Biology subjects

Soriano-Arroquia, A.

Publications and source records attributed to Soriano-Arroquia, A..

4 recordsLinked to original sources

bioRxiv2025

miR-196a-5p and miR-342-3p mediate skeletal muscle and thermogenic adipose tissue crosstalk through extracellular vesicles

Small extracellular vesicles (small EVs) are nanovesicles found in tissues and body fluids that contain regulatory molecules including microRNAs, termed exomiRs. Research in murine models has demonstrated that exercise can trigger the release of small EVs into the circulation. The aim of this study was to study exomiR release in humans pre and post exercise and to characterise the function of these microRNAs especially in relation to thermogenic fat. We found that exercise increased the release of exomiR-196a-5p in endurance athletes, a microRNA that induces UCP1 expression and browning of white adipocytes. We observed that myotubes specifically release miR-196a-5p within small EVs after in vitro exercise-mimicking conditions such as electrical pulse stimulation and cAMP treatment. Likewise, the expression at basal levels of the exercise-induced exomiR-342-3p negatively correlated with BMI and age. EV proteomics revealed a positive correlation between FABP4+ and miR-342-3p, suggesting an adipocyte cell origin. Overexpression of miR-342-3p increased Myogenin levels during skeletal muscle cell differentiation, indicating a positive role in muscle differentiation. Our results suggest that oxidative extreme metabolic capacities in endurance athletes contribute to the enhanced release of circulatory exomiRs after exercise mediating bi-directional crosstalk between skeletal muscle and thermogenic adipose tissue. Graphical abstractO_LISerum-EVs from endurance athletes increase UCP1 expression in white adipocytes. C_LIO_LImiR-196a and miR-342-3p are increased in serum-EVs from endurance athletes. C_LIO_LIMuscle cells release EVs enriched in miR-196a after electrical pulse stimulation. C_LIO_LImiR-196a and miR-342-3p have browning and myogenic potential, respectively. C_LI O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=143 SRC="FIGDIR/small/656129v1_ufig1.gif" ALT="Figure 1"> View larger version (31K): org.highwire.dtl.DTLVardef@1bd9b25org.highwire.dtl.DTLVardef@114a549org.highwire.dtl.DTLVardef@6f863borg.highwire.dtl.DTLVardef@1d5c528_HPS_FORMAT_FIGEXP M_FIG C_FIG

cell biology↗

bioRxiv2024

Unveiling Ageing-Associated and Caloric Restriction-Associated Changes in miRNA Expression in Rat Skeletal Muscle and the Mechanisms Mediating their Effects on Muscle Cell Function

The mechanisms underlying skeletal muscle ageing, whilst poorly understood, are thought to involve dysregulated micro (mi)RNA expression. Using young and aged rat skeletal muscle tissue, we applied high-throughput RNA sequencing to comprehensively study alterations in miRNA expression occurring with age, as well as the impact of caloric restriction (CR) on these changes. Furthermore, the function of the proteins targeted by these age- and CR-associated miRNAs was ascertained. Numerous known and novel age-associated miRNAs were identified of which CR normalised 45.5% to youthful levels. Our results suggested miRNAs upregulated with age to downregulated proteins involved in muscle tissue development and metabolism, as well as longevity pathways, such as AMPK and autophagy. Furthermore, our results found miRNAs downregulated with age to upregulate pro-inflammatory proteins, particularly those involved in innate immunity and the complement and coagulation cascades. Interestingly, CR was particularly effective at normalising miRNAs upregulated with age, rescuing their associated protein coding genes but was less effective at rescuing anti-inflammatory miRNAs downregulated with age. Lastly, the effects of a specific miRNA, miR-96-5p, identified by our analysis to be upregulated with age, were studied in culture C2C12 myoblasts. We demonstrated miR-96-5p to decrease cell viability and markers of mitochondrial biogenesis, myogenic differentiation and autophagy. Overall, our results provide useful information regarding how miRNA expression changes in skeletal muscle, as well as the consequences of these changes and how they are ameliorated by CR.

molecular biology↗

bioRxiv2024

From Planning Stage To FAIR Data: A Practical Metadatasheet For Biomedical Scientists

Datasets consist of measurement data and metadata. Metadata provides context, essential for understanding and (re-)using data. Various metadata standards exist for different methods, systems and contexts. However, relevant information resides at differing stages across the data-lifecycle. Often, this information is defined and standardized only at publication stage, which can lead to data loss and workload increase. In this study, we developed Metadatasheet, a metadata standard based on interviews with members of two biomedical consortia and systematic screening of data repositories. It aligns with the data-lifecycle allowing synchronous metadata recording within Microsoft Excel, a widespread data recording software. Additionally, we provide an implementation, the Metadata Workbook, that offers user-friendly features like automation, dynamic adaption, metadata integrity checks, and export options for various metadata standards. By design and due to its extensive documentation, the proposed metadata standard simplifies recording and structuring of metadata for biomedical scientists, promoting practicality and convenience in data management. This framework can accelerate scientific progress by enhancing collaboration and knowledge transfer throughout the intermediate steps of data creation.

bioinformatics↗

bioRxiv2019

miR-181a Regulates p62/SQSTM1, Parkin and Protein DJ-1 Promoting Mitochondrial Dynamics in Skeletal Muscle Ageing

One of the key mechanisms underlying skeletal muscle functional deterioration during ageing is disrupted mitochondrial dynamics. Regulation of mitochondrial dynamics is essential to maintain a healthy mitochondrial population and prevent the accumulation of damaged mitochondria, however the regulatory mechanisms are poorly understood. We demonstrated loss of mitochondrial content and disrupted mitochondrial dynamics in muscle during ageing concomitant with dysregulation of miR-181a target interactions. Using functional approaches and mitoQc assay, we have established that miR-181a is an endogenous regulator of mitochondrial dynamics through concerted regulation of Park2, p62/SQSTM1 and DJ-1 in vitro. Downregulation of miR-181a with age was associated with an accumulation of autophagy-related proteins and abnormal mitochondria. Restoring miR-181a levels in old mice prevented accumulation of p62, DJ-1 and PARK2, improved mitochondrial quality and muscle function. These results provide physiological evidence for the potential of microRNA-based interventions for age-related muscle atrophy and of wider significance for diseases with disrupted mitochondrial dynamics.\n\n\n\nO_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=107 SRC=\"FIGDIR/small/805176v1_ufig1.gif\" ALT=\"Figure 1\">\nView larger version (54K):\norg.highwire.dtl.DTLVardef@1d6d4c7org.highwire.dtl.DTLVardef@12b6940org.highwire.dtl.DTLVardef@10aed74org.highwire.dtl.DTLVardef@6b5b34_HPS_FORMAT_FIGEXP M_FIG C_FIG

physiology↗