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Candida Biofilms
Published in Chaminda Jayampath Seneviratne, Microbial Biofilms, 2017
Chaminda Jayampath Seneviratne, Thuyen Truong, Yue Wang
Dispersal is the least understood and perhaps the most complicated process involved in both fungal and bacterial biofilms. As a part of their life cycle, members of the Candida biofilm community singly or as a group may detach from the biofilm and disseminate through a fluid phase to seed new sites. Genome-wide studies have shown that Set3, an NAD-dependent histone deacetylation complex, modulates the expression of NRG1 [49], which encodes a transcriptional regulator of biofilm dispersal [50]. Nrg1 is a well-known transcriptional repressor of filamentation [51], and Set3 complex mutants are hyperfilamentous [52]. The typical dispersal of C. albicans cells from biofilms is found to be in the yeast form, possibly due to the effect of Nrg1 and Set3 complex [50]. Thus, manipulations that increase filamentous cells and decrease yeast-form cells may reduce biofilm dispersal [53]. Studies by Murad et al. revealed that the dispersal stage of the fungal biofilm has an association with disease progression. In C. albicans, deletion of the NRG1 gene completely attenuated virulence in a murine model of systemic candidiasis [54]. However, as deleting NRG1 causes a constitutive filamentous growth of C. albicans cells, it is not certain that the effect is due solely to biofilm dispersal. If targeted well, blocking the biofilm dispersal stage may provide an alternative strategy for developing novel therapeutic options in the future for controlling Candida biofilm–associated infections.
Genetic influences on antisocial behaviour, problem substance use and schizophrenia: evidence from quantitative genetic and molecular genetic studies
Published in John C. Gunn, Pamela J. Taylor, Forensic Psychiatry, 2014
Pamela J Taylor, Marianne BM van den Bree, Nigel Williams, Terrie E Moffitt
So, together, the positive association data in three genetic locations and the fact that all studies have reported more significant results from haplotypic analysis than from single marker analysis suggest that the true causative variants directly increasing susceptibility to schizophrenia, or psychosis more generally, have not yet been found (Williams et al., 2004, 2006; Stefansson et al., 2002). In addition, the high number of different associated haplotypes that have been reported, especially at DTNBP1 and NRG1, indicates either substantial heterogeneity in linkage disequilibrium structure in different populations or the presence of multiple risk alleles, perhaps both.
NRG1 PLGA MP locally induce macrophage polarisation toward a regenerative phenotype in the heart after acute myocardial infarction
Published in Journal of Drug Targeting, 2019
S. Pascual-Gil, G. Abizanda, E. Iglesias, E. Garbayo, F. Prósper, M. J. Blanco-Prieto
Another factor that is mandatory to consider regarding MP administration is when to administer the treatment. On one hand, piMac are predominant during the first days after AMI and aiMac exert their role afterwards [26]. On the other hand, each type of macrophage may respond in a different way to NRG1 PLGA MP. Moreover, one of the main NRG1 therapeutic actions is the promotion of cardiomyocyte proliferation [33]. After AMI, although the majority of the cardiomyocytes’ death occurs during ischaemia, necrosis and apoptosis processes can continue for up to 3 days [34]. This creates a therapeutic window for arresting cell death using NRG1. In addition, patients promptly treated after the onset of symptoms of AMI will have the best outcomes [35]. In this study we evaluated how NRG1 PLGA MP administration could diversely affect heart inflammatory response depending on the time of treatment administration (15 min, 24, 72 and 168 h after AMI induction). We selected these time points because they are clinically relevant and cover the therapeutic window of NRG1. Surprisingly, we demonstrated that inflammatory response was not modified by the time at which the treatment was administered (Figure 4(B)), and NRG1 PLGA MP treated animals showed a similar macrophage polarisation to control animals regardless of the time of treatment administration. Clinically, this means that PLGA MP could be administered whenever needed in order to meet the therapeutic window of the encapsulated GF, without undesired inflammatory issues.
Circulating neuregulin-1 levels in polycystic ovary syndrome
Published in Journal of Obstetrics and Gynaecology, 2019
NRG1 is a cytokine that belongs to a family of proteins structurally related to epidermal growth factors (EGF) and it is expressed by cells of an endothelial and mesenchymal origin (Meyer et al. 1997). EGF induces division, differentiation, survival, proliferation, and the migration of the many cells, including the somatic cells of the developing follicle (Richani and Gilchrist 2017). NG1 binds to the erythroblastic leukaemia viral oncogene homologues 3 and 4 (ErbB3 and 4) receptors (Britsch 2007). The ErbB receptor tyrosine kinase family consists of four members such as ErbB1/EGFR/HER1, ErbB2/HER2, ErbB3/HER3, and ErbB4/HER4. The ErbB3 and ErbB4 receptors were detected in the reproductive tract (Prigent et al. 1992; Srinivasan et al. 1998). NRG1 binds to tyrosine kinase receptors ErbB3 and ErbB4, which form homodimers or ErbB2 heterodimers, and thus dimerisation activates ErbB receptor phosphorylation, activating a number of downstream signalling proteins (Carraway and Cantley 1994).
Association of Neuregulin 1 rs7835688 G > C, rs16879552 T > C and rs2439302 G > C Polymorphisms with Susceptibility to Non-Syndromic Hirschsprung’s Disease
Published in Fetal and Pediatric Pathology, 2021
Seyed Hamed Hosseini-Jangjou, Seyed Alireza Dastgheib, Majid Aflatoonian, Abdolhamid Amooee, Reza Bahrami, Elham Salehi, Jalal Sadeghizadeh-Yazdi, Hossein Neamatzadeh
HSCR is a complex and heterogeneous genetic disease, where alterations at different molecular levels are required for the development of the disease [2, 10]. It is evident that a wide spectrum of mutations at different genes causes HSCR, although the occurrence and severity of HSCR from many cases remain unexplained [16]. NRG1 plays a pivotal role in the neural circuitry generation, axon ensheathment, neuronal migration, synaptic plasticity, myelination and neurotransmission [17]. The human gene encoding NRG1 (MIM: 142445) is mapped to chromosome 8p, spanning about 1.2 Mb and contains more than 23000 variants [18]. The NRG1/ErbB system promotes neuronal survival and plays an important role in the maintenance of the ENS [19, 20]. Some functional studies indicate that NRG1 polymorphisms might play a role in the pathogenesis of non-syndromic HSCR [21, 22]. Over the course of the past few years, the association of NRG1 polymorphisms with HSCR risk had been repeatedly verified in different Asian populations, but there was no study in the Iranian population. This is the first assessment of the frequency of NRG1 polymorphisms in Iranian children with HSCR. Our study is the first assessment of any association of rs7835688 G > C and rs16879552 T > C polymorphisms of the NRG1 gene with HSCR risk using a TaqMan genotyping assay, and provides further insights into the contribution of the NRG1 rs7835688 G > C, rs16879552 T > C and rs2439302 G > C polymorphisms in the molecular genetic pathogenesis of HSCR. Our results showed that NRG1 rs7835688 G > C, rs16879552 T > C and rs2439302 G > C polymorphisms were not significantly associated with increased risk of HSCR in our population.