scholarly journals Transgenic expression of oncogenic BRAF induces loss of stem cells in the mouse intestine, which is antagonized by β-catenin activity

Oncogene ◽  
2014 ◽  
Vol 34 (24) ◽  
pp. 3164-3175 ◽  
Author(s):  
P Riemer ◽  
A Sreekumar ◽  
S Reinke ◽  
R Rad ◽  
R Schäfer ◽  
...  
Keyword(s):  
Stem Cells ◽  
Transgenic Expression ◽  
Mouse Intestine

scholarly journals Wip1 Phosphatase Regulates p53-Dependent Apoptosis of Stem Cells and Tumorigenesis in the Mouse Intestine

2007 ◽  
Vol 1 (2) ◽  
pp. 180-190 ◽  
Author(s):  
Oleg N. Demidov ◽  
Oleg Timofeev ◽  
Hnin N.Y. Lwin ◽  
Calvina Kek ◽  
Ettore Appella ◽  
...  
Keyword(s):  
Stem Cells ◽  
Wip1 Phosphatase ◽  
Mouse Intestine

scholarly journals Sertoli cell-only phenotype and scRNA-seq define PRAMEF12 as a factor essential for spermatogenesis in mice

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Zhengpin Wang ◽  
Xiaojiang Xu ◽  
Jian-Liang Li ◽  
Cameron Palmer ◽  
Dragan Maric ◽  
...  
Keyword(s):  
Stem Cells ◽  
Sertoli Cell ◽  
Reproductive Medicine ◽  
Spermatogonial Stem Cells ◽  
Transcriptional Analysis ◽  
Seminiferous Tubules ◽  
Transgenic Expression ◽  
Genetic Ablation ◽  
Male Germline ◽  
Lower Expression

AbstractSpermatogonial stem cells (SSCs) have the dual capacity to self-renew and differentiate into progenitor spermatogonia that develop into mature spermatozoa. Here, we document that preferentially expressed antigen of melanoma family member 12 (PRAMEF12) plays a key role in maintenance of the spermatogenic lineage. In male mice, genetic ablation of Pramef12 arrests spermatogenesis and results in sterility which can be rescued by transgenic expression of Pramef12. Pramef12 deficiency globally decreases expression of spermatogenic-related genes, and single-cell transcriptional analysis of post-natal male germline cells identifies four spermatogonial states. In the absence of Pramef12 expression, there are fewer spermatogonial stem cells which exhibit lower expression of SSC maintenance-related genes and are defective in their ability to differentiate. The disruption of the first wave of spermatogenesis in juvenile mice results in agametic seminiferous tubules. These observations mimic a Sertoli cell-only syndrome in humans and may have translational implications for reproductive medicine.

scholarly journals Transgenic expression of cyclooxygenase-2 in mouse intestine epithelium is insufficient to initiate tumorigenesis but promotes tumor progression

2009 ◽  
Vol 273 (2) ◽  
pp. 225-232 ◽  
Author(s):  
Mazin A. Al-Salihi ◽  
A. Terrece Pearman ◽  
Thao Doan ◽  
Ethan C. Reichert ◽  
Daniel W. Rosenberg ◽  
...  
Keyword(s):  
Tumor Progression ◽  
Cyclooxygenase 2 ◽  
Transgenic Expression ◽  
Mouse Intestine

scholarly journals Protein arginine methyltransferase 1 regulates cell proliferation and differentiation in adult mouse adult intestine

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Lu Xue ◽  
Lingyu Bao ◽  
Julia Roediger ◽  
Yijun Su ◽  
Bingyin Shi ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cell Proliferation ◽  
Intestinal Epithelium ◽  
Adult Stem Cells ◽  
Adult Mouse ◽  
Intestinal Development ◽  
Arginine Methyltransferase ◽  
Mouse Intestine ◽  
Protein Arginine Methyltransferase 1 ◽  
Crypt Base

Abstract Background Adult stem cells play an essential role in adult organ physiology and tissue repair and regeneration. While much has been learnt about the property and function of various adult stem cells, the mechanisms of their development remain poorly understood in mammals. Earlier studies suggest that the formation of adult mouse intestinal stem cells takes place during the first few weeks after birth, the postembryonic period when plasma thyroid hormone (T3) levels are high. Furthermore, deficiency in T3 signaling leads to defects in adult mouse intestine, including reduced cell proliferation in the intestinal crypts, where stem cells reside. Our earlier studies have shown that protein arginine methyltransferase 1 (PRMT1), a T3 receptor coactivator, is highly expressed during intestinal maturation in mouse. Methods We have analyzed the expression of PRMT1 by immunohistochemistry and studied the effect of tissue-specific knockout of PRMT1 in the intestinal epithelium. Results We show that PRMT1 is expressed highly in the proliferating transit amplifying cells and crypt base stem cells. By using a conditional knockout mouse line, we have demonstrated that the expression of PRMT1 in the intestinal epithelium is critical for the development of the adult mouse intestine. Specific removal of PRMT1 in the intestinal epithelium results in, surprisingly, more elongated adult intestinal crypts with increased cell proliferation. In addition, epithelial cell migration along the crypt-villus axis and cell death on the villus are also increased. Furthermore, there are increased Goblet cells and reduced Paneth cells in the crypt while the number of crypt base stem cells remains unchanged. Conclusions Our finding that PRMT1 knockout increases cell proliferation is surprising considering the role of PRMT1 in T3-signaling and the importance of T3 for intestinal development, and suggests that PRMT1 likely regulates pathways in addition to T3-signaling to affect intestinal development and/or homeostasis, thus affecting cell proliferating and epithelial turn over in the adult.

scholarly journals Deletion of Polycomb Repressive Complex 2 From Mouse Intestine Causes Loss of Stem Cells

2016 ◽  
Vol 151 (4) ◽  
pp. 684-697.e12 ◽  
Author(s):  
Martijn A.J. Koppens ◽  
Gergana Bounova ◽  
Gaetano Gargiulo ◽  
Ellen Tanger ◽  
Hans Janssen ◽  
...  
Keyword(s):  
Stem Cells ◽  
Polycomb Repressive Complex ◽  
Polycomb Repressive Complex 2 ◽  
Mouse Intestine

scholarly journals Overcoming reprogramming resistance of Fanconi anemia cells

Blood ◽  
2012 ◽  
Vol 119 (23) ◽  
pp. 5449-5457 ◽  
Author(s):  
Lars U. W. Müller ◽  
Michael D. Milsom ◽  
Chad E. Harris ◽  
Rutesh Vyas ◽  
Kristina M. Brumme ◽  
...  
Keyword(s):  
Stem Cells ◽  
Fanconi Anemia ◽  
Ex Vivo ◽  
Normal Karyotype ◽  
Patient Specific ◽  
Dna Double Strand Breaks ◽  
Gene Correction ◽  
Hematopoietic Stem ◽  
Transgenic Expression ◽  
Reprogramming Efficiency

Abstract Fanconi anemia (FA) is a recessive syndrome characterized by progressive fatal BM failure and chromosomal instability. FA cells have inactivating mutations in a signaling pathway that is critical for maintaining genomic integrity and protecting cells from the DNA damage caused by cross-linking agents. Transgenic expression of the implicated genes corrects the phenotype of hematopoietic cells, but previous attempts at gene therapy have failed largely because of inadequate numbers of hematopoietic stem cells available for gene correction. Induced pluripotent stem cells (iPSCs) constitute an alternate source of autologous cells that are amenable to ex vivo expansion, genetic correction, and molecular characterization. In the present study, we demonstrate that reprogramming leads to activation of the FA pathway, increased DNA double-strand breaks, and senescence. We also demonstrate that defects in the FA DNA-repair pathway decrease the reprogramming efficiency of murine and human primary cells. FA pathway complementation reduces senescence and restores the reprogramming efficiency of somatic FA cells to normal levels. Disease-specific iPSCs derived in this fashion maintain a normal karyotype and are capable of hematopoietic differentiation. These data define the role of the FA pathway in reprogramming and provide a strategy for future translational applications of patient-specific FA iPSCs.

Proliferation and multi-differentiation potentials of human mesenchymal stem cells on thermoresponsive PDMS surfaces grafted with PNIPAAm

2010 ◽  
Vol 30 (6) ◽  
pp. 455-455 ◽  
Author(s):  
Dongyan Shi ◽  
Dan Ma ◽  
Feiqing Dong ◽  
Chen Zong ◽  
Liyue Liu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Human Mesenchymal Stem Cells
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