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Signalling Pathways in The Regulation of Cellular Responses to Exercise
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Anders Gudiksen, Stine Ringholm, Henriette Pilegaard
CaMKII phosphorylation has been shown to be elevated in human SkM during prolonged exercise, with a marked peak already after 1 minute of exercise (102), and the exercise-induced CAMKII phosphorylation in human SkM has been reported to be intensity dependent (26). The finding that transgenic mice expressing a constitutively active form of CAMKIV in SkM had elevated messenger RNA (mRNA) levels of the transcriptional coactivator PGC-1α mRNA (135) suggested that Ca2+ regulates PGC-1α transcription in response to acute exercise. In accordance, the PGC-1α mRNA increased in primary rat SkM cells when the cytosolic Ca2+ concentration was raised by incubation in the Ca2+ ionophore, ionomycin, or ryanodine receptor agonis, caffeine (70). These responses were prevented by treatment with the calcineurin inhibitor cyclosporine A and reduced by the CAMK inhibitor KN-62 (70). In accordance, prior treatment with cyclosporine A or KN-62 also prevented a contraction-induced increase in PGC-1α mRNA in rat EDL muscle ex vivo (70). Similarly, 5 days of incubation of L6 myotubes in ionomycin or caffeine increased cytochrome oxidase I (COXI), cytochrome c, and citrate synthase protein content and incubation in the ryanodine receptor inhibitor, dantrolene, or the Ca2+ chelator EGTA (90) or the CAMK inhibitor KN93 (89) prevented these effects. This indicates that both calcineurin and CAMK are involved in gene regulation. However, an increased cytochrome c mRNA content in myotubes incubated in the Ca2+ ionophore A23187 was prevented by simultaneous incubation in the PKC inhibitor staurosporine, but not the CAMK inhibitor KN-62. Moreover, incubation with a mitogen-activated protein kinase (MAPK) inhibitor prevented the Ca2+-induced increase in cytochrome c transcriptional activity, and extracellular signal-regulated kinase (ERK)1/2 phosphorylation showed an early increase (32). This suggests that a Ca2+ PKA ERK-dependent pathway is involved in regulation of gene expression of mitochondrial proteins, but it should be noted that not all PKC isoforms are activated by Ca2+, as mentioned earlier. Together these studies indicate that Ca2+ plays an important role in transcriptional regulation of PGC-1α and oxidative proteins in SkM through ERK1/2, calcineurin and CAMK-mediated regulation. Because PGC-1α has been shown to regulate the transcription of a broad range of mitochondrial proteins and mitochondrial volume in mouse SkM (44, 72), Ca2+ signalling is thought to be central in exercise training–induced mitochondrial biogenesis in SkM through effects on PGC-1α transcription. Ca2+ has also been suggested to regulate the transcription of the myokine interleukin (IL)-6 in SkM, which is supported by an observed increase in IL-6 mRNA in myotubes incubated in the Ca2+ ionophore calcimycin A23187 (124) (Figure 8.2).
Host-directed therapies for malaria and tuberculosis: common infection strategies and repurposed drugs
Published in Expert Review of Anti-infective Therapy, 2022
Piyush Baindara, Sonali Agrawal, O. L. Franco
Baicalin is a flavone glycoside and is reported to enhance autophagic flux and Mtb clearance in infected macrophages by inhibiting the PI3K/Akt/mTOR signaling pathway [184]. Calcimycin is a polyether antibiotic from Streptomyces chartreusensis and was recently reported to inhibit intracellular Mtb through autophagy induction via eliciting the upregulation of intracellular calcium levels by binding to P2RX7 receptor [185]. Another autophagy inducer is Ambroxol, which is a mucoactive drug, and interestingly, mucokinetic activity of ambroxol is found to induce the autophagic flux by activation of TFEB nuclear translocation in the murine tuberculosis model [186]. Psychotropic drugs like nortriptyline are also reported to induce the autophagic flux by increasing the rate of phagosome formation in Mtb-infected macrophages [111].
Artificial oocyte activation: physiological, pathophysiological and ethical aspects
Published in Systems Biology in Reproductive Medicine, 2019
George Anifandis, Alexandros Michopoulos, Alexandros Daponte, Katerina Chatzimeletiou, Mara Simopoulou, Christina I. Messini, Nikolas P. Polyzos, Katerina Vassiou, Konstantinos Dafopoulos, Dimitrios G. Goulis
Intra-cytoplasmic sperm injection (ICSI) has established its role as an effective infertility treatment. Nevertheless, multiple ICSI failures can be encountered in infertile couples with low oocyte yield in combination with abnormal semen parameters. One of the factors associated with ICSI failure is oocyte activation deficiency (AOD). The latter is considered a result of sperm-derived molecules, such as phospholipase C-zeta (PLCζ), that is not capable of producing adequate Ca+2 oscillations for oocyte activation. Apart from these natural activators, other stimulants, such as Ca+2 ionophore A23187 (calcimycin), ionomycin and strontium chloride have been applied to overcome AOD and ICSI failure. The present narrative review aims to discuss and critically appraise the literature on the role of Ca+2 oscillations in oocyte activation and summarize the evidence concerning the use of natural and artificial factors, as agents for artificial oocyte activation (AOA) in both animals and humans. Physiological, pathophysiological and ethical aspects of AOA will be discussed as well.
Anti-inflammatory effects of Artemisia scoparia and its active constituent, 3,5-dicaffeoyl-epi-quinic acid against activated mast cells
Published in Immunopharmacology and Immunotoxicology, 2018
Sun-Young Nam, Na-Ra Han, So-Young Rah, Youngwan Seo, Hyung-Min Kim, Hyun-Ja Jeong
Fetal bovine serum (FBS) and Isocove’s modified Dulbecco’s medium (IMDM) were purchased from Gibco BRL (Grand Island, NY). Dimethyl sulfoxide (DMSO) and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), phorbol myristate acetate (PMA), A23187 (calcimycin; C29H37N3O6) and bicinchoninic acid (BCA) were obtained from Sigma Chemical Co (St. Louis, MO). TSLP, TNF-α, IL-1β and IL-6 antibodies were procured from R&D Systems Inc. (Minneapolis, MN). Caspase-1, NF-κB, poly-ADP-ribose polymerase, phosphorylated (p)-c-Jun N-terminal kinases (JNK), JNK, p-p38, p38, p-extracellular signal-regulated kinases (ERK), ERK, p-IκBα and tubulin antibodies were obtained from Santa Cruz Biotechnology (Dallas, TX).