scholarly journals High expression of SARS-CoV2 viral entry-related proteins in human limbal stem cells

Author(s):  
Yuzuru Sasamoto ◽  
Catherine A.A. Lee ◽  
Masahito Yoshihara ◽  
Gabrielle Martin ◽  
Bruce R. Ksander ◽  
...  
2006 ◽  
Vol 69 (12) ◽  
pp. 983-991 ◽  
Author(s):  
Enzo Di Iorio ◽  
Vanessa Barbaro ◽  
Stefano Ferrari ◽  
Claudio Ortolani ◽  
Michele De Luca ◽  
...  

2021 ◽  
Vol 11 (8) ◽  
pp. 1576-1581
Author(s):  
Yiwei Shen ◽  
Xue Li ◽  
Xiaoke Wu ◽  
Yi Li ◽  
Yiwei Shen ◽  
...  

SIRT1 is known to be closely associated with cellular senescence, while the relationship between miR-487a-3p and SIRT1 and their role in mesenchymal stem cells (MSCs) remains unclear. MiRDB analysis showed SIRT1 is a target of miR-487a-3p. Here we investigated whether miR-487a-3p modulates senescence of mesenchymal stem cells by targeting SIRT1. The human MSCs (hMSCs) were divided into control group (NC group), miR-487a-3p Mimics group, pCMV-SIRT+miR-487a-3p Mimics group followed by analysis of miR-487a-3p expression by qPCR and protein level of SIRT1, P21 and P53 by western blot. Dual luciferin report assay verified the binding of miR-487a-3p to SIRT1 mRNA and β-galactosidase activity staining detected hMSCs senescence. miR-487a-3p level was significantly elevated after miR-487a-3p Mimics treatment (P <0.01) without difference between miR-487a-3p Mimics group and pCMV-SIRT1 group+miR-487a-3pMimics (P >0.05). miR-487a-3p mimics significantly decreased SIRT1 level (P < 0.01), which was reversed by pCMVSIRT1 plasmid transfection (P <0.05). Moreover, miR-487a-3p could bind SIRT1 mRNA 3′-UTR region. Further more, miR-487a-3p Mimics induced cellular senescence as displayed by increased β-galactosidase activity (P <0.01) and increased level of senescence-related proteins P21 and P53 (P < 0.01), which were all reversed by overexpression of SIRT1 (P < 0.05). In conclusion, miR-487a-3p reduced SIRT1 expression, thus promoting hMSCs senescence, while overexpression of SIRT1 could counteract the senescence of hMSCs induced by miR-487a-3p.


2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi23-vi23
Author(s):  
Alexandra Calinescu ◽  
Zain Sultan ◽  
McKenzie Kauss ◽  
Wajd Al-Holou ◽  
Jason Heth

Abstract Glioblastoma (GBM) is the most common and deadly primary brain tumor in adults. Recurrence of the disease is attributed in part to the presence of Glioma Stem Cells (GSC), which are resistant to chemo- and radiotherapy and can initiate tumor formation. Molecularly, GSCs resemble the mesenchymal subtype that is associated with worse prognosis. GSCs share many characteristics with Neural Stem Cells (NSCs) including proliferative potential, migratory capacity, telomerase activity, diverse progeny and similar gene signature, however differ fundamentally from NSCs in their tumor forming ability. RNA-Seq analysis of GSCs and NSCs illustrates significant enrichment in GSCs of transcription factors (TFs) known to be dysregulated in cancer, chief among them being SIX1, a developmental TF with documented roles in progression of multiple cancers. Overexpression of SIX1 in A172 GBM cells enhances proliferation, promotes resistance to radiotherapy and alters expression of a core set of 4 developmental TFs (POU3F2, SALL2, OLIG2 and SOX2) capable to reprogram differentiated GBM cells into GSCs (Suva et al., 2014). Analysis of SIX1 in surgical samples from glioma patients illustrates that high expression of SIX1 correlates with tumor grade, finding corroborated in the TCGA and CGGA data sets. Surprisingly, primary NSCs, after extended time in culture, increase their proliferation rate, acquire a mesenchymal transcriptional signature akin to GSCs, including high expression of SIX1, and form deadly tumors when implanted into the brains of mice. Comparing the epigenetic landscape of transformed and normal NSCs we identify a significant enrichment of accessible chromatin at promoter and enhancer loci in transformed NSCs, including at regulatory regions of SIX1 and of genes that define mesenchymal GBM. These data suggest that SIX1 may represent an upstream regulator of the GSC phenotype and may drive malignant transformation of NSCs. Genetic and epigenetic loss of function analyses are ongoing to test this hypothesis.


2019 ◽  
Vol 8 (2) ◽  
pp. 41
Author(s):  
Zarka Stoycheva ◽  
Yana Manolova ◽  
Yordan Yordanov

2016 ◽  
Vol 5 (83) ◽  
pp. 6182-6185
Author(s):  
Subbiah Vasan Chandrakumar ◽  
Sudalaiyandi Ganapathirajesh ◽  
Shanmugasami Kavitha ◽  
Sundararajalu Abirami ◽  
Mohanasundaram Vijayalakshmi ◽  
...  

Cornea ◽  
2007 ◽  
Vol 26 (4) ◽  
pp. 473-478 ◽  
Author(s):  
Ahmed Galal ◽  
Juan J Perez-Santonja ◽  
Jose Luis Rodriguez-Prats ◽  
Marta Abad ◽  
Jorge Alio

Author(s):  
Edward J. Holland ◽  
Mayank Gupta

The corneal epithelium is a rapidly regenerating, stratified squamous epithelium. Homeostasis of corneal epithelial cells is an important prerequisite, not only for the integrity of the ocular surface, but also for the visual function. The maintenance of a healthy corneal epithelium under both normal and wound-healing conditions is achieved by a population of stem cells located in the basal layer of limbal epithelium. The Limbus represents the transition zone between the peripheral cornea and the bulbar conjunctiva. The stem cells from the limbus generate the transient amplifying cells that migrate, proliferate, and differentiate to replace lost or damaged corneal epithelial cells. In patients with aniridia, there is a primary dysfunction of these limbal stem cells (see Figure 6.1). The cornea is affected clinically in 90 percent of the patients with aniridia. In most cases, the cornea in aniridic patients appears normal and transparent during infancy and childhood. However, during the early teens, the cornea begins to show changes. The early changes are marked by the in-growth of opaque epithelium from the limbal region into the peripheral cornea, which represents conjunctival epithelial cells, goblet cells, and blood vessels in the corneal epithelium. These changes gradually progress toward the central cornea and may cause corneal epithelial erosions and epithelial abnormalities that eventually culminate in opacification of the corneal stroma, which leads to vision loss. With the gradual loss of limbal stem cells, the entire cornea becomes covered with conjunctival cells. Eventually, many patients develop total limbal stem cell deficiency. These abnormalities usually become more pronounced with aging. The corneal abnormalities seen in aniridia are collectively termed “aniridic keratopathy”. Significant corneal opacification may occasionally be the initial manifestation of aniridia. Abnormal tear film stability and meibomian gland dysfunction are also observed in patients with aniridia. This can lead to dry eyes, aggravating corneal erosion and ulceration observed in aniridic patients. Sometimes, aniridia is associated with “Peter’s anomaly,” in which central corneal opacity is present at birth along with defects in the corneal endothelium and Descemet’s membrane.


2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Fang Li ◽  
Jianglin Chen ◽  
Mengjia Gong ◽  
Yang Bi ◽  
Chengchen Hu ◽  
...  

Mesenchymal stem cells (MSCs) are multipotent progenitor cells in adult tissues. The aim of this study is to isolate and identify synovial fluid-derived mesenchymal stromal cells (SF-MSCs) from the popliteal cyst fluid of pediatric patients. SF-MSCs were collected from the popliteal cyst fluid of pediatric patients during cystectomy surgery. After cyst fluid extraction and adherent culturing, in vitro morphology, growth curve, and cell cycle were observed. The expression of stem cell surface markers was analyzed by flow cytometry, and expression of cell marker protein was detected by immunofluorescence. SF-MSCs were cultured in osteogenic, adipogenic, and chondrogenic differentiation medium. The differentiation potential of SF-MSCs was analyzed by alkaline phosphatase (Alizarin Red), Oil Red O, and Alcian blue. Antibody detection of human angiogenesis-related proteins was performed compared with bone marrow mesenchymal stem cells (BM-MSCs). The results show that SF-MSCs from the popliteal cyst fluid of pediatric patients showed a shuttle appearance and logarithmic growth. Flow cytometry analysis revealed that SF-MSCs were negative for hematopoietic lineage markers (CD34, CD45) and positive for MSC markers (CD44, CD73, CD90, and CD105). Interstitial cell marker (vimentin) and myofibroblast-like cell marker alpha-smooth muscle actin (α-SMA) were positive. These cells could differentiate into osteogenic, adipogenic, and chondrogenic lineages, respectively. Several types of human angiogenesis-related proteins were detected in the cell secretory fluid. These results show that we successfully obtained SF-MSCs from the popliteal cyst fluid of pediatric patients, which have the potential to be a valuable source of MSCs.


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