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Published in Valerio Voliani, Nanomaterials and Neoplasms, 2021
Gunter Schmid, Wolfgang G. Kreyling, Ulrich Simon
Pan et al. pointed out that for Au1.4MS and Au15MS, the major cell-death pathway is oxidative stress [58]. All indicators of oxidative stress, reactive oxygen species (ROS), mitochondrial potential and integrity, and mitochondrial substrate reduction are compromised. In addition, they performed mRNA expression analysis using Affymetrix gene chips. The results are illustrated in Fig. 15.17. In a so-called heat map presentation, it is illustrated that a group of growth-related genes (PTGER4, EDN1, NR4A1, C5orf13, NR4A3, EGR3, FOS, EMP1, CALD1, SERPINE1, EGR1, DUSP5, ATF3, DUSP2) were upregulated in HeLa cells treated with both Au1.4MS (the signature of these particles is “s”: small) and Au15MS (the signature of these particles is “b”: big) at 1 h after the onset of treatment (s1h_1, s1h_2, b1h_1, b1h_2). This reflected an initial growth response triggered by addition of fresh media along with the Au1.4MS and Au15MS, which illustrates a well-known short-term phenomenon of cell culture and confirms the validity of the gene chip expression study. A separate clustering of the gene expression changes following treatment with the non-toxic Au15MS confirmed an overlapping, almost identical group of genes (EGR1, NR4A1, DUSP5, PPP1R3B, EDN1, FOS, EGR1, EDN1, ADAMTS1, ATF3, PTGER4, CYR61) as upregulated at 1 h after medium exchange irrespective of toxicity.
Age-specific response of skeletal muscle extracellular matrix to acute resistance exercise: A pilot study
Published in European Journal of Sport Science, 2019
Barbara Wessner, Michael Liebensteiner, Werner Nachbauer, Robert Csapo
It is well known that MMPs, particularly gelatinase A (MMP2) and gelatinase B (MMP9) play an important role in the adaptive modifications of skeletal muscle induced by physical exercise (Lo Presti, Hopps, & Caimi, 2017). One of the most interesting findings of our study was the age-specific response of MMP9 to the exercise stimulus: the MMP9 mRNA expression was increased in young but decreased in older subjects. These results are in line with a study in young recreationally active men, where MMP9 mRNA and protein levels were elevated 3 h post knee extension exercises (Patel et al., 2017). To our knowledge no other study so far has reported the exercise-associated MMP9 response in older healthy subjects, but in several models of muscular dystrophy the pharmacological inhibition of MMP9 has been suggested to improve skeletal muscle structure and function and to reduce muscle injury, inflammation and fibre necrosis (Li, Mittal, Makonchuk, Bhatnagar, & Kumar, 2009). However, at later stages of the disease the inhibition of MMP9 may lead to accumulation of fibroadipose tissue and reduced muscle strength (Shiba et al., 2015) showing the multifaceted role of MMP9. Studies performed to investigate the inflammatory processes triggered by resistance exercise may help to interpret the downregulation of MMP9 found in older subjects. One particularly interesting study has suggested that muscles of old adults could be “primed” for a stress response. Such priming is indicated by higher baseline levels of STAT3, NF-κB and HSP70 in muscles of old adults, which may increase the sensitivity to cellular stress and promote inflammatory reactions (Thalacker-Mercer, Dell’Italia, Cui, Cross, & Bamman, 2010). The close connection of the ECM to inflammatory pathways is also evident as the induction of ADAMTS1 gene expression observed in our study could be caused by the infiltration of immune cells to sites of exercise-induced muscle injury. ADAMTS1 functions as an extracellular signal that promotes satellite cell activation and muscle regeneration, at least in young mice (Du et al., 2017).