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Pathogenesis: Molecular mechanisms of osteoporosis
Published in Peter V. Giannoudis, Thomas A. Einhorn, Surgical and Medical Treatment of Osteoporosis, 2020
Anastasia E. Markatseli, Theodora E. Markatseli, Alexandros A. Drosos
With regard to local factors, studies have shown that OPG, RANKL, and receptor activator of nuclear factor-κB (RANK), which are members of the superfamily of ligands and receptors of tumor necrosis factor (TNF), play an essential role in the regulation of bone remodeling (48–50). It is noteworthy that both OPG and RANKL are produced by osteoblasts. In particular, RANKL affects the fusion of osteoclast precursors in order to create a multinuclear mature osteoclast. The mechanism by which this differentiation of osteoclasts is achieved is the activation of the expression of c-Fos by RANKL (51). In contrast, OPG inhibits osteoclast differentiation (52). Moreover, macrophage colony-stimulating factor (M-CSF) modulates the proliferation of osteoclast progenitors and their differentiation into mature osteoclasts (53). M-CSF is expressed by osteoblasts and contributes to the maintenance of the survival of osteoclast precursors as well as to the suppression of apoptosis of mature osteoclasts (54,55). Therefore, osteoblasts produce activators (RANKL, M-CSF) and inhibitors (OPG) of osteoclast differentiation.
Gene Targeting Models of Epilepsy: Technical and Analytical Considerations
Published in Steven L. Peterson, Timothy E. Albertson, Neuropharmacology Methods in Epilepsy Research, 2019
Expression of the immediate early gene transcription factor c-fos is rapidly induced in response to seizure activity. To identify neural substrates of AGSs in 5-HT2C receptor mutant mice, AGS-induced patterns of c-fos-like immunoreactivity were examined. Staining was observed in subcortical structures associated with auditory processing in a pattern similar to those found in other AGS-susceptible strains. Because no X-linked genes have been implicated in AGS-susceptibility in these other strains, it is likely that AGSs may be produced not only by the absence of 5-HT2C receptors, but also by additional independent genetic mechanisms. This epilepsy syndrome is also the first audiogenic seizure model for which the causative genetic perturbation has been identified. Greater detail concerning sound-induced seizures may be found in Chapter 6.
Internet Pornography: Addiction or Sexual Dysfunction?
Published in Philipa A Brough, Margaret Denman, Introduction to Psychosexual Medicine, 2019
This dopaminergic system is modulated by various neurotransmitter systems, including cholinergic, opioid, cannabinoid, GABAergic (main inhibitory mediation) and glutamatergic (main excitatory mediation). The route travelled backwards and forwards is known as the mesocorticolimbic pathway or reward-motivation pathway. Activation of this dopamine system mediates the rewarding effect not only of drug but also of non-drug or behavioural stimuli (10). There are many other additional contributing factors, and particularly of interest is the transcription factor deltaFosB, a Fos family protein, which can be thought of as the ‘molecular switch’ for addiction in its role as mediator of reward memory. Its presence and behaviour appear to be genetically determined, suggesting genetic susceptibility to addictive behaviour. It is known to accumulate in the nucleus accumbens following induction by chronic as opposed to acute exposure to drugs of abuse. It has also been shown to accumulate in the same area following chronic overconsumption of natural rewards, demonstrably running and sucrose drinking (consuming sugary drinks). This causes a state of sensitisation and increased incentive drive for the reward (11).
Multiple brain regions are involved in reaction to acute restraint stress in CYLD-knockout mice
Published in Stress, 2023
Yuan-Yuan Han, Jian-Wen Zhou, Zhi-Wei Guo, Zhuo-Qing Wu, Zai-Yong Zhang, De-xiang Liu, Cheng Long
In this study, we explored the impact of environmental challenges on Cyld−/− mice by evaluating whether and how CYLD-knockout mice respond to the acute challenge posed by a single episode of ARS. The elevated plus maze (EPM) test was employed to assess anxious behavior in CYLD-knockout mice following ARS. We also used c-Fos immunochemical staining to characterize activated brain areas in CYLD-knockout mice after ARS. It is upregulated soon after a stimulus is delivered, so c-Fos is known as an early response gene and shows activity-dependent expression; consequently, it has been widely used to identify stimulation-induced neuronal activation (Bullitt, 1990). Our data highlight several new brain regions for studying the role of CYLD in the central nervous system.
c-Fos is upregulated in the genital tubercle of DEHP-induced hypospadiac rats and the prepuce of patients with hypospadias
Published in Systems Biology in Reproductive Medicine, 2021
Han Xiang, Shao Wang, Xiaoyan Kong, Yihang Yu, Lianju shen, Chunlan Long, Xing Liu, Guang-Hui Wei
The proto-oncogene c-Fos (Piechaczyk and Blanchard 1994) is involved in the regulation of numerous genes that control growth and differentiation in many tissues (Barrett et al. 2017). c-Fos functions largely to promote growth, cell survival, oncogenesis, tumor invasion, and metastasis (Zhang et al. 2007). The c-Fos protein regulates gene expression as part of a dimeric AP-1 complex, typically with a member of the c-Jun family of transcription factors. Of note, c-jun N-terminal kinase (JNK) 1/2 has been reported to be upregulated in patients with hypospadias and thus might play a role in the development of external male genitalia defects (Li et al. 2013). The evidence described above suggests that c-Fos might play a role in the etiology of hypospadias. Thus, we sought to verify the changes in c-Fos in hypospadiac patients.
Advances in understanding the mechanisms of retinal degenerations
Published in Clinical and Experimental Optometry, 2020
In order to study these retinal plasticity changes in more detail, we generated a transgenic mouse in which neurons are labelled by a transgenic beta galactosidase reporter system when they are activated. This mouse, called the rd1‐FTL mouse, carries a mutation in the beta subunit of phosphodiesterase 6 that leads to retinal degeneration via a similar mutation to human autosomal recessive RP,50 together with an axonally targeted transgenic beta galactosidase reporter system that is under the control of the c‐fos promoter.51 C‐fos is an intermediate gene that is activated following neural activity, cell death or plasticity.200251,52 FTL mice have been used to study activated circuits in the brain and retina – neurons labelled with beta galactosidase (blue) when activated.200251,52