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Advanced Light-Sheet Microscopy to Explore Brain Structure on an Organ-Wide Scale
Published in Francesco S. Pavone, Shy Shoham, Handbook of Neurophotonics, 2020
Ludovico Silvestri, Francesco S. Pavone
Single-cell mapping in entire cleared mouse brain is particularly suited to investigate whole-brain behavior-specific neuronal activation by looking at the expression of immediate early genes. Renier and colleagues used immunohistochemistry (based on the iDISCO protocol: Renier et al., 2014) to map activation in explorative tasks and in parental behaviors (Renier et al., 2016). Ye and co-authors used a similar approach, although based on the use of a transgenic animal rather than immunolabeling, to study whole-brain effects of appetitive versus aversive stimuli (Ye et al., 2016). This latter study was also complemented by tracing of activation-specific axonal bundles, and by optogenetic stimulation of a subset of neurons defined by their activation, leading to an exquisite global view of the brain-wide circuits involved in punishment and reward. Activation mapping using immediate early gene expression has also been performed by Susaki and colleagues (Susaki et al., 2014). The same authors also applied LSFM to image the entire marmoset brain, opening the possibility of studying primate nervous system at an organ-wide level, but still with cellular resolution (Figure 10.2d).
Mechanical Signaling in the Urinary Bladder
Published in Jiro Nagatomi, Eno Essien Ebong, Mechanobiology Handbook, 2018
Aruna Ramachandran, Ramaswamy Krishnan, Rosalyn M. Adam
Although alterations in production of ECM proteins following bladder wall distension have been well documented, the molecular events underlying changes in ECM protein expression have not been fully elucidated. The immediate early gene Cyr61/CCN1 encodes a secreted, cysteine-rich, heparin-binding protein and functions as an ECM-associated signaling molecule. Cyr61 was shown to be induced in BSMC following cyclic stretch-relaxation, in a protein kinase C-, ROCK-, and PI3K/Akt-dependent manner [100]. Cyr61 and another immediate early gene product, connective tissue growth factor (CTGF/CCN2), also identified as mechanosensitive in BSMC [101], were found to be induced in the detrusor smooth muscle following PBOO in rats, with expression sustained for the duration of obstruction [102]. Among their various diverse functions, Cyr61 and CTGF are key regulators of wound healing and regulate the expression of various matrix-associated, angiogenic, and ECM-remodeling proteins such as MMPs, TIMPs, VEGF, and integrins [103,104].
Transcranial Magnetic and Electric Stimulation
Published in Ben Greenebaum, Frank Barnes, Biological and Medical Aspects of Electromagnetic Fields, 2018
Shoogo Ueno, Masaki Sekino, Tsukasa Shigemitsu
The immediate early gene expression in rat brain was compared between high-frequency (25 Hz) 2 T rTMS and electroconvulsive stimulation (ECS) (Ji et al., 1998). The rTMS was administered to awake rats by using a round coil (5 cm diameter). The coil was held above the rat’s head at close proximity to the site of stimulation at the orbit level. ECS was applied as follows: car clip electrodes connected to an ECT stimulator (unit 7801, Ugo Basile, Varese, Italy) were used on awake male adult rats. To induce maximal convulsive seizures, 1 s stimulation at 100 Hz, 5 ms pulse width, 90 mA electric current were chosen. Results were that ECS induces a rapid increase of c-fos mRNA expression through the brain in the hippocampus and neocortex. On the other hand, a single rTMS application produces a more discrete stimulation of c-fos mRNA expression. Most notably, rTMS results in strongly increased c-fos expression, predominately in the paraventricular nucleus of the thalamus (PVT) and specific cortical regions, and moderate expression in regions controlling circadian rhythms. ECS induces strong activation of c-fos expression in all cortical regions and hippocampus, but weaker activation in the PVT and suprachiasmatic nucleus (SCN).
Expression levels of selected cytokines and microRNAs in response to vitamin D supplementation in ultra-marathon runners
Published in European Journal of Sport Science, 2020
D. Pastuszak-Lewandoska, D. Domańska-Senderowska, J. Kiszałkiewicz, P. Szmigielska, A. Snochowska, W. Ratkowski, M. Spieszny, T. Klocek, P. Godlewski, P. Cięszczyk, E. Brzeziańska-Lasota, A. V. September, M. J. Laguette
The immediate early gene expression, as a first line of transcriptional responses stimulated by the physical effort, including the transcription of pro-inflammatory cytokines, can be modulated by the relevant miRNAs. Previous reports have demonstrated that in response to an exercise stimulus, miRNAs can alter gene expression levels (Radom-Aizik, Zaldivar, Leu, Galassetti, & Cooper, 2008, 2010), although the correlations between cytokines and their regulatory miRNAs have not been studied. Evidence from studies has indirectly explored the dose-dependent inflammatory miRNA response to acute aerobic exercise associated with control of the exercise-induced inflammatory cascade (de Gonzalo-Calvo et al., 2015). The significant inverse correlations found in our study in T1 support a down-regulation exerted by hsa-miRNA-155 and -miR-223 against IL-6. However, this was not observed after the UM, possibly because of the sample size of this study.
The cationic (calcium and lead) and enzyme conundrum
Published in Journal of Toxicology and Environmental Health, Part B, 2018
Jane Kasten-Jolly, David A. Lawrence
In cultures of PC12 cells, Pb increased PKC activity at 0.01 μM but reduced PKC activity at a concentration of 10 mM. This was attributed to the ability of 0.01 μM Pb to elevate cytosolic free calcium concentration. It was further observed that 10 μM Pb increased the level of ROS, which led to greater cytotoxicity and cell death. This effect might be enhanced by the addition of glutamate. The cytotoxicity might be partially blocked by a PKC inhibitor (staurosporine) and NMDA antagonist (MK-801). Therefore, in cases of Pb exposure, PKC activation and intracellular calcium together augment glutamate receptor mediated ROS formation and subsequent cell death (Jadhav, Ramesh, and Gunasekar 2000). In a study of immediate early gene expression, such as for c-fos, c-jun, and egr-1, in PC12 cells exposed to Pb, Kim et al. (2000) noted that activation of PKC was required for immediate early gene expression. Pb failed to increase c-fos mRNA in PC12 cells that were depleted of PKC or incubated in the presence of the PKC inhibitor H-7. A study performed in CL3 cells, a human non-small-cell lung adenocarcinoma cell, linked the activation of EGFR, epidermal growth factor receptor, by Pb exposure to the Ras/Raf-1/ERK signaling pathway with initiation through PKCα activation (Wang et al. 2009). CL3 cells were incubated in the presence of Pb (300 μM) or EGF (50–100 ng/ml) for 30 min. Results showed that Pb enhanced expression of Ras-GTP and p-Raf-1 and that this rise might be eliminated by pre-incubation of the CL3 cells with inhibitors of PKCα or RAS (RasN17). Further, Pb increased tyrosine kinase activity and this could be blocked by pre-incubation with inhibitors of EGFR (PD153035) or the Src family protein kinases (SU8656), suggesting that they are responsible for the tyrosine kinase activation in the Pb-treated CL3 cells. Overall, data indicated that Pb exposure first activated EGFR which then activated a Src family protein kinase leading to activation of PKCα and concomitant signaling through the ERK1/2 cascade via RAS and Raf-1. Tian, Sun, and Suszkiw (2000) examined the influence of Pb exposure on expression of tyrosine hydroxylase (TH) and choline acetyltransferase (ChAT) with respect to Pb-activation of cPKC in PC12 cells. It was observed that 0.53 μM Pb increased TH activity 150% after a 2 hr exposure, while ChAT activity was lowered to 45% after 6 hr Pb exposure. PKC activity increased to 200% after 2 hr of Pb exposure and then fell to control levels by 48 hr. An inhibitor of PKC activity (RÖ32-0342) suppressed the rise in TH activity, but did not markedly affect activity of ChAT. Therefore, it was concluded that PKC activation is involved in the early upregulation phase of TH activity perhaps through phosphorylation of TH. However, PKC does not modulate the prolonged upregulation of TH and downregulation of ChAT, which probably is mediated in the nucleus at their transcription sites.