Cigarette smoke challenges bone marrow mesenchymal stem cell capacities in guinea pig

Tura-Ceide, Olga; Lobo, Borja; Paul, Tanja; Puig-Pey, Raquel; Coll-Bonfill, Núria; García-Lucio, Jéssica; Smolders, Valérie F. E. D.; Blanco, Isabel; Barberà, Joan Albert; Peinado, Víctor I.

doi:10.1186/s12931-017-0530-0

Cited by 20 publications

(17 citation statements)

References 43 publications

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“…Cigarette smoke, a major risk factor for COPD, has been shown to reduce the repair potential of endothelial progenitor cells [139] and bone marrow mesenchymal stem cells by interfering with cell homing and proliferation capacities [140]. Thus, stem cell exhaustion might contribute to COPD pathogenesis by reducing the endogenous renewal and repair capacity of the lung by local as well as recruited cells.…”

Section: Stem Cell Exhaustionmentioning

confidence: 99%

Lung ageing and COPD: is there a role for ageing in abnormal tissue repair?

et al. 2017

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Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death worldwide, with increasing prevalence, in particular in the elderly. COPD is characterised by abnormal tissue repair resulting in (small) airways disease and emphysema. There is accumulating evidence that ageing hallmarks are prominent features of COPD. These ageing hallmarks have been described in different subsets of COPD patients, in different lung compartments and also in a variety of cell types, and thus might contribute to different COPD phenotypes. A better understanding of the main differences and similarities between normal lung ageing and the pathology of COPD may improve our understanding of the mechanisms driving COPD pathology, in particular in those patients that develop the most severe form of COPD at a relatively young age, i.e. severe early-onset COPD patients.In this review, after introducing the main concepts of lung ageing and COPD pathology, we focus on the role of (abnormal) ageing in lung remodelling and repair in COPD. We discuss the current evidence for the involvement of ageing hallmarks in these pathological features of COPD. We also highlight potential novel treatment strategies and opportunities for future research based on our current knowledge of abnormal lung ageing in COPD.

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Section: Stem Cell Exhaustionmentioning

confidence: 99%

Lung ageing and COPD: is there a role for ageing in abnormal tissue repair?

et al. 2017

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“…Dysfunctional PCs show excessive apoptosis and are unable to respond to external injuries to mediate proper lung tissue healing [26]. Previous results from our group showed in an experimental animal model, that short-term exposure to CS induced PCs dysfunction, affecting pulmonary homing and proliferation [27]. In vitro, CS altered the rate of proliferation, senescence, differentiation and migration capacity of PCs [27].…”

Section: Discussionmentioning

confidence: 99%

Progenitor cell mobilisation and recruitment in pulmonary arteries in chronic obstructive pulmonary disease

et al. 2019

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Background Pulmonary vascular abnormalities are a characteristic feature of chronic obstructive pulmonary disease (COPD). Cigarette smoking is the most important risk factor for COPD. It is believed that its constant exposure triggers endothelial cell damage and vascular remodelling. Under pathological conditions, progenitor cells (PCs) are mobilized from the bone marrow and recruited to sites of vascular injury. The aim of the study was to investigate whether in COPD the number of circulating PCs is related to the presence of bone marrow-derived cells in pulmonary arteries and the association of these phenomena to both systemic and pulmonary endothelial dysfunction. Methods Thirty-nine subjects, 25 with COPD, undergoing pulmonary resection because of a localized carcinoma, were included. The number of circulating PCs was assessed by flow cytometry using a triple combination of antibodies against CD45, CD133 and CD34. Infiltrating CD45 + cells were identified by immunohistochemistry in pulmonary arteries. Endothelial function in systemic and pulmonary arteries was measured by flow-mediated dilation and adenosine diphosphate-induced vasodilation, respectively. Results COPD patients had reduced numbers of circulating PCs ( p < 0.05) and increased numbers of CD45 + cells (< 0.05) in the pulmonary arterial wall than non-COPD subjects, being both findings inversely correlated (r = − 0.35, p < 0.05). In pulmonary arteries, the number of CD45 + cells correlated with the severity of vascular remodelling (r = 0.4, p = 0.01) and the endothelium-dependent vasodilation (r = − 0.3, p = 0.05). Systemic endothelial function was unrelated to the number of circulating PCs and changes in pulmonary vessels. Conclusion In COPD, the decrease of circulating PCs is associated with their recruitment in pulmonary arteries, which in turn is associated with endothelial dysfunction and vessel remodelling, suggesting a mechanistic link between these phenomena. Our findings are consistent with the notion of an imbalance between endothelial damage and repair capacity in the pathogenesis of pulmonary vascular abnormalities in COPD. Electronic supplementary material The online version of this article (10.1186/s12931-019-1024-z) contains supplementary material, which is available to authorized users.

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“…Recent studies have reported that cigarette smoke or cigarette smoke components have cytotoxic effects on stem cells. Exposure of short‐term cigarette smoke induced dysfunction to cell homing and cell survival of bone marrow‐derived mesenchymal stem cells . An in vitro study showed that exposure of human umbilical cord blood cells to 3–9 mM nicotine decreased cell proliferation in a dose dependent manner and increased apoptosis .…”

Section: Discussionmentioning

confidence: 99%

“…Exposure of short-term cigarette smoke induced dysfunction to cell homing and cell survival of bone marrow-derived mesenchymal stem cells. 26 An in vitro study showed that exposure of human umbilical cord blood cells to 3-9 mM nicotine decreased cell proliferation in a dose dependent manner and increased apoptosis. 27 In addition, an in vivo study showed that the proliferation capacity of mesenchymal stem cells isolated from chronic smokers was about 2.5-fold less than that from non-smokers.…”

Section: Discussionmentioning

confidence: 99%

Apoptotic effects of cigarette smoke extracts on mouse embryonic stem cells via oxidative stress

Kim

Hwang

et al. 2019

Environmental Toxicology

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Abstarct Previous studies have reported that cigarette smoke and cigarette smoke extract (CSE) have negative effects on embryonic development. However, no studies have investigated the mechanism through which CSE affects the cellular signaling pathway leading to apoptosis and oxidative stress in embryonic cells, or how the two pathways are cross‐linked. Thus, we studied the effects of CSE on apoptosis and oxidative stress in mouse embryonic stem cells (mESCs). Specifically, we measured changes in cell viability in response to CSEs (3R4F and two domestic cigarettes CSE 1 and 2) using a water soluble tetrazolium (WST) assay and a neutral red uptake (NRU) assay, which revealed that cell viability decreased in a concentration‐dependent manner. Western blot analysis revealed that the expression of cyclin D1 and cyclin E1 was decreased and that of p21 and p27 was increased by CSE. Additionally, the number of terminal deoxynucleotidyl transferase (TUNEL)‐stained cells was increased by CSE, while the levels of Bax and Caspase‐3 increased and Bcl‐2 decreased. Moreover, a 2′,7′‐dichlorofluorescin diacetate (DCF‐DA) assay and reactive oxygen species (ROS)‐Glo H2O2 assay confirmed that ROS were generated in response to CSE and that they were associated with up‐regulated Keaf‐1 and CHOP. Overall, the results revealed that cigarette smoke extract (CSE) inhibited cell proliferation by regulating cell cycle‐related protein expression and increased oxidative stress by regulating the expression of Kelch‐like ECH‐associated protein 1 (Keap‐1) and CCAAT/enhancer‐binding protein homologous protein (CHOP), resulting in apoptosis in mESCs.

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Cigarette smoke challenges bone marrow mesenchymal stem cell capacities in guinea pig

Cited by 20 publications

References 43 publications

Lung ageing and COPD: is there a role for ageing in abnormal tissue repair?

Lung ageing and COPD: is there a role for ageing in abnormal tissue repair?

Progenitor cell mobilisation and recruitment in pulmonary arteries in chronic obstructive pulmonary disease

Apoptotic effects of cigarette smoke extracts on mouse embryonic stem cells via oxidative stress

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