scholarly journals ElevatedO-GlcNAc Levels Activate Epigenetically Repressed Genes and Delay Mouse ESC Differentiation Without Affecting Naïve to Primed Cell Transition

Stem Cells ◽  
2014 ◽  
Vol 32 (10) ◽  
pp. 2605-2615 ◽  
Author(s):  
Christopher M. Speakman ◽  
Tanja C.E. Domke ◽  
Wikrom Wongpaiboonwattana ◽  
Kelly Sanders ◽  
Manikhandan Mudaliar ◽  
...  
Keyword(s):  
Primed Cell ◽  
Cell Transition

scholarly journals Infarct in the Heart: What’s MMP-9 Got to Do with It?

Biomolecules ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 491
Author(s):  
Mediha Becirovic-Agic ◽  
Upendra Chalise ◽  
Michael J. Daseke ◽  
Shelby Konfrst ◽  
Jeffrey D. Salomon ◽  
...  
Keyword(s):  
Wound Healing ◽  
Cardiac Repair ◽  
Dual Effect ◽  
Strong Connection ◽  
The Past ◽  
Left Ventricle Remodeling ◽  
Inflammation Resolution ◽  
Metalloproteinase 9 ◽  
Cell Transition

Over the past three decades, numerous studies have shown a strong connection between matrix metalloproteinase 9 (MMP-9) levels and myocardial infarction (MI) mortality and left ventricle remodeling and dysfunction. Despite this fact, clinical trials using MMP-9 inhibitors have been disappointing. This review focuses on the roles of MMP-9 in MI wound healing. Infiltrating leukocytes, cardiomyocytes, fibroblasts, and endothelial cells secrete MMP-9 during all phases of cardiac repair. MMP-9 both exacerbates the inflammatory response and aids in inflammation resolution by stimulating the pro-inflammatory to reparative cell transition. In addition, MMP-9 has a dual effect on neovascularization and prevents an overly stiff scar. Here, we review the complex role of MMP-9 in cardiac wound healing, and highlight the importance of targeting MMP-9 only for its detrimental actions. Therefore, delineating signaling pathways downstream of MMP-9 is critical.

Progesterone alters human cervical epithelial and stromal cell transition and migration: Implications in cervical remodeling during pregnancy and parturition

2021 ◽  
pp. 111276
Author(s):  
Ourlad Alzeus G. Tantengco ◽  
Lauren S. Richardson ◽  
Joy Vink ◽  
Talar Kechichian ◽  
Paul Mark B. Medina ◽  
...  
Keyword(s):  
Stromal Cell ◽  
Cervical Remodeling ◽  
And Migration ◽  
Cell Transition

scholarly journals Immune regulators SIB1 and LSD1 antagonistically regulate PhANGs via the GLK transcription factors

2020 ◽  
Author(s):  
Mengping Li ◽  
Keun Pyo Lee ◽  
Tong Liu ◽  
Vivek Dogra ◽  
Jianli Duan ◽  
...  
Keyword(s):  
Cell Death ◽  
Transcription Factors ◽  
Critical Level ◽  
Negative Regulator ◽  
Chloroplast Biogenesis ◽  
Sensor Protein ◽  
Primed Cell ◽  
Light Harvesting Antenna ◽  
Signaling Components ◽  
Fine Tune

AbstractGOLDEN2-LIKE (GLK) transcription factors drive the expression of photosynthesis-associated nuclear genes (PhANGs), indispensable for chloroplast biogenesis. We previously demonstrated that the salicylic acid (SA)-induced SIGMA FACTOR-BINDING PROTEIN1 (SIB1), a transcription coregulator and positive regulator of SA-primed cell death, interacts with GLKs. The SIB1-GLK interaction raises the level of light-harvesting antenna proteins in the photosystem II, aggravating photoinhibition and singlet oxygen (1O2) burst. 1O2 then contributes to SA-primed cell death via EXECUTER1 (EX1, 1O2 sensor protein)-mediated retrograde signaling upon reaching a critical level. We now reveal that LESION-SIMULATING DISEASE 1 (LSD1), a transcription coregulator and negative regulator of SA-primed cell death, interacts with GLKs to repress their activities. Consistently, the overexpression of LSD1 represses the expression of PhANGs, but the loss of LSD1 increases their expression. The SA-induced SIB1 then counteractively interacts with GLKs, leading to EX1-mediated cell death. Collectively, we provide a working model that mutually exclusive SA-signaling components SIB1 and LSD1 antagonistically regulate GLKs to fine-tune the expression of PhANGs, priming SA-induced cell death, and sustaining 1O2 homeostasis, respectively.

scholarly journals Basal stem cell fate specification is mediated by SMAD signaling in the developing human lung

2018 ◽  
Author(s):  
Alyssa J. Miller ◽  
Qianhui Yu ◽  
Michael Czerwinski ◽  
Yu-Hwai Tsai ◽  
Renee F. Conway ◽  
...  
Keyword(s):  
Single Cell ◽  
Progenitor Cells ◽  
Cell Fate ◽  
Basal Cell ◽  
Human Lung ◽  
Branching Morphogenesis ◽  
Basal Cells ◽  
Smad Signaling ◽  
Cell Fate Decisions ◽  
Cell Transition

AbstractBasal stem cells (basal cells), located in the bronchi and trachea of the human lung epithelium, play a critical role in normal airway homeostasis and repair, and have been implicated in the development of diseases such as cancer1-4. Additionally, basal-like cells contribute to alveolar regeneration and fibrosis following severe injury5-8. However, the developmental origin of basal cells in humans is unclear. Previous work has shown that specialized progenitor cells exist at the tips of epithelial tubes during lung branching morphogenesis, and in mice, give rise to all alveolar and airway lineages9,10. These ‘bud tip progenitor cells’ have also been described in the developing human lung11-13, but the mechanisms controlling bud tip differentiation into specific cell lineages, including basal cells, are unknown. Here, we interrogated the bud tip-to-basal cell transition using human tissue specimens, bud tip progenitor organoid cultures11, and single-cell transcriptomics. We used single-cell mRNA sequencing (scRNAseq) of developing human lung specimens from 15-21 weeks gestation to identify molecular signatures and cell states in the developing human airway epithelium. We then inferred differentiation trajectories during bud tip-to-airway differentiation, which revealed a previously undescribed transitional cell state (‘hub progenitors’) and implicated SMAD signaling as a regulator of the bud tip-to-basal cell transition. We used bud tip progenitor organoids to show that TGFT1 and BMP4 mediated SMAD signaling robustly induced the transition into functional basal-like cells, and these in vitro-derived basal cells exhibited clonal expansion, self-renewal and multilineage differentiation. This work provides a framework for deducing and validating key regulators of cell fate decisions using single cell transcriptomics and human organoid models. Further, the identification of SMAD signaling as a critical regulator of newly born basal cells in the lung may have implications for regenerative medicine, basal cell development in other organs, and understanding basal cell misregulation in disease.

scholarly journals Single cell transcriptomics of human epidermis identifies basal stem cell transition states

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Shuxiong Wang ◽  
Michael L. Drummond ◽  
Christian F. Guerrero-Juarez ◽  
Eric Tarapore ◽  
Adam L. MacLean ◽  
...  
Keyword(s):  
Stem Cell ◽  
Single Cell ◽  
Transition States ◽  
Human Epidermis ◽  
Cell Transition

scholarly journals Tracing the Pre-B to Immature B Cell Transition in Human Leukemia Cells Reveals a Coordinated Sequence of Primary and SecondaryIGKGene Rearrangement,IGKDeletion, andIGLGene Rearrangement

2004 ◽  
Vol 174 (1) ◽  
pp. 367-375 ◽  
Author(s):  
Florian Klein ◽  
Niklas Feldhahn ◽  
Jana L. Mooster ◽  
Mieke Sprangers ◽  
Wolf-Karsten Hofmann ◽  
...  
Keyword(s):  
B Cell ◽  
Leukemia Cells ◽  
Human Leukemia ◽  
Human Leukemia Cells ◽  
Cell Transition
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