Hubs and Webs in Platelet Intracellular Signalling

In this issue of Systems Biology and Physiology Reports A.A. Martyanov and M.A. Panteleev suggested a review on platelet intracellular signalling network, which is a second part in the discussion on the molecular relationships between platelet activation and responses [1]. The review contains seven thousands words and two hundred references and yet it is not complete, as there are still unclear parts in platelet signalling, especially in its inhibition [2-4]. In an effort to comprehend the platelet activation pattern, I drew a signalling scheme based on the review and data from other authors [2, 3].

Scheme of platelet intracellular signalling with focus on cytosolic calcium as a “Hub”. Cytosolic calcium concentration is given in the shades of red. Almost all types of platelet receptor agonists lead to activation of phospholipase C (PLC), followed by calcium release from intracellular stores (DTS). Calcium concentration is rapidly reduced by calcium-dependent ATPases (SERCA and PMCA). Also, it could be reduced by binding with some buffering proteins, including its effector-proteins (indicated with red dots). Platelet mitochondria also can function as a calcium buffer and, simultaneously, be regulated by calcium concentration. Direct activation is shown by solid green arrows, direct inhibition - by solid red arrows. Indirect interactions are shown by dashed lines. Abbreviations. AC – adenylate cyclase, α2AAR - α2A-adrenergic receptor, CDGEF - CalDAGGEFI, COX – cyclooxygenase, DAG - diacylglycerol, DTS - dense tubular system, Fbg – fibrinogen, IP3R - receptor for inositol-1,4,5-trisphosphate (IP3), Mit - a mitochondrion, mPTP - mitochondrial permeability transition pore, NCLX - mitochondrial sodium/calcium exchanger, OCS - open canalicular system, P2Y - purinergic receptor, PAR - protease-activated receptor, PIP2 - phosphoinositol-4,5-bisphosphate, PIP3 - phosphoinositol-3,4,5-trisphosphate, PI(P)n – phosphoinositides, PKA – protein kinase A, PKG – protein kinase G, PKC – protein kinase C, PL – phospholipid, PLA2 – phospholipase A2, PMCA - plasma membrane calcium ATPase, PR - PGI2 receptor, P-Tyr – phosphorylated tyrosine residue, SERCA - sarcoplasmic/endoplasmic reticulum calcium ATPase, sGC – soluble guanylate cyclase, TR - thromboxane A2 (TxA2) receptor, TRPC - transient receptor potential channel, UNI - mitochondrial uniporter, vWF – von Willebrand Factor, Y-Pase – tyrosine phosphatase.

Overview of the neutralizing antibody and memory B cell response kinetics in SARS-CoV-2 convalescent and/or mRNA vaccinated individuals.

COVID-19 pandemics triggered by the SARS-CoV-2 virus have caused millions of deaths worldwide and have led to expedited developments of various effective vaccines that, if administered, could prevent and/or circumvent the infection and reduce the death toll. Since the start of the pandemics multiple research groups around the world have been involved in the analysis of immune responses of various human cohorts to the SARS-CoV-2 infection and vaccines. Now, over 1.5 years later, the scientific community has accumulated extensive data about both the development of an immune response to SARS-CoV-2 following infection, as well as its rate of fading off. Kinetic analysis of the immune response generated by vaccines is also emerging, enabling the possibility of making comparisons and predictions. In this review we will focus on the comparing B cell and antibody immune responses to the SARS-CoV-2 infection as opposed to mRNA vaccines for the SARS-CoV-2 S-protein, which have been utilized to immunize hundreds of millions of people and analyzed in multiple studies.

#B-cells#COVID-19#vaccines#immune response

Systems approaches meet biology and physiology: why do we need yet another journal?

Modern biological science in the past 50 years has made a spectacular journey providing us fascinating insights into the nature of living organisms and leading to accumulation of incredible amount of information. Nowadays, we observe introduction of the new systems approaches that allow us to supplement the qualitative nature of the life sciences by quantitative and mechanism-driven analysis. More and more scientists are becoming attracted by the unique opportunities that are provided by the novel synthetic approaches, encompassed by the systems biology, systems physiology and systems pharmacology in various fields. Right now, it is not simply mathematical or computational modelling of biological systems: a wide range of tools, including various approaches from big data field, progressive statistical methods, "omics" and others, are used to get insight into the mechanism of health and disease.
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