platelets are eliminated through the spleen. CTLs – cytotoxic T-lymphocytes; Treg – T-regulatory cell; Th – T-helper; Breg – B-regulatory cell; BAFF – B-cell activating factor.
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#autoimmunity#ITP#platelets#acute/chronic ITP#computational modeling#murine models