Biology subjects

Mis, K.

Publications and source records attributed to Mis, K..

3 recordsLinked to original sources

bioRxiv2026

Intrinsic IL-6 expression reduces rhIL-6-induced JAK/STAT activation and promotes glucose and oleic acid oxidation in cultured human myoblasts

Interleukin-6 (IL-6), produced by skeletal muscle and extramuscular tissues, regulates skeletal muscle function through the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway. However, the interaction between intrinsic (locally produced) IL-6 and extrinsic (circulating) IL-6 in skeletal muscle remains unclear. We investigated whether and how intrinsic expression of IL-6 in cultured primary human myoblasts influences their response to extrinsic stimulation with recombinant human IL-6 (rhIL-6). Using gene silencing, we found that suppression of intrinsic IL-6 enhanced rhIL-6-induced phosphorylation of STAT1 and STAT3. Silencing STAT3 also increased rhIL-6-induced STAT1 phosphorylation, but silencing STAT1 had no effect on STAT3 phosphorylation. Pretreatment of myoblasts with neutralising anti-IL-6 antibodies increased phosphorylation of STAT1 and STAT3 induced by 50 ng/mL rhIL-6, whereas pretreatment with 5 ng/mL rhIL-6 reduced this response. Despite increased JAK/STAT signalling, IL-6 silencing decreased glucose and oleic acid uptake and oxidation under both basal and rhIL-6-stimulated conditions. Collectively, our results imply that intrinsic IL-6 restrains activation of the JAK/STAT pathway by extrinsic IL-6, but acts synergistically with it to promote myoblast energy metabolism.

cell biology↗

bioRxiv2025

Low-load blood flow restriction training and ischemia modulate expression of Na+,K+-ATPase and FXYDs in human skeletal muscle

Anterior cruciate ligament (ACL) rupture leads to muscle deconditioning and downregulation of Na+,K+-ATPase (NKA). Low-load blood flow restriction (LL-BFR) training was shown to improve muscle function after ACL injury, but its effects on NKA are unknown. We analysed expression of NKA and its FXYD regulators in knee muscles from ACL-injured subjects undergoing LL-BFR, low-load training with sham blood flow restriction (LL-Sham), or no training (Control). Additionally, we dissected effects of ischemia components by subjecting cultured human myotubes to glucose deprivation and/or hypoxia. The LL-BFR group had higher vastus lateralis mRNA levels of NKA1, NKA{beta}3, and FXYD5 than the LL-Sham group. In vitro, NKA1, NKA{beta}1, and NKA{beta}3 mRNA and NKA1 and NKA{beta}1 protein levels were downregulated by sustained ischemia and glucose deprivation, but not hypoxia, while FXYD5 protein was upregulated by glucose deprivation. Conversely, intermittent ischemia had no effect on NKA or FXYD expression. In conclusion, our study shows that LL-BFR training induces specific transcriptional adaptations in vastus lateralis after ACL injury, potentially contributing to functional improvements. Moreover, it shows that glucose availability plays a major role in modulating NKA and FXYD expression in muscle cells under ischemic conditions. NEW & NOTEWORTHYO_LIThis is the first study exploring effects of low-load BFR training on Na+,K+-ATPase (NKA) and FXYD expression in knee muscles after anterior cruciate ligament injury. C_LIO_LIEffects of ischemia components were analysed by subjecting cultured human myotubes to glucose deprivation and/or hypoxia. C_LIO_LILL-BFR training induces specific transcriptional adaptations in vastus lateralis after ACL injury, potentially contributing to functional improvements. C_LIO_LIGlucose plays a major role in modulating NKA and FXYD expression in cultured myotubes under ischemic conditions. C_LI

physiology↗

bioRxiv2025

PDK1: one abbreviation, two kinases, relentless confusion

Despite peer review, hundreds of biomedical articles contain errors due to identical abbreviations that refer to different proteins. This includes PDK1, denoting both pyruvate dehydrogenase kinase 1 and 3-phosphoinositide-dependent protein kinase 1. Our analysis shows that one-out-of-five articles with the term PDK1 on PubMed, published in 2019-2026, state incorrect antibodies, refer to incorrect sequences for PCR, gene silencing, or plasmids, merge the properties of the two proteins, or incorrectly cite the other protein. Confusion extends to websites of biotechnology providers, where PDK1 antibodies and recombinant proteins were misattributed. To mitigate PDK1 abbreviation misuse, we recommend using unique protein abbreviations, clear antibody and sequence identification, and implementation of more rigorous peer review processes, supported by our newly developed PDK1-TermTracker citation network visualization and analysis service.

biochemistry↗