Search bioRxiv⌕ Search

Biology subjects

Tomkova, K.

Publications and source records attributed to Tomkova, K..

3 recordsLinked to original sources

Translational toolkit for reproducible, cross-study profiling of human ageing hallmarks in human blood and tissue

BackgroundAgeing is a complex, multi-dimensional process, underpinned by interacting biological hallmarks that collectively contribute to functional decline and increased susceptibility to disease. While considerable progress has been made in delineating individual ageing pathways, translation into human studies has been hindered by methodological heterogeneity and a lack of standardised, multi-system approaches. Here, we describe a validated, high-resolution toolkit for the simultaneous quantification of multiple ageing hallmarks in clinically accessible human samples, encompassing cellular senescence, immune ageing, inflammation, mitochondrial function, mTOR signalling, autophagy, genomic instability, and stem cell exhaustion. MethodsBlood (25ml) was obtained from young and aged donors (26-81y). Deep immunophenotyping was performed using a novel 30-colour spectral flow cytometry panel. T-cell mTOR activation and autophagic flux were assessed by flow cytometry. Metabolic flux was measured by Seahorse. From whole blood (4 ml), muscle, and adipose tissue (AT) (obtained during elective hip arthroplasty) RNA, DNA, AT stem cells, and myoblasts were isolated. DNA copy number and senescent cell burden were assessed by q-PCR and SA-{beta}-gal staining, respectively. FindingsUtilising this toolkit, we identified pronounced age-related immune remodelling, increased senescent T-cell burden, diminished mitochondrial capacity and altered mTOR-autophagy signalling between healthy young and aged donors. Furthermore, metabolism was significantly affected by anti-coagulant and freezing sample before analysis. InterpretationThis integrated platform provides a foundation for reproducible, cross-study analyses and facilitates translational investigation of interventions targeting health-span extension. FundingWellcome Leap Dynamic Resilience program (co-funded by Temasek Trust).

immunology↗

Discordance between biomarkers of iron status in plasma and myocardium across iron replete, iron deficiency, and iron replacement states.

It is unclear whether plasma measures of iron status reflect iron status in tissues. This study compared the effects of iron deficiency or treatment with intravenous iron on plasma versus myocardial measures of iron metabolism and mitochondrial dysfunction in mice and humans. The human study included 31 people undergoing cardiac surgery. Twenty-two (71%) were iron deficient. The mouse study included 88 mice randomly allocated to iron replete diet group (Controls, n=29), an Iron Deficient diet (n=31) or an iron deficient diet followed by IV Iron administration (n=28). Outcomes included plasma iron and ferritin concentrations, and myocardial total iron, ferritin, IRP1 binding, and mitochondrial complex activity and DNA damage. In the human study, plasma ferritin positively correlated with myocardial ferritin (r2=0.155, p=0.012). People with iron deficiency had significantly lower myocardial ferritin levels than those without iron deficiency. There were no differences or significant correlations for other outcomes. In the mouse study, plasma ferritin negatively correlated with myocardial ferritin (r2=0.113, p=0.004), and iron deficiency reduced myocardial ferritin levels (p=0.018) as well as the binding affinity of myocardial IRP1 to the Ferritin heavy chain mRNA (p=0.033). Intravenous iron had divergent effects on plasma (increased) and myocardial (decreased) ferritin levels, and increased IRP1 binding affinity and mitochondrial respiratory complex activity (p=0.049). These finding suggest that measures of iron metabolism and iron deficiency in plasma do not consistently reflect myocardial iron status across iron replete, iron deficient, and iron replacement states.

molecular biology↗

Second Generation Antibodies Neutralize Emerging SARS-CoV-2 Variants of Concern

Recently emerged SARS-CoV-2 variants show resistance to some antibodies that were authorized for emergency use. We employed hybridoma technology combined with authentic virus assays to develop second-generation antibodies, which were specifically selected for their ability to neutralize new variants of SARS-CoV-2. AX290 and AX677, two monoclonal antibodies with non-overlapping epitopes, exhibit subnanomolar or nanomolar affinities to the receptor binding domain of the viral Spike protein carrying amino acid substitutions N501Y, N439K, E484K, K417N, and a combination N501Y/E484K/K417N found in the circulating virus variants. The antibodies showed excellent neutralization of an authentic SARS-CoV-2 virus representing strains circulating in Europe in spring 2020 and also the variants of concern B.1.1.7 and B.1.351. Finally, the combination of the two antibodies prevented the appearance of escape mutations of the authentic SARS-CoV-2 virus. The neutralizing properties were fully reproduced in chimeric mouse-human versions, which may represent a promising tool for COVID-19 therapy.

microbiology↗