CRISPR-Cas9-mediated induction of large chromosomal inversions in human bronchial epithelial cells

Angelopoulou, Andriani; Papaspyropoulos, Angelos; Papantonis, Argyris; Gorgoulis, Vassilis G.

doi:10.1016/j.xpro.2022.101257

Cited by 6 publications

(4 citation statements)

References 9 publications

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“…An alternative to generate knockout clones is the use of knock-out strategies in hiPSCs 54 and the use of these cells to generate airway epithelial cells. Another, albeit suboptimal, alternative is establishing an immortalized PBEC line in order to clonally expand gene-edited cells 55 .…”

Section: Discussionmentioning

confidence: 99%

Isolating Bronchial Epithelial Cells from Resected Lung Tissue for Biobanking and Establishing Well-Differentiated Air-Liquid Interface Cultures

Ninaber

Does

Hiemstra

2023

JoVE

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The airway epithelial cell layer forms the first barrier between lung tissue and the outside environment and is thereby constantly exposed to inhaled substances, including infectious agents and air pollutants. The airway epithelial layer plays a central role in a large variety of acute and chronic lung diseases, and various treatments targeting this epithelium are administered by inhalation. Understanding the role of epithelium in pathogenesis and how it can be targeted for therapy requires robust and representative models. In vitro epithelial culture models are increasingly being used and offer the advantage of performing experiments in a controlled environment, exposing the cells to different kinds of stimuli, toxicants, or infectious agents. The use of primary cells instead of immortalized or tumor cell lines has the advantage that these cells differentiate in culture to a pseudostratified polarized epithelial cell layer with a better representation of the epithelium compared to cell lines.Presented here is a robust protocol, that has been optimized over the past decades, for the isolation and culture of airway epithelial cells from lung tissue. This procedure allows successful isolation, expansion, culture, and mucociliary differentiation of primary bronchial epithelial cells (PBECs) by culturing at the air-liquid interface (ALI) and includes a protocol for biobanking. Furthermore, the characterization of these cultures using cell-specific marker genes is described. These ALI-PBEC cultures can be used for a range of applications, including exposure to whole cigarette smoke or inflammatory mediators, and co-culture/infection with viruses or bacteria.

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Section: Discussionmentioning

confidence: 99%

Isolating Bronchial Epithelial Cells from Resected Lung Tissue for Biobanking and Establishing Well-Differentiated Air-Liquid Interface Cultures

Ninaber

Does

Hiemstra

2023

JoVE

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“…However, ADT may rather induce a reversible type of senescence which lacks the characteristics of DNA damage [ 148 ]. Along those lines, escape from senescence has been found to be an important mechanism contributing to tumor progression [ 145 , 149 , 150 ]. Interestingly, although several potential links with developmental pathways remain to be established, Notch signaling has been found associated with cellular senescence in prostate cancer, as upon PTEN loss, Notch pathway inhibition leads to senescence [ 78 ].…”

Section: Discussionmentioning

confidence: 99%

Interplay of Developmental Hippo–Notch Signaling Pathways with the DNA Damage Response in Prostate Cancer

Mourkioti

Angelopoulou

Belogiannis

et al. 2022

Cells

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Prostate cancer belongs in the class of hormone-dependent cancers, representing a major cause of cancer incidence in men worldwide. Since upon disease onset almost all prostate cancers are androgen-dependent and require active androgen receptor (AR) signaling for their survival, the primary treatment approach has for decades relied on inhibition of the AR pathway via androgen deprivation therapy (ADT). However, following this line of treatment, cancer cell pools often become resistant to therapy, contributing to disease progression towards the significantly more aggressive castration-resistant prostate cancer (CRPC) form, characterized by poor prognosis. It is, therefore, of critical importance to elucidate the molecular mechanisms and signaling pathways underlying the progression of early-stage prostate cancer towards CRPC. In this review, we aim to shed light on the role of major signaling pathways including the DNA damage response (DDR) and the developmental Hippo and Notch pathways in prostate tumorigenesis. We recapitulate key evidence demonstrating the crosstalk of those pathways as well as with pivotal prostate cancer-related ‘hubs’ such as AR signaling, and evaluate the clinical impact of those interactions. Moreover, we attempt to identify molecules of the complex DDR–Hippo–Notch interplay comprising potentially novel therapeutic targets in the battle against prostate tumorigenesis.

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“…Previous research in the cancer field has shown that, under certain conditions, OIS cells may exit senescence and reenter the cell cycle in a process collectively referred to as escape from OIS (30,31,(326)(327)(328). It was recently demonstrated that as a result of genomic instability and chromatin refolding changes in OIS cells, activation of the circadian gene BHLHE40 was sufficient to drive the escape from OIS, leading to the manifestation of aggressive oncogenic behavior (36,329). Given that genomic instability and epigenetic alterations are a frequent underlying cause of CVDs (107,119,120), it would be important to investigate whether escape from senescence is a possibility in cardiac disease and to delineate the molecular mechanisms through which it may occur.…”

Section: Future Perspectivesmentioning

confidence: 99%

Cellular senescence and cardiovascular diseases: moving to the “heart” of the problem

Evangelou

Vasileiou

Papaspyropoulos

et al. 2023

Physiological Reviews

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Cardiovascular diseases (CVDs) constitute the prime cause of global mortality with an immense impact on patient quality of life and disability. Clinical evidence has revealed a strong connection between cellular senescence and worse cardiac outcomes in the majority of CVDs concerning both ischemic and non-ischemic cardiomyopathies. Cellular senescence is characterized by cell cycle arrest accompanied by alterations in several metabolic pathways, resulting in morphological and functional changes. Metabolic rewiring of senescent cells results in marked paracrine activity, through a unique secretome, often exerting deleterious effects on neighboring cells. Here, we recapitulate the hallmarks and key molecular pathways involved in cellular senescence in the cardiac context and summarize the different roles of senescence in the majority of CVDs. In the last few years, the possibility of eliminating senescent cells in various pathological conditions is being increasingly explored, giving rise to the field of senotherapeutics. Therefore, we additionally attempt to clarifythe current state of this field with a focus on cardiac senescence, and discuss the potential of implementing senolytics as atreatment option in heart disease.

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CRISPR-Cas9-mediated induction of large chromosomal inversions in human bronchial epithelial cells

Cited by 6 publications

References 9 publications

Isolating Bronchial Epithelial Cells from Resected Lung Tissue for Biobanking and Establishing Well-Differentiated Air-Liquid Interface Cultures

Isolating Bronchial Epithelial Cells from Resected Lung Tissue for Biobanking and Establishing Well-Differentiated Air-Liquid Interface Cultures

Interplay of Developmental Hippo–Notch Signaling Pathways with the DNA Damage Response in Prostate Cancer

Cellular senescence and cardiovascular diseases: moving to the “heart” of the problem

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