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A Review on L-Asparaginase
Published in Se-Kwon Kim, Marine Biochemistry, 2023
Treating cells with the cytotoxic compound may lead to various cell fates. Due to the necrosis that the cells undergo, they lose membrane integrity and die quickly as a result of cell lysis. The cells will lose their vigorously growing and dividing capacity (a reduction in cell viability), or the cells can begin a program of controlled cell death (apoptosis).
Gene Therapy in Oral Tissue Regeneration
Published in Vincenzo Guarino, Marco Antonio Alvarez-Pérez, Current Advances in Oral and Craniofacial Tissue Engineering, 2020
Fernando Suaste, Patricia González-Alva, Alejandro Luis, Osmar Alejandro
Gene therapy has become a powerful tool in the treatment of clinical diseases of the oral cavity. The potential to manipulate the different cell types of the complex craniofacial system, by stimulating them with a combination of growth factors and later their reintegration into the damaged tissue, is a promising strategy to avoid surgical procedures. However, despite the advantages of this genetic strategy, severe limitations still prevent its use as a clinical therapy in humans For example, to have sustained expression of a specific factor and promote specific cell reprogramming, the integration of transgene into the genome of the host cell is essentially required. Moreover, leading to devastating consequences for cell fate that can lead to the development of cancer. Future guidelines in gene therapy to avoid such reactions in the cell should aim the development of vectors whose transfection mechanism, whether transient or stable, is controlled, as well as improve specificity to infect a particular cell type.
Vitamin C and Somatic Cell Reprogramming
Published in Qi Chen, Margreet C.M. Vissers, Cancer and Vitamin C, 2020
Vitamin C can also reprogram the epigenome of adult stem cells. Epigenetic dysregulation is a hallmark of hematopoietic stem cell (HSC) transformation, and impaired TET function is a driver of blood cell malignancies [20,21]. By enhancing TET function, vitamin C has been shown to block aberrant self-renewal and slow down leukemia progression, highlighting its potential therapeutic benefit for the treatment of patients with hematopoietic malignancies [22,23]. The ability of vitamin C to directly modulate the epigenome has expanded our appreciation of this essential vitamin in the regulation of cell fate that has widespread application in the fields of stem cell biology and regenerative medicine and in the treatment of cancer.
Endogenous lung stem cells for lung regeneration
Published in Expert Opinion on Biological Therapy, 2019
It is clear from recent studies that perceptions of stem cells existing in a hierarchical order with relatively fixed cell fate choices at each stage of differentiation were naïve. It is increasingly obvious that the lung has evolved with considerable redundancy in its reparative tool box, with duplication of stem cells that give rise to critical specialized epithelial cells and plasticity of mature specialized cells increasing the capacity for wound healing after injury. With dedicated efforts to map the cellular profile of the lung by single-cell transcriptomics, more cell subsets, and new cell types will be discovered, which I am sure will uncover unforeseen reparative routes through which the lung responds to injury and disease. Indeed, comprehensive single cell (sc)RNA-Seq analysis of the human and mouse airway epithelium by two independent research teams recently discovered a number of new cell types, including a rare type of airway cell they named pulmonary ionocytes which express the highest levels of the Cftr gene, mutations to which cause cystic fibrosis [69,70]. In a technological advance, D.T. Montoro and colleagues coupled lineage tracing with scRNA-Seq over time to provide the first evidence that new ionocytes may be derived from basal cells [69]. The team also discovered high proliferative epithelial zones in the airways (named hillocks) that are comprised of stratified epithelial layers of newly identified Trp63+ Keratin 13 (Krt13)+ basal cells and secretory cells but lacked luminal ciliated cells [69].
Targeting Hedgehog pathway in pediatric acute myeloid leukemia: challenges and opportunities
Published in Expert Opinion on Therapeutic Targets, 2019
Andrea Pession, Annalisa Lonetti, Salvatore Bertuccio, Franco Locatelli, Riccardo Masetti
The Hedgehog (Hh) pathway is a key signaling system that controls proliferation and differentiation of embryonic cells, whereas in adult organisms it is involved in the control of tissue homeostasis and regeneration by regulating adult stem cell proliferation, apoptosis, and self-renewal. The canonical Hh pathway involves a paracrine or autocrine mechanism. The ligands Sonic (Shh), Indian (Ihh) and Desert (Dhh) Hedgehog bind the transmembrane receptor Patched (PTCH) that functions as a negative regulator of the pathway through inhibition of Smoothened (Smo). Hh ligand binding results in activation of Smo that, in turn, activates members of the GLI family of zincfinger transcription factors, which translocate to the nucleus to regulate the transcription of Hh target genes (GLI1 acts as a positive regulator, GLI3 acts as a repressor and GLI2 acts both as either a positive or negative transcriptional regulator) (Figure 1). In this context, the balance of GLI activators and repressors defines the cell fate. Importantly, Hh signaling can also be activated via non-canonical Smo-independent pathways, including PI3K/Akt and RAS/RAF/MEK/ERK signaling cascades [1] (Figure 1).
Direct cellular reprogramming and inner ear regeneration
Published in Expert Opinion on Biological Therapy, 2019
Patrick J. Atkinson, Grace S. Kim, Alan G. Cheng
As regeneration does not occur in the mature mammalian cochlea, there have been considerable efforts aimed at coercing supporting cells to regenerate lost hair cells (Figure 2), with cellular reprogramming being a major focus. The targeted manipulation of cell fate through the introduction of transcription factors is broadly termed cellular reprogramming. Over three decades ago, the introduction of a single transcription factor, MyoD, was shown to convert fibroblasts directly to myoblasts in vitro [47], shifting the notion that somatic cell fate is fixed. The plasticity of somatic cell fate was further highlighted by work carried out by Takahashi and colleagues, who successfully induced pluripotency with a cocktail of four transcription factors, the so-called ‘Yamanaka factors’ [48]. Since these studies, many reprogramming approaches to induce pluripotency have been used prior to implementing guided differentiation protocols [49]. Moreover, new strategies to directly convert a cell’s identity (without a preceding dedifferentiation event) have been examined in a growing number of organ systems [50–52]. This new strategy, of ‘direct cellular reprogramming’ will be the focus of the remainder of this review. For a comprehensive discussion of cellular reprogramming more broadly, we refer the avid reader to the following reviews [53–55].