China
Africa
Explore chapters and articles related to this topic
Ion Channels in Human Pluripotent Stem Cells and Their Neural Derivatives
Published in Tian-Le Xu, Long-Jun Wu, Nonclassical Ion Channels in the Nervous System, 2021
Ritika Raghavan, Robert Juniewicz, Maharaib Syed, Michael Lin, Peng Jiang
GABAergic interneurons can also be generated using the direct reprogramming method with high efficiency. By expressing the transcription factors Foxg1, Sox2, Ascl1, Dlx5, and Lhx6 in in human fibroblasts, researchers were able to produce functional GABAergic interneurons in vitro (51). The electrophysiological activity of these neurons was measured using patch clamp analysis. As early as week four post-differentiation, these neurons acquired the ability to fire APs repetitively at high frequencies, typical of the interneurons. GABAergic inhibitory synaptic neurotransmission of the fibroblast-derived GABAergic interneurons was also detected (51). Other studies have shown that using transcription factors, such as Ascl1, Dlx2, NKX2.1, and Lhx6, hPSCs can be rapidly induced to differentiate to GABAergic interneurons. GABAergic interneurons generated using this method produce mature APs and exhibit synapse activities within 5 to 8 weeks (13,15).
Introduction to Oral and Craniofacial Tissue Engineering
Published in Vincenzo Guarino, Marco Antonio Alvarez-Pérez, Current Advances in Oral and Craniofacial Tissue Engineering, 2020
María Verónica Cuevas González, Eduardo Villarreal-Ramírez, Adriana Pérez-Soria, Pedro Alberto López Reynoso, Vincenzo Guarino, Marco Antonio Alvarez-Pérez
Bone Morphogenetic Proteins (BMP) are a group of proteins involved in multiple development processes which include skeletal formation, embryogenesis, hematopoiesis and neurogenesis. These proteins belong to the Transforming Growth Factor Beta superfamily, and over 20 members have been characterized. Four groups are formed to classify these proteins based on its amino acid sequence similarity: BMP2/4, BMP5/6/7/8a/8b, BMP9/10, and BMP12/13/14. These proteins are synthetized as a large precursor from 400–500 aa, which has three main domains, N-terminal secretion signal, a prodomain and a C-terminal region that constitutes the mature protein. Most of BMPs have seven cysteine residues in the C-terminal region, which are involved in its self-assembly and is known as a cysteine knot. BMPs functioning depends on the structural arrangement as homo- or heterodimers, which in turn are associated with specific membrane serine/threonine receptors denoted as type I and type II to trigger two main signal pathways: Smad (mothers against decapentaplegic) dependent pathway and Mitogen-Activated Protein Kinase (MAPK) pathway. This BMPs-MAPK signal pathway has shown its potential as an inductor of mesenchymal stem cells differentiation into osteoblasts, this extracellular signal is transduced inside the nucleus via the activation of ERK1/2, p38, INK 1/2/3 cascades which activate specific transcriptional factors (RUNX2, DLX5, and Osterix) related with the osteoblastic commitment and initiate the production of bone matrix proteins, leading to bone morphogenesis (Ripamonti 2019; Anusuya et al. 2016).
Individual conditions grouped according to the international nosology and classification of genetic skeletal disorders*
Published in Christine M Hall, Amaka C Offiah, Francesca Forzano, Mario Lituania, Michelle Fink, Deborah Krakow, Fetal and Perinatal Skeletal Dysplasias, 2012
Christine M Hall, Amaka C Offiah, Francesca Forzano, Mario Lituania, Michelle Fink, Deborah Krakow
Genetics: Heterogeneous disorder, six subtypes known: SHFM1 maps to chromosome 7q21 and recently mutations in the gene DLX5 have been identified in one family, SHFM2 maps to chromosome Xq26, SHFM3 is caused by duplication of chromosome 10q24, SHFM4 is caused by mutation in the TP63 gene (chromosome 3), SHFM5 maps to chromosome 2q31, SHFM6 is caused by mutation in the WNT10B gene on chromosome 12q13. Inheritance is autosomal dominant in SHFM 1, 3 and 4, X-linked recessive in SHFM2, unknown in SHFM5, autosomal recessive in SHFM6. Penetrance is incomplete.
A comprehensive overview on utilizing electromagnetic fields in bone regenerative medicine
Published in Electromagnetic Biology and Medicine, 2019
Esmaeel Azadian, Bahar Arjmand, Zohreh Khodaii, Abdolreza Ardeshirylajimi
To investigate the possible role of Notch signaling pathway in osteogenesis, Bagheri et al. (2018) ran an in vitro study on bone marrow hMSCs using PEMFs. As expected, PEMF increased the expression of osteocalcin and osteogenic transcription factors (Runx2, Dlx5, Osterix) and promoted ALP activity, ECM mineralization. Interestingly, PEMF treatment affects some of Notch signaling pathway components (receptors, ligands, and nuclear target genes); it enhanced the expression of Notch4 (a Notch receptor), Dll4 (ligand), and the nuclear target genes of Hey1, Hes1, and Hes5. In addition, it has been shown that the inhibition of this pathway led to a significant reduction in the expression of osteogenic markers (Runx2, Dlx5, Osterix) and nuclear target genes (Hes1 and Hes5).
Contribution of Human Trophoblast Progenitor Cells to Neurogenesis in Rat Focal Cerebral Ischemia Model
Published in Brain Injury, 2021
Kerem Yanar, Muge Molbay, Eylem Özaydın-Goksu, Gozde Unek, Emre Cetindağ, Ali Unal, Emin Turkay Korgun
DLX2 and DLX5 are important transcriptional factors in neuronal fate, differentiation, and development. To determine whether hTPC treatment affects DLX2 and DLX5 expression after ischemia, we demonstrated immunohistochemistry analysis, which shows that the DLX2 is expressed mainly in motor neurons, and its level did not change after ischemia or after hTPC treatment. On the other hand, DLX5, which is expressed in both motor neurons and neuroglial cells, levels are greatly reduced in neurons and neuroglial cells after ischemia, but increased after hTPC treatment, especially in motor neurons (Figure 8, Figure 9).
Integrated analysis of human transcriptome data for Rett syndrome finds a network of involved genes
Published in The World Journal of Biological Psychiatry, 2020
Friederike Ehrhart, Susan L. Coort, Lars Eijssen, Elisa Cirillo, Eric E. Smeets, Nasim Bahram Sangani, Chris T. Evelo, Leopold M.G. Curfs
Genes that are involved in RTT disorder development and progression, according to previously published studies, are MECP2, CDKL5, EGR2, PTPN1, BDNF, GAMT, FKBP5, IGF2, DLX5, DLX6, SGK1, MPP1, FXYD1, UBE3A and GRID1 (Ehrhart et al. 2016). These genes were found again in the data, but the reported outcome shows a greater variability than reported in literature. BDNF e.g., is mostly reported to be down regulated in RTT (or model systems). We found a significant downregulation only in one fibroblast and one iPSC sample, in other samples gene expression changes were not significant and occurred in both directions. We did not find a significant change in expression profile for either DLX5 or DLX6 and can therefore support the hypothesis that it is not involved in RTT disorder progression (Schule et al. 2007; Miyano et al. 2008). A general observation was that the gene expression patterns vary greatly among the different samples, which matches previous observations, e.g., from Colantuoni et al. (2001) and Tanaka et al. (2014). This study investigated iPSCs derived from RTT patients (and a clone with healthy X-chromosome as control) and all of them had different causative MECP2 mutations. The result was that gene expression profiles for those patients were very different. In our study, too, there is no single mutation occurring twice in the sample datasets. Low overlap of previously known genes and identified by the data-driven approach was reported several times previously (e.g., an epilepsy study (Rogic and Pavlidis 2009)), and all these studies revealed new genes which were not yet known to be involved in disease progression (Roder et al. 2012; Mistry et al. 2013; Raddatz et al. 2014; Ch'ng et al. 2015).