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Intestinal Immune Adaptation and Necrotizing Enterocolitis
Published in David J. Hackam, Necrotizing Enterocolitis, 2021
The mature small intestinal mucosa is characterized by gland-like crypts and fingerlike protrusions called villi. These structural features provide a protected stem cell niche and ensure efficient food degradation and nutrient uptake, respectively. The small intestinal epithelium encompasses six major epithelial cell lineages, Lgr5+ stem cells, the pool of rapidly proliferating transit-amplifying (TA) cells, and antimicrobial peptide-secreting Paneth cells situated at the crypt base as well as mucus-producing goblet cells, tuft cells, enteroendocrine cells, and absorptive enterocytes that constitute the villus epithelium. Lgr5+ stem cells and the rapidly proliferating TA cells are maintained by high concentrations of Wnt ligands and Notch signaling in the crypt region (6). The differentiation program for the epithelial lineages is initiated by reduced Wnt ligand exposure and Notch signaling when cells migrate upward along the crypt–villus axis and leave the crypt. Major pathways such as BMP as well as lineage-specific transcription factors (e.g., HES1 for absorptive enterocytes, SOX8 for M cells, ATOH1 for the secretory lineages and in combination with SOX9 for Paneth cells) (7-9) drive specific expression profiles. They facilitate a balanced cell differentiation to generate all epithelial lineages. Apoptosis and exfoliation at the villus tip facilitate constant renewal of the epithelial layer every 5 to 7 days. Also, the adult colon epithelium, mainly responsible for electrolyte and water absorption, undergoes constant renewal. It lacks the villus protrusions but harbors stem cells and rapid amplifying cells within the long and deep colonic crypts.
Detection of a Large Novel α-Thalassemia Deletion in an Autochthonous Belgian Family
Published in Hemoglobin, 2019
Laura Heireman, Ariane Luyckx, Katrien De Schynkel, Annelies Dheedene, Mélanie Delaunoy, Anne-Sophie Adam, Béatrice Gulbis, Johan Dierick
As the deletion was extended in the ATR-16 syndrome locus, at first diagnosis of this rare contiguous gene deletion syndrome was presumed. The ATR-16 syndrome results from a deletion (1-2 Mb) at the telomeric short arm of chromosome 16p13.3 removing both α-globin genes and genes involved in central nervous system development and function nearby the α-globin locus [1,2,4,8]. The ATR-16 syndrome is characterized by mild intellectual disability, facial and skeletal abnormalities and developmental delay [1,3,8,9]. Harteveld [10] narrowed the region for which haploinsufficiency leads to mental retardation and dysmorphic features typical for ATR-16 down to a ∼800 kb region localized between 0.9 and 1.7 Mb from the telomere of 16p. About 14 known genes or gene families are located in this locus [10]. Pfeifer [8] identified a deletion of the SOX8 gene as a possible contributor to the mental impairment seen in the ATR-16 syndrome. In contrast, Bezerra et al. [11] described a Brazilian family characterized by haploinsufficiency of SOX8 but without intellectual disability or dysmorphic features. The deleted region observed in the current family is very small compared to deletions described in ATR-16 syndrome and does not contain the ∼800 kb region associated with intellectual disability and dysmorphic features, thereby excluding a full-blown ATR-16 syndrome [9].
Circ_0008365 Suppresses Apoptosis, Inflammation and Extracellular Matrix Degradation of IL-1β-treated Chondrocytes in Osteoarthritis by Regulating miR-324-5p/BMPR2/NF-κB Signaling Axis
Published in Immunological Investigations, 2022
Zilong Zhang, Teng Zhao, Haiwei Xu, Xing Wu
Circular RNAs (circRNAs) have vital regulatory roles in cell differentiation and development of eukaryotes (Di Timoteo et al. 2020). Several circRNAs have been used as molecular targets for OA prediction and treatment (Yu et al. 2018). CircRNAs can regulate the progression of human diseases via competing endogenous RNA (ceRNA) network. For instance, circEXOC6B regulated cell proliferation and invasion in ovarian cancer by sponging miR-421 to increase RUS1 level (Wang et al. 2020). CircRNA_0084043 facilitated the progression of diabetic retinopathy by regulating miR-140-3p/TGFA axis (Li et al. 2020). Downregulation of circHIPK3 promoted chondrocyte apoptosis in OA via targeting miR-124 to inhibit SOX8 expression (Wu et al. 2020).
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
The neurons and glial cells of Sox10 knockout mice were affected to varying degrees. Some nerve cells could still be specified and develop, Sox10 is a transcription factor that belongs to the SoxE family, which also includes Sox8 and Sox9, but Sox10 plays a more important role. It was found that the neurons and glial cells of Sox10 knockout mice were affected to varying degrees, even without the sox10 some nerve cells could still be specified and develop but no glial cells could form either in vivo or in vitro [20, 21]. Therefore, Sox10 is essential for the formation and development of glial cells in the PNS. Surprisingly, however, we found that the expression of Sox10 decreased in the TAK 165 group, in which an ErbB2 blocking agent was added, but there was no obvious change in the HRG-off group, in which HRG was not added. One of the reason for this phenomenon may be the high level of neuregulin-1 expression in the HRG-off group, because the amount of neuregulin-1 has reached a saturation state, excessive neuregulin-1 cannot cause obvious biological effects. Another possibility, Neuregulin 1 gene has a variety of spliceosome, including I type ARIA (acetylcholine receptor inducing factor), type II glial cell growth factor (gial growth factor, GGF) as well as the type III sensorimotor derived factor (chipmaker sensory and motor derived factor, SMDF) [22], and heregulin I and its main with the survival of the schwann cells and promote the growth of axons [14], but type III neuregulinsand Sox10 have the most closely related functions. Therefore, the HRG-off group showed no significant impact on the expression of Sox10. The inhibitor of the neuregulin-1/ErbB signaling pathway disrupts the entire signaling pathway and affects the expression of Sox10. This demonstrates that Sox10 is affected by the neuregulin-1/ErbB signaling pathway rather than by heregulin.