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Etiopathogenesis
Published in Vineet Relhan, Vijay Kumar Garg, Sneha Ghunawat, Khushbu Mahajan, Comprehensive Textbook on Vitiligo, 2020
Dario Didona, Biagio Didona, Giovanni Paolino, Raffaele Dante Caposiena Caro
Both peripheral nerve sheath and melanocytes arise from neural crest cells (NCC). These cells migrate from the neural tube to dorsolateral and ventral directions [38] (Figure 5.5). On the one hand, cells with only a dorsolateral trajectory are committed to melanocytic fate; on the other hand, cells with a ventral trajectory are committed to neuronal, glial/melanocyte, or endoneurial fibroblast fate [38]. It has been shown that SOX10+ NCCs fail to initiate the neuronogenesis, adopting a glial pathway to give rise to Schwann cells and melanocytes, highlighting the link between pigmentary disorders (as vitiligo) and neural cells [38]. Neuregulin 1 is an axon-derived growth factor which, when overexpressed, promotes glial fate and suppresses melanocytic activity [39]. Furthermore, melanocytes with the overexpression of embryo retinal epithelium can dedifferentiate back to their unpigmented glial progenitor [39].
Schizophrenia
Published in Ben Green, Problem-based Psychiatry, 2018
Recent research has continued to search for a gene for schizophrenia. No specific gene has yet materialised and this would be the case for a heterogeneous illness. Some ‘susceptibility’ gene candidates have been proposed such as neuregulin which is involved in neuronal and glial cell growth and synaptic plasticity and dybindin which controls symptom function and signalling.
100 MCQs from Dr. David Browne and Colleagues
Published in David Browne, Selena Morgan Pillay, Guy Molyneaux, Brenda Wright, Bangaru Raju, Ijaz Hussein, Mohamed Ali Ahmed, Michael Reilly, MCQs for the New MRCPsych Paper A, 2017
Dr Karen Fleming, Dr Michael Kenewali, Dr Manas Sarkar, Dr Daniel White
Much work has been done to identify susceptibility genes in schizophrenia and bipolar disorder. The current evidence implicates specific genes in both disorders. Evidence supports neuregulin 1 (NGR1), dysbindin (DTNBP1), DISC1, D-amino acid oxidase activator (DAOA (G72)), D-amino acid oxidase (DAO) and regulator of G-protein signalling (RGS4) as schizophrenia susceptibility loci. For bipolar disorder the strongest evidence supports DAOA (G72) and brain-derived neurotrophic factor (BDNF). Increasing evidence suggests an overlap in genetic susceptibility across the traditional classification system that dichotomised psychotic disorders into schizophrenia or bipolar disorder, most notably with association findings at DAOA (G72), DISC1, and NGR1. (1, p 572)
The significance of the neuregulin-1/ErbB signaling pathway and its effect on Sox10 expression in the development of terminally differentiated Schwann cells in vitro
Published in International Journal of Neuroscience, 2021
Xizhong Yang, Cuijie Ji, Xinyue Liu, Chaoqun Zheng, Yanxin Zhang, Ruowu Shen, Zangong Zhou
This study explored the effects of the neuregulin 1/ErbB system and Sox10 on the differentiation of SCs, the results of which were consistent with previous studies [17]. According to our results, the expression of neuregulin-1 did not differ significantly in three groups, but the expression of sox10 was decreased in the TAK165 group compared with that in the control group. However, there was no significant difference in the expression of sox between the control group and the HRG-off group. Neuregulin-1 promotes the differentiation of neural crest stem cells into glial cells, and it promotes the survival, proliferation and migration of Schwann cell precursors [18]. Neuregulin-1 is one of the most important signaling molecules in myelination [18]. It affects the activity of SCs after a neurological injury [19]. It can be seen from the results that neuregulin-1 is always expressed stably throughout the undifferentiated period and the entire induction period. Thus, in the process of differentiation, high (stable) expression of neuregulin-1 also indicates its importance in the differentiation of Schwann-like cells. We identify signaling by ErbB receptor tyrosine kinase as an important regulator of SC development with respect to SC proliferation, apoptosis, and support of neurite growth. In the presence of other induced factors, the morphology and protein markers of the HRG-off group changed a lot compared with the control group, which indicates the significance of heregulin in the terminal differentiation of Schwann-like cells.
NRG1 and NRG2 fusions in non-small cell lung cancer (NSCLC): seven years between lights and shadows
Published in Expert Opinion on Therapeutic Targets, 2021
Domenico Trombetta, Angelo Sparaneo, Federico Pio Fabrizio, Concetta Martina Di Micco, Antonio Rossi, Lucia Anna Muscarella
At the same time as exploring the epidemiological context of fusions involving the neuregulins genes, the molecular and pathological features of NRG1-positive tumors have taken shape over the past two years: the NRG1 fusions appeared molecularly, pathologically, and clinically more heterogeneous than previously recognized. NRG1 and NRG2 are strictly related to aberrant ErbB activation, cell proliferation, and invasion, and have been frequently identified in tumors that are pan-negative for other main molecular drivers [4,5,7]. Before translating the neuregulins fusions into the clinical practice, the scientific community must make its way between lights and shadows and address any major points toward the full characterization of the genomic rearrangements involving the NRG1 and NRG2 genes. There is increasing attention and need to clarify the associated clinical-pathological background of cancer patients and their impact on patients’ responses to various agents. All these points are strictly related to the understanding of the oncogenic role and cellular effects elicited by the different NRG1 and NRG2 fusions variants [1].
Matrix metallopeptidase 9 and placental growth factor may correlate with collateral status based on whole-brain perfusion combined with multiphase computed tomography angiography
Published in Neurological Research, 2021
Bo Yang, Yarong Ding, Xin Liu, Yuan Cai, Xinxuan Yang, Qixuan Lu, Weibin Gu, Liping Liu, Yuehua Pu
Identifying the related factors and biomarkers of collateral circulation is the prerequisite to find treatment targets for improving collateral circulation. Differences of collateral assessment tools in studies may affect the consistency of the results on influence factors. Metabolic syndrome, hyperuricemia and older age [8] are associated with poor leptomeningeal collateral status in patients with acute ischemic stroke [9]. Younger age, dyslipidemia and lower creatinine levels were predictors of better collaterals in acute ischemic stroke patients from proximal MCA occlusions [10]. Several serum biomarkers have proved to be correlated with coronary collateral circulation in patients with coronary artery disease. Neuregulin-1 [11], endostatin [12], YKL-40 [13] may be useful biomarkers for coronary collateral development and potential target for therapeutic angiogenesis in patients with coronary artery disease.