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Artículos de revistas sobre el tema "Lung Stem Cell"

Autor: Grafiati

Publicado: 11 de marzo de 2023

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1

Kim, Carla F. "Paving the road for lung stem cell biology: bronchioalveolar stem cells and other putative distal lung stem cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 293, no. 5 (2007): L1092—L1098. http://dx.doi.org/10.1152/ajplung.00015.2007.

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New discoveries in stem cell biology are making the biology of solid tissues increasingly complex. Important seminal studies demonstrating the presence of damage-resistant cell populations together with new isolation and characterization techniques suggest that stem cells exist in the adult lung. More detailed in vivo molecular and cellular characterization of bronchioalveolar stem cells (BASCs), other putative lung stem and progenitor cells, and differentiated cells is needed to determine the lineage relationships in adult lung. Lung diseases such as cystic fibrosis or chronic obstructive pulmonary disease, as well as the most common form of lung cancer in the United States, all involve apparent bronchiolar and alveolar cell defects. It is likely that the delicate balance of stem, progenitor, and differentiated cell functions in the lung is critically affected in patients with these devastating diseases. Thus the discovery of BASCs and other putative lung stem cells will lay the foundation for new inroads to understanding lung biology related to lung disease.

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2

Sentek, Hanna, and Diana Klein. "Lung-Resident Mesenchymal Stem Cell Fates within Lung Cancer." Cancers 13, no. 18 (2021): 4637. http://dx.doi.org/10.3390/cancers13184637.

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Lung-resident mesenchymal stem cells (LR-MSCs) are non-hematopoietic multipotent stromal cells that predominately reside adventitial within lung blood vessels. Based on their self-renewal and differentiation properties, LR-MSCs turned out to be important regulators of normal lung homeostasis. LR-MSCs exert beneficial effects mainly by local secretion of various growth factors and cytokines that in turn foster pulmonary regeneration including suppression of inflammation. At the same time, MSCs derived from various tissues of origins represent the first choice of cells for cell-based therapeutic applications in clinical medicine. Particularly for various acute as well as chronic lung diseases, the therapeutic applications of exogenous MSCs were shown to mediate beneficial effects, hereby improving lung function and survival. In contrast, endogenous MSCs of normal lungs seem not to be sufficient for lung tissue protection or repair following a pathological trigger; LR-MSCs could even contribute to initiation and/or progression of lung diseases, particularly lung cancer because of their inherent tropism to migrate towards primary tumors and metastatic sites. However, the role of endogenous LR-MSCs to be multipotent tumor-associated (stromal) precursors remains to be unraveled. Here, we summarize the recent knowledge how ‘cancer-educated’ LR-MSCs impact on lung cancer with a focus on mesenchymal stem cell fates.

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3

Ionescu, Lavinia, Roisin N. Byrne, Tim van Haaften, et al. "Stem cell conditioned medium improves acute lung injury in mice: in vivo evidence for stem cell paracrine action." American Journal of Physiology-Lung Cellular and Molecular Physiology 303, no. 11 (2012): L967—L977. http://dx.doi.org/10.1152/ajplung.00144.2011.

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Mortality and morbidity of acute lung injury and acute respiratory distress syndrome remain high because of the lack of pharmacological therapies to prevent injury or promote repair. Mesenchymal stem cells (MSCs) prevent lung injury in various experimental models, despite a low proportion of donor-derived cell engraftment, suggesting that MSCs exert their beneficial effects via paracrine mechanisms. We hypothesized that soluble factors secreted by MSCs promote the resolution of lung injury in part by modulating alveolar macrophage (AM) function. We tested the therapeutic effect of MSC-derived conditioned medium (CdM) compared with whole MSCs, lung fibroblasts, and fibroblast-CdM. Intratracheal MSCs and MSC-CdM significantly attenuated lipopolysaccharide (LPS)-induced lung neutrophil influx, lung edema, and lung injury as assessed by an established lung injury score. MSC-CdM increased arginase-1 activity and Ym1 expression in LPS-exposed AMs. In vivo, AMs from LPS-MSC and LPS-MSC CdM lungs had enhanced expression of Ym1 and decreased expression of inducible nitric oxide synthase compared with untreated LPS mice. This suggests that MSC-CdM promotes alternative macrophage activation to an M2 “healer” phenotype. Comparative multiplex analysis of MSC- and fibroblast-CdM demonstrated that MSC-CdM contained several factors that may confer therapeutic benefit, including insulin-like growth factor I (IGF-I). Recombinant IGF-I partially reproduced the lung protective effect of MSC-CdM. In summary, MSCs act through a paracrine activity. MSC-CdM promotes the resolution of LPS-induced lung injury by attenuating lung inflammation and promoting a wound healing/anti-inflammatory M2 macrophage phenotype in part via IGF-I.

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4

Kuo, Ming-Han, Pei-Yu Chen, Yi-Ping Yang, et al. "Cytokine and Epigenetic Regulation of Programmed Death-Ligand 1 in Stem Cell Differentiation and Cancer Cell Plasticity." Stem Cells 39, no. 10 (2021): 1298–309. http://dx.doi.org/10.1002/stem.3429.

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Abstract Programmed death-ligand 1 (PD-L1), an immune checkpoint ligand, is recognized as a potential target for cancer immunotherapy as well as for the induction of transplantation tolerance. However, how the crosstalk between stem cell programming and cytokine signaling regulates PD-L1 expression during stem cell differentiation and cancer cell plasticity remains unclear. Herein, we reported that PD-L1 expression was regulated by SOX2 during embryonic stem cell (ESC) differentiation and lung cancer cell plasticity. PD-L1 was induced during ESC differentiation to fibroblasts and was downregulated during SOX2-mediated reprogramming of fibroblasts to induced pluripotent stem cells (iPSCs). Furthermore, SOX2 activation affected cancer cell plasticity and inhibited PD-L1 expression in lung cancer cells. We discovered that the H3K27ac signal at the PD-L1 locus was enhanced during ESC differentiation to fibroblasts as well as during cancer plasticity of SOX2-positive lung cancer cells to SOX2-negative counterparts. Romidepsin, an epigenetic modifier, induced PD-L1 expression in lung cancer cells, whereas TGF-β stimulation downregulated SOX2 but upregulated PD-L1 expression in lung cancer cells. Furthermore, in addition to PD-L1, the expressions of EGFR and its ligand HBEGF were downregulated by activation of endogenous SOX2 expression during lung cancer cell plasticity and iPSC reprogramming, and the activation of EGFR signaling by HBEGF upregulated PD-L1 expression in lung cancer cells. Together, our results reveal the crosstalk between SOX2 programming and cytokine stimulation influences PD-L1 expression, and these findings may provide insights into PD-L1-mediated therapeutics.

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5

Kotton, Darrell N., and Alan Fine. "Lung stem cells." Cell and Tissue Research 331, no. 1 (2007): 145–56. http://dx.doi.org/10.1007/s00441-007-0479-2.

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6

Omar, Said A., Amal Abdul-Hafez, Sherif Ibrahim, et al. "Stem-Cell Therapy for Bronchopulmonary Dysplasia (BPD) in Newborns." Cells 11, no. 8 (2022): 1275. http://dx.doi.org/10.3390/cells11081275.

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Premature newborns are at a higher risk for the development of respiratory distress syndrome (RDS), acute lung injury (ALI) associated with lung inflammation, disruption of alveolar structure, impaired alveolar growth, lung fibrosis, impaired lung angiogenesis, and development of bronchopulmonary dysplasia (BPD) with severe long-term developmental adverse effects. The current therapy for BPD is limited to supportive care including high-oxygen therapy and pharmacotherapy. Recognizing more feasible treatment options to improve lung health and reduce complications associated with BPD is essential for improving the overall quality of life of premature infants. There is a reduction in the resident stem cells in lungs of premature infants with BPD, which strongly suggests a critical role of stem cells in BPD pathogenesis; this warrants the exploration of the potential therapeutic use of stem-cell therapy. Stem-cell-based therapies have shown promise for the treatment of many pathological conditions including acute lung injury and BPD. Mesenchymal stem cells (MSCs) and MSC-derived extracellular vesicles (EVs) including exosomes are promising and effective therapeutic modalities for the treatment of BPD. Treatment with MSCs and EVs may help to reduce lung inflammation, improve pulmonary architecture, attenuate pulmonary fibrosis, and increase the survival rate.

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7

Wu, Huijuan, and Nan Tang. "Stem cells in pulmonary alveolar regeneration." Development 148, no. 2 (2021): dev193458. http://dx.doi.org/10.1242/dev.193458.

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ABSTRACTThe lungs are constantly exposed to the external environment and are therefore vulnerable to insults that can cause infection and injury. Maintaining the integrity and barrier function of the lung epithelium requires complex interactions of multiple cell lineages. Elucidating the cellular players and their regulation mechanisms provides fundamental information to deepen understanding about the responses and contributions of lung stem cells. This Review focuses on advances in our understanding of mammalian alveolar epithelial stem cell subpopulations and discusses insights about the regeneration-specific cell status of alveolar epithelial stem cells. We also consider how these advances can inform our understanding of post-injury lung repair processes and lung diseases.

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8

OTTO, W. R. "Lung stem cells." International Journal of Experimental Pathology 78, no. 5 (2003): 291–310. http://dx.doi.org/10.1046/j.1365-2613.1997.370366.x.

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9

MAIUTHED, ARNATCHAI, WIPA CHANTARAWONG, and PITHI CHANVORACHOTE. "Lung Cancer Stem Cells and Cancer Stem Cell-targeting Natural Compounds." Anticancer Research 38, no. 7 (2018): 3797–809. http://dx.doi.org/10.21873/anticanres.12663.

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10

Yin, Huijing, Bo Jing, Dongliang Xu, et al. "Identification of Active Bronchioalveolar Stem Cells as the Cell of Origin in Lung Adenocarcinoma." Cancer Research 82, no. 6 (2022): 1025–37. http://dx.doi.org/10.1158/0008-5472.can-21-2445.

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Abstract While initiation is established as a critical step in tumorigenesis, the identity of the cell of origin for lung adenocarcinoma and the mechanism controlling susceptibility to initiation remain elusive. Here we show that lung tumor suppressor Gprc5a-knockout (KO) mice are susceptible to initiation of lung tumorigenesis. Bronchioalveolar stem cells (BASC) and alveolar type 2 (AT2) cells were aberrantly expanded in Gprc5a-KO mouse lungs compared with those in wild-type (WT) mice, suggesting that Gprc5a-KO might confer susceptibility to initiation by increasing the cell of origin in mouse lungs. BASCs from Gprc5a-KO mice (KO-BASC) exhibited significantly increased stemness and self-renewal potential and reduced differentiation capacity compared with BASCs from WT mice (WT-BASC). AT2 cells did not possess self-renewal potential regardless of Gprc5a status. KO-BASCs expressed a stem-like gene profile with upregulated Abcg2, EGFR, and NF-κB signaling compared with WT-BASCs. Blockade of EGFR and NF-κB signaling inhibited both expansion of BASC and AT2 cells and lung tumorigenesis. Abcg2 was expressed in active KO-BASCs as well as in lung tumor cells but not in quiescent WT-BASCs or AT2 cells, supporting that lung adenocarcinoma cells are derived from Abcg2-positive KO-BASCs (active). Taken together, Gprc5a deletion leads to expansion of active BASCs via dysregulated EGFR and NF-κB signaling that confers susceptibility to initiation of lung tumorigenesis, marking Abcg2-positive BASCs as candidate cell of origin for lung adenocarcinoma. Significance: Identification of active bronchioalveolar stem cells as lung adenocarcinoma cells of origin provides insights into mechanisms of lung tumorigenesis and could facilitate development of effective strategies for cancer prevention and therapy. See related commentary by Osborne and Minna, p. 972

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11

Weiss, D. J., J. K. Kolls, L. A. Ortiz, A. Panoskaltsis-Mortari, and D. J. Prockop. "Stem Cells and Cell Therapies in Lung Biology and Lung Diseases." Proceedings of the American Thoracic Society 5, no. 5 (2008): 637–67. http://dx.doi.org/10.1513/pats.200804-037dw.

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12

Weiss, D. J., I. Bertoncello, Z. Borok, et al. "Stem Cells and Cell Therapies in Lung Biology and Lung Diseases." Proceedings of the American Thoracic Society 8, no. 3 (2011): 223–72. http://dx.doi.org/10.1513/pats.201012-071dw.

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13

Parekh, Kalpaj R., Janna Nawroth, Albert Pai, Shana M. Busch, Christiana N. Senger, and Amy L. Ryan. "Stem cells and lung regeneration." American Journal of Physiology-Cell Physiology 319, no. 4 (2020): C675—C693. http://dx.doi.org/10.1152/ajpcell.00036.2020.

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The ability to replace defective cells in an airway with cells that can engraft, integrate, and restore a functional epithelium could potentially cure a number of lung diseases. Progress toward the development of strategies to regenerate the adult lung by either in vivo or ex vivo targeting of endogenous stem cells or pluripotent stem cell derivatives is limited by our fundamental lack of understanding of the mechanisms controlling human lung development, the precise identity and function of human lung stem and progenitor cell types, and the genetic and epigenetic control of human lung fate. In this review, we intend to discuss the known stem/progenitor cell populations, their relative differences between rodents and humans, their roles in chronic lung disease, and their therapeutic prospects. Additionally, we highlight the recent breakthroughs that have increased our understanding of these cell types. These advancements include novel lineage-traced animal models and single-cell RNA sequencing of human airway cells, which have provided critical information on the stem cell subtypes, transition states, identifying cell markers, and intricate pathways that commit a stem cell to differentiate or to maintain plasticity. As our capacity to model the human lung evolves, so will our understanding of lung regeneration and our ability to target endogenous stem cells as a therapeutic approach for lung disease.

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14

Trounson, Alan, Kyle Kolaja, Thomas Petersen, Klaus Weber, Maralee McVean, and Kathleen A. Funk. "Stem Cell Research." International Journal of Toxicology 34, no. 4 (2015): 349–51. http://dx.doi.org/10.1177/1091581815581423.

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Stem cells have great potential in basic research and are being slowly integrated into toxicological research. This symposium provided an overview of the state of the field, stem cell models, described allogenic stem cell treatments and issues of immunogenicity associated with protein therapeutics, and tehn concentrated on stem cell uses in regenerative medicine focusing on lung and testing strategies on engineered tissues from a pathologist’s perspective.

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15

Haddad, Imad Y. "Stem cell transplantation and lung dysfunction." Current Opinion in Pediatrics 25, no. 3 (2013): 350–56. http://dx.doi.org/10.1097/mop.0b013e328360c317.

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16

Purnell, Beverly A. "Fibroblasts as lung stem cell niche." Science 359, no. 6380 (2018): 1114.10–1116. http://dx.doi.org/10.1126/science.359.6380.1114-j.

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17

Schrepfer, S., T. Deuse, H. Reichenspurner, M. P. Fischbein, R. C. Robbins, and M. P. Pelletier. "Stem Cell Transplantation: The Lung Barrier." Transplantation Proceedings 39, no. 2 (2007): 573–76. http://dx.doi.org/10.1016/j.transproceed.2006.12.019.

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18

Pine, Sharon R., Blair Marshall, and Lyuba Varticovski. "Lung Cancer Stem Cells." Disease Markers 24, no. 4-5 (2008): 257–66. http://dx.doi.org/10.1155/2008/396281.

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Lung cancer remains a major cause of cancer-related lethality because of high incidence and recurrence in spite of significant advances in staging and therapies. Recent data indicates that stem cells situated throughout the airways may initiate cancer formation. These putative stem cells maintain protumorigenic characteristics including high proliferative capacity, multipotent differentiation, drug resistance and long lifespan relative to other cells. Stem cell signaling and differentiation pathways are maintained within distinct cancer types, and destabilization of this machinery may participate in maintenance of cancer stem cells. Characterization of lung cancer stem cells is an area of active research and is critical for developing novel therapies. This review summarizes the current knowledge on stem cell signaling pathways and cell markers used to identify the lung cancer stem cells.

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19

Hamad, Hussein, and Birgitte Brinkmann Olsen. "Cannabidiol Induces Cell Death in Human Lung Cancer Cells and Cancer Stem Cells." Pharmaceuticals 14, no. 11 (2021): 1169. http://dx.doi.org/10.3390/ph14111169.

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Currently, there is no effective therapy against lung cancer due to the development of resistance. Resistance contributes to disease progression, recurrence, and mortality. The presence of so-called cancer stem cells could explain the ineffectiveness of conventional treatment, and the development of successful cancer treatment depends on the targeting also of cancer stem cells. Cannabidiol (CBD) is a cannabinoid with anti-tumor properties. However, the effects on cancer stem cells are not well understood. The effects of CBD were evaluated in spheres enriched in lung cancer stem cells and adherent lung cancer cells. We found that CBD decreased viability and induced cell death in both cell populations. Furthermore, we found that CBD activated the effector caspases 3/7, increased the expression of pro-apoptotic proteins, increased the levels of reactive oxygen species, as well as a leading to a loss of mitochondrial membrane potential in both populations. We also found that CBD decreased self-renewal, a hallmark of cancer stem cells. Overall, our results suggest that CBD is effective against the otherwise treatment-resistant cancer stem cells and joins a growing list of compounds effective against cancer stem cells. The effects and mechanisms of CBD in cancer stem cells should be further explored to find their Achilles heel.

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20

Wagner, Darcy E., Laertis Ikonomou, Sarah E. Gilpin, et al. "Stem Cells, Cell Therapies, and Bioengineering in Lung Biology and Disease 2019." ERJ Open Research 6, no. 4 (2020): 00123–2020. http://dx.doi.org/10.1183/23120541.00123-2020.

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A workshop entitled “Stem Cells, Cell Therapies and Bioengineering in Lung Biology and Diseases” was hosted by the University of Vermont Larner College of Medicine in collaboration with the National Heart, Lung and Blood Institute, the Alpha-1 Foundation, the Cystic Fibrosis Foundation, the International Society for Cell and Gene Therapy and the Pulmonary Fibrosis Foundation. The event was held from July 15 to 18, 2019 at the University of Vermont, Burlington, Vermont. The objectives of the conference were to review and discuss the current status of the following active areas of research: 1) technological advancements in the analysis and visualisation of lung stem and progenitor cells; 2) evaluation of lung stem and progenitor cells in the context of their interactions with the niche; 3) progress toward the application and delivery of stem and progenitor cells for the treatment of lung diseases such as cystic fibrosis; 4) progress in induced pluripotent stem cell models and application for disease modelling; and 5) the emerging roles of cell therapy and extracellular vesicles in immunomodulation of the lung. This selection of topics represents some of the most dynamic research areas in which incredible progress continues to be made. The workshop also included active discussion on the regulation and commercialisation of regenerative medicine products and concluded with an open discussion to set priorities and recommendations for future research directions in basic and translation lung biology.

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21

Nystedt, Johanna, Heidi Anderson, Jonne Tikkanen, et al. "Cell Surface Structures Influence Lung Clearance Rate of Systemically Infused Mesenchymal Stromal Cells." STEM CELLS 31, no. 2 (2013): 317–26. http://dx.doi.org/10.1002/stem.1271.

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22

Parikh, S. D., V. Levina, T. Wang, M. K. Gibson, and A. E. Lokshin. "Radioresistance of Non-small Cell Lung Cancer Stem Cells." International Journal of Radiation Oncology*Biology*Physics 75, no. 3 (2009): S542—S543. http://dx.doi.org/10.1016/j.ijrobp.2009.07.1240.

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23

Song, Ye Na, and Man Ryul Lee. "Single-cell transcriptomics of lung organoids." Organoid 1 (October 19, 2021): e9. http://dx.doi.org/10.51335/organoid.2021.1.e9.

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The in vitro application of human pluripotent stem cell- or adult stem cell-derived lung organoids has the potential to revolutionize lung disease research, but there are several limitations in the consistent implementation of lung organoids resulting from the structural diversity of the lung tissues and the variety of cell types (more than 40 resident cell types) populating these tissues. However, the evaluation of these complexities using a combination of lung organoids and single-cell transcriptomics has made it possible to identify several key cell types and sub-populations critical to the development of robust in vitro organoid models. Recent studies have started to use stem cells to produce these organoids, making it possible to mimic complex 3-dimensional tissues. Furthermore, single-cell mRNA sequencing allows critical comparisons of the transcriptome, which may help focus future research in the field of lung disease.

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24

Elias, Anthony. "Hematopoietic Stem Cell Transplantation for Small Cell Lung Cancer." Chest 116 (December 1999): 531S—538S. http://dx.doi.org/10.1378/chest.116.suppl_3.531s.

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25

Rizzo, J. Douglas, Anthony D. Elias, Patrick J. Stiff, et al. "Autologous stem cell transplantation for small cell lung cancer." Biology of Blood and Marrow Transplantation 8, no. 5 (2002): 273–80. http://dx.doi.org/10.1053/bbmt.2002.v8.pm12064365.

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26

Tachezy, Michael, Hilke Zander, Gerrit Wolters-Eisfeld, et al. "Activated Leukocyte Cell Adhesion Molecule (CD166): An “Inert” Cancer Stem Cell Marker for Non-Small Cell Lung Cancer?" STEM CELLS 32, no. 6 (2014): 1429–36. http://dx.doi.org/10.1002/stem.1665.

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27

Yamashita, Naoki, Tetsuya So, Takeaki Miyata, et al. "Cancer stem cell markers in lung adenocarcinoma." Personalized Medicine Universe 9 (October 31, 2020): 64–65. http://dx.doi.org/10.46459/pmu.2020002.

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28

Cruz, Fernanda F., and Patricia R. M. Rocco. "Stem-cell extracellular vesicles and lung repair." Stem Cell Investigation 4, no. 9 (2017): 78. http://dx.doi.org/10.21037/sci.2017.09.02.

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29

Whitson, Bryan A., Ryan C. Shelstad, Marshall I. Hertz, Rosemary F. Kelly, Jonathan D’Cunha, and Sara J. Shumway. "Lung transplantation after hematopoietic stem cell transplantation." Clinical Transplantation 26, no. 2 (2011): 254–58. http://dx.doi.org/10.1111/j.1399-0012.2011.01482.x.

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30

Tzouvelekis, Argyris, Paschalis Ntolios, and Demosthenes Bouros. "Stem Cell Treatment for Chronic Lung Diseases." Respiration 85, no. 3 (2013): 179–92. http://dx.doi.org/10.1159/000346525.

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31

Miyata, Takeaki, Takashi Yoshimatsu, Tetsuya So, et al. "Cancer stem cell markers in lung cancer." Personalized Medicine Universe 4 (July 2015): 40–45. http://dx.doi.org/10.1016/j.pmu.2015.03.007.

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32

Koch, Lin-Kristin, Hui Zhou, Jörg Ellinger, et al. "Stem cell marker expression in small cell lung carcinoma and developing lung tissue." Human Pathology 39, no. 11 (2008): 1597–605. http://dx.doi.org/10.1016/j.humpath.2008.03.008.

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33

Xing, Dongqi, J. Michael Wells, Samantha S. Giordano, et al. "Induced pluripotent stem cell-derived endothelial cells attenuate lipopolysaccharide-induced acute lung injury." Journal of Applied Physiology 127, no. 2 (2019): 444–56. http://dx.doi.org/10.1152/japplphysiol.00587.2018.

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The chemokine receptors CXCR1/2 and CCR2/5 play a critical role in neutrophil and monocyte recruitment to sites of injury and/or inflammation. Neutrophil-mediated inflammation and endothelial cell (EC) injury are unifying factors in the pathogenesis of the acute respiratory distress syndrome. This study tested the hypothesis that systemic administration of rat-induced pluripotent stem cell (iPS)-derived ECs (iPS-ECs) overexpressing CXCR1/2 or CCR2/5 attenuates lipopolysaccharide (LPS)-induced acute lung injury. Rat iPS-ECs were transduced with adenovirus containing cDNA of CXCR1/2 or CCR2/5. Ovariectomized Sprague-Dawley rats (10 wk old) received intraperitoneal injection of LPS and intravenous infusion of 1) saline vehicle, 2) AdNull-iPS-ECs (iPS-ECs transduced with empty adenoviral vector), 3) CXCR1/2-iPS-ECs (iPS-ECs overexpressing CXCR1/2), or 4) CCR2/5-iPS-ECs (iPS-ECs overexpressing CCR2/5) at 2 h post-LPS. Rats receiving intraperitoneal injection of saline served as sham controls. Later (4 h), proinflammatory cytokine/chemokine mRNA and protein levels were measured in total lung homogenates by real-time RT-PCR and Luminex multiplex assays, and neutrophil and macrophage infiltration in alveoli was measured by immunohistochemical staining. Pulmonary microvascular permeability was assessed by the Evans blue technique, and pulmonary edema was estimated by wet-to-dry lung weight ratios. Albumin levels and neutrophil counts were assessed in bronchoalveolar lavage fluid at 24 h post-LPS. Both CXCR1/2-iPS-ECs and CCR2/5-iPS-ECs significantly reduced LPS-induced proinflammatory mediator expression, neutrophil and macrophage infiltration, pulmonary edema, and vascular permeability compared with controls. These provocative findings provide strong evidence that targeted delivery of iPS-ECs overexpressing CXCR1/2 or CCR2/5 prevents LPS-induced acute lung injury. NEW & NOTEWORTHY We have developed a novel approach to address neutrophil-mediated inflammation and endothelial damage by targeted delivery of rat-induced pluripotent stem cell (iPS)-derived endothelial cell (ECs)overexpressing chemokine receptors CXCR1/2 and CCR2/5 in injured lung tissue in a model of acute lung injury. We have demonstrated that intravenously transfused CXCR1/2-iPS-ECs and CCR2/5-iPS-ECs are recruited to lipopolysaccharide-injured lungs and attenuate lipopolysaccharide-induced parenchymal lung injury responses, including inflammatory mediator expression, inflammatory cell infiltration, and vascular leakage compared with controls.

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34

Rasky, Andrew, David M. Habiel, Susan Morris, et al. "Inhibition of the stem cell factor 248 isoform attenuates the development of pulmonary remodeling disease." American Journal of Physiology-Lung Cellular and Molecular Physiology 318, no. 1 (2020): L200—L211. http://dx.doi.org/10.1152/ajplung.00114.2019.

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Stem cell factor (SCF) and its receptor c-kit have been implicated in inflammation, tissue remodeling, and fibrosis. Ingenuity Integrated Pathway Analysis of gene expression array data sets showed an upregulation of SCF transcripts in idiopathic pulmonary fibrosis (IPF) lung biopsies compared with tissue from nonfibrotic lungs that are further increased in rapid progressive disease. SCF248, a cleavable isoform of SCF, was abundantly and preferentially expressed in human lung fibroblasts and fibrotic mouse lungs relative to the SCF220 isoform. In fibroblast-mast cell coculture studies, blockade of SCF248 using a novel isoform-specific anti-SCF248 monoclonal antibody (anti-SCF248), attenuated the expression of COL1A1, COL3A1, and FN1 transcripts in cocultured IPF but not normal lung fibroblasts. Administration of anti-SCF248 on days 8 and 12 after bleomycin instillation in mice significantly reduced fibrotic lung remodeling and col1al, fn1, acta2, tgfb, and ccl2 transcript expression. In addition, bleomycin increased numbers of c-kit+ mast cells, eosinophils, and ILC2 in lungs of mice, whereas they were not significantly increased in anti-SCF248-treated animals. Finally, mesenchymal cell-specific deletion of SCF significantly attenuated bleomycin-mediated lung fibrosis and associated fibrotic gene expression. Collectively, these data demonstrate that SCF is upregulated in diseased IPF lungs and blocking SCF248 isoform significantly ameliorates fibrotic lung remodeling in vivo suggesting that it may be a therapeutic target for fibrotic lung diseases.

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35

Pacienza, Natalia, Diego Santa-Cruz, Ricardo Malvicini, et al. "Mesenchymal Stem Cell Therapy Facilitates Donor Lung Preservation by Reducing Oxidative Damage during Ischemia." Stem Cells International 2019 (August 5, 2019): 1–13. http://dx.doi.org/10.1155/2019/8089215.

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Lung transplantation is a lifesaving therapy for people living with severe, life-threatening lung disease. The high mortality rate among patients awaiting transplantation is mainly due to the low percentage of lungs that are deemed acceptable for implantation. Thus, the current shortage of lung donors may be significantly reduced by implementing different therapeutic strategies which facilitate both organ preservation and recovery. Here, we studied whether the anti-inflammatory effect of human umbilical cord-derived mesenchymal stem cells (HUCPVCs) increases lung availability by improving organ preservation. We developed a lung preservation rat model that mimics the different stages by which donor organs must undergo before implantation. The therapeutic schema was as follows: cardiac arrest, warm ischemia (2 h at room temperature), cold ischemia (1.5 h at 4°C, with Perfadex), and normothermic lung perfusion with ventilation (Steen solution, 1 h). After 1 h of warm ischemia, HUCPVCs (1×106 cells) or vehicle was infused via the pulmonary artery. Physiologic data (pressure-volume curves) were acquired right after the cardiac arrest and at the end of the perfusion. Interestingly, although lung edema did not change among groups, lung compliance dropped to 34% in the HUCPVC-treated group, while the vehicle group showed a stronger reduction (69%, p<0.0001). Histologic assessment demonstrated less overall inflammation in the HUCPVC-treated lungs. In addition, MPO activity, a neutrophil marker, was reduced by 41% compared with vehicle (p<0.01). MSC therapy significantly decreased tissue oxidative damage by controlling reactive oxygen species production. Accordingly, catalase and superoxide dismutase enzyme activities remained at baseline levels. In conclusion, these results demonstrate that the anti-inflammatory effect of MSCs protects donor lungs against ischemic injury and postulates MSC therapy as a novel tool for organ preservation.

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36

Hennrick, Kenneth T., Angela G. Keeton, Suparna Nanua, et al. "Lung Cells from Neonates Show a Mesenchymal Stem Cell Phenotype." American Journal of Respiratory and Critical Care Medicine 175, no. 11 (2007): 1158–64. http://dx.doi.org/10.1164/rccm.200607-941oc.

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37

Martin, J., K. Helm, P. Ruegg, M. Varella-Garcia, E. Burnham, and S. Majka. "Adult lung side population cells have mesenchymal stem cell potential." Cytotherapy 10, no. 2 (2008): 140–51. http://dx.doi.org/10.1080/14653240801895296.

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38

Ouyang, Xiaoping, Xinlin Shi, Na Huang та ін. "WDR72 Enhances the Stemness of Lung Cancer Cells by Activating the AKT/HIF-1α Signaling Pathway". Journal of Oncology 2022 (7 листопада 2022): 1–12. http://dx.doi.org/10.1155/2022/5059588.

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Objectives. Lung cancer is a common malignant tumor with high morbidity and mortality rate. Lung cancer stem cells are crucial in the development of lung cancer. In this study, we investigate WD repeat-containing protein 72 (WDR72) on lung cancer cell stemness and explore its underlying mechanism. Methods. WDR72 expression was investigated in lung cancer tissues and lung cancer stem cells by Western blot and RT-qPCR. The stemness of lung cancer stem cells was verified by the sphere-forming experiment and the abundance of stem cell markers. For the purpose of determining lung cancer stem cell growth, metastasis, and apoptosis, the CCK-8 assay, colony formation, Transwell migration, and flow cytometry were carried out. The ability of tumorigenesis in vivo was explored by xenograft tumor mouse models. Results. Up-regulation of WDR72 was found in lung cancer tissues and lung cancer stem cells. WDR72 overexpression significantly activated the AKT/HIF-1α signaling pathway. Application of PI3K/AKT pathway inhibitor LY29004 was able to counteract the impacts of WDR72 upregulation on genes related to stemness, growth, migration, and apoptosis in lung cancer stem cells. The sphere formation of lung cancer stem cells was significantly diminished after inhibiting the AKT/HIF-1α pathway. The promotion of WDR72 overexpression on lung cancer stem cell proliferation and metastasis was also eliminated by LY29004 treatment. Conclusion. WDR72 activates the AKT/HIF-1α signaling pathway to enhance the stemness of lung cancer stem cells and promote the growth and metastasis of lung cancer.

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39

Inamdar, Ajinkya C., and Arati A. Inamdar. "Mesenchymal stem cell therapy in lung disorders: Pathogenesis of lung diseases and mechanism of action of mesenchymal stem cell." Experimental Lung Research 39, no. 8 (2013): 315–27. http://dx.doi.org/10.3109/01902148.2013.816803.

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40

Kotton, Darrell N., Ross Summer, and Alan Fine. "Lung stem cells: New paradigms." Experimental Hematology 32, no. 4 (2004): 340–43. http://dx.doi.org/10.1016/j.exphem.2004.01.009.

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41

Alder, Jonathan K., Christina E. Barkauskas, Nathachit Limjunyawong, et al. "Telomere dysfunction causes alveolar stem cell failure." Proceedings of the National Academy of Sciences 112, no. 16 (2015): 5099–104. http://dx.doi.org/10.1073/pnas.1504780112.

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Telomere syndromes have their most common manifestation in lung disease that is recognized as idiopathic pulmonary fibrosis and emphysema. In both conditions, there is loss of alveolar integrity, but the underlying mechanisms are not known. We tested the capacity of alveolar epithelial and stromal cells from mice with short telomeres to support alveolar organoid colony formation and found that type 2 alveolar epithelial cells (AEC2s), the stem cell-containing population, were limiting. When telomere dysfunction was induced in adult AEC2s by conditional deletion of the shelterin component telomeric repeat-binding factor 2, cells survived but remained dormant and showed all the hallmarks of cellular senescence. Telomere dysfunction in AEC2s triggered an immune response, and this was associated with AEC2-derived up-regulation of cytokine signaling pathways that are known to provoke inflammation in the lung. Mice uniformly died after challenge with bleomycin, underscoring an essential role for telomere function in AEC2s for alveolar repair. Our data show that alveoloar progenitor senescence is sufficient to recapitulate the regenerative defects, inflammatory responses, and susceptibility to injury that are characteristic of telomere-mediated lung disease. They suggest alveolar stem cell failure is a driver of telomere-mediated lung disease and that efforts to reverse it may be clinically beneficial.

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42

Nacarino-Palma, Ana, Claudia M. Rejano-Gordillo, Francisco J. González-Rico, et al. "Loss of Aryl Hydrocarbon Receptor Favors K-RasG12D-Driven Non-Small Cell Lung Cancer." Cancers 13, no. 16 (2021): 4071. http://dx.doi.org/10.3390/cancers13164071.

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Non-small cell lung adenocarcinoma (NSCLC) bearing K-RasG12D mutations is one of the most prevalent types of lung cancer worldwide. Aryl hydrocarbon receptor (AHR) expression varies in human lung tumors and has been associated with either increased or reduced lung metastasis. In the mouse, Ahr also adjusts lung regeneration upon injury by limiting the expansion of resident stem cells. Here, we show that the loss of Ahr enhances K-RasG12D-driven NSCLC in mice through the amplification of stem cell subpopulations. Consistent with this, we show that K-RasG12D;Ahr−/− lungs contain larger numbers of cells expressing markers for both progenitor Clara (SCGB1A1 and CC10) and alveolar type-II (SFTPC) cells when compared to K-RasG12D;Ahr+/+-driven tumors. They also have elevated numbers of cells positive for pluripotent stem cells markers such as SOX2, ALDH1, EPCAM, LGR5 and PORCN. Typical pluripotency genes Nanog, Sox2 and c-Myc were also upregulated in K-RasG12D;Ahr−/− lung tumors as found by RNAseq analysis. In line with this, purified K-RasG12D/+;Ahr−/− lung cells generate larger numbers of organoids in culture that can subsequently differentiate into bronchioalveolar structures enriched in both pluripotency and stemness genes. Collectively, these data indicate that Ahr antagonizes K-RasG12D-driven NSCLC by restricting the number of cancer-initiating stem cells. They also suggest that Ahr expression might represent a good prognostic marker to determine the progression of K-RasG12D-positive NSCLC patients.

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43

Savukinas, Ulrika Blank, Sara Rolandsson Enes, Annika Andersson Sjöland, and Gunilla Westergren-Thorsson. "Concise Review: The Bystander Effect: Mesenchymal Stem Cell-Mediated Lung Repair." STEM CELLS 34, no. 6 (2016): 1437–44. http://dx.doi.org/10.1002/stem.2357.

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Li, Feng, Jinxi He, Jun Wei, William C. Cho, and Xiaoming Liu. "Diversity of Epithelial Stem Cell Types in Adult Lung." Stem Cells International 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/728307.

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Lung is a complex organ lined with epithelial cells. In order to maintain its homeostasis and normal functions following injuries caused by varied extraneous and intraneous insults, such as inhaled environmental pollutants and overwhelming inflammatory responses, the respiratory epithelium normally undergoes regenerations by the proliferation and differentiation of region-specific epithelial stem/progenitor cells that resided in distinct niches along the airway tree. The importance of local epithelial stem cell niches in the specification of lung stem/progenitor cells has been recently identified. Studies using cell differentiating and lineage tracing assays,in vitroand/orex vivomodels, and genetically engineered mice have suggested that these local epithelial stem/progenitor cells within spatially distinct regions along the pulmonary tree contribute to the injury repair of epithelium adjacent to their respective niches. This paper reviews recent findings in the identification and isolation of region-specific epithelial stem/progenitor cells and local niches along the airway tree and the potential link of epithelial stem cells for the development of lung cancer.

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45

Pan, Zhenhua, Meidi Zhang, Fengyu Zhang, et al. "Single-Cell Transcriptomics Unveils the Dedifferentiation Mechanism of Lung Adenocarcinoma Stem Cells." International Journal of Molecular Sciences 24, no. 1 (2022): 482. http://dx.doi.org/10.3390/ijms24010482.

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Lung adenocarcinoma (LUAD) is a major subtype of lung cancer, and its prognosis is still poor due to therapy resistance, metastasis, and recurrence. In recent years, increasing evidence has shown that the existence of lung cancer stem cells is responsible for the propagation, metastasis, therapy resistance, and recurrence of the tumor. During their transition to cancer stem cells, tumor cells need to inhibit cell differentiation and acquire invasive characteristics. However, our understanding of the property and role of such lung cancer stem cells is still limited. In this study, lung adenocarcinoma cancer stem cells (LCSCs) were enriched from the PC-9 cell line in a serum-free condition. PC-9 cells grew into spheres and showed higher survival rates when exposed to gefitinib: the drug used for the treatment of LUAD. Additionally, we found that the canonical stemness marker protein CD44 was significantly increased in the enriched LCSCs. Then, LCSCs were inoculated into the groin of nude mice for 1.5 months, and tumors were detected in the animals, indicating the strong stemness of the cells. After that, we performed single-cell RNA sequencing (scRNA-seq) on 7320 LCSCs and explored the changes in their transcriptomic signatures. We identified cell populations with a heterogeneous expression of cancer stem marker genes in LCSCs and subsets with different degrees of differentiation. Further analyses revealed that the activation of the FOXM1 (oncoprotein) transcription factor is a key factor in cell dedifferentiation, which enables tumor cells to acquire an epithelial-mesenchymal transition phenotype and increases the LCSC surface marker CD44. Moreover, we found that the combination of CD44, ABCG2, and ALCAM was a specific marker for LCSCs. In summary, this study identified the potential factors and molecular mechanisms underlying the stemness properties of LUAD cancer cells; it could also provide insight into developing novel and effective therapeutic approaches.

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46

Tropea, Kristen A., Eva Leder, Muhammad Aslam, et al. "Bronchioalveolar stem cells increase after mesenchymal stromal cell treatment in a mouse model of bronchopulmonary dysplasia." American Journal of Physiology-Lung Cellular and Molecular Physiology 302, no. 9 (2012): L829—L837. http://dx.doi.org/10.1152/ajplung.00347.2011.

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Bronchopulmonary dysplasia (BPD) remains a major complication of prematurity resulting in significant morbidity and mortality. The pathology of BPD is multifactorial and leads to alveolar simplification and distal lung injury. Previous studies have shown a beneficial effect of systemic treatment with bone marrow-derived mesenchymal stromal cells (MSCs) and MSC-conditioned media (MSC-CM) leading to amelioration of the lung parenchymal and vascular injury in vivo in the hyperoxia murine model of BPD. It is possible that the beneficial response from the MSCs is at least in part due to activation of endogenous lung epithelial stem cells. Bronchioalveolar stem cells (BASCs) are an adult lung stem cell population capable of self-renewal and differentiation in culture, and BASCs proliferate in response to bronchiolar and alveolar lung injury in vivo. Systemic treatment of neonatal hyperoxia-exposed mice with MSCs or MSC-CM led to a significant increase in BASCs compared with untreated controls. Treatment of BASCs with MSC-CM in culture showed an increase in growth efficiency, indicating a direct effect of MSCs on BASCs. Lineage tracing data in bleomycin-treated adult mice showed that Clara cell secretory protein-expressing cells including BASCs are capable of contributing to alveolar repair after lung injury. MSCs and MSC-derived factors may stimulate BASCs to play a role in the repair of alveolar lung injury found in BPD and in the restoration of distal lung cell epithelia. This work highlights the potential important role of endogenous lung stem cells in the repair of chronic lung diseases.

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Pitt, Bruce R., and Luis A. Ortiz. "Stem cells in lung biology." American Journal of Physiology-Lung Cellular and Molecular Physiology 286, no. 4 (2004): L621—L623. http://dx.doi.org/10.1152/ajplung.00392.2003.

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Abreu, Soraia Carvalho, Tatiana Maron-Gutierrez, Cristiane Sousa Nascimento Baez Garcia, Marcelo Marcos Morales, and Patricia Rieken Macedo Rocco. "Stem cells and respiratory diseases." Brazilian Archives of Biology and Technology 51, spe (2008): 23–30. http://dx.doi.org/10.1590/s1516-89132008000700005.

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Stem cells have a multitude of clinical implications in the lung. This article is a critical review that includes clinical and experimental studies of MedLine and SciElo database in the last 10 years, where we highlight the effects of stem cell therapy in acute respiratory distress syndrome or more chronic disorders such as lung fibrosis and emphysema. Although, many studies have shown the beneficial effects of stem cells in lung development, repair and remodeling; some important questions need to be answered to better understand the mechanisms that control cell division and differentiation, therefore enabling the use of cell therapy in human respiratory diseases.

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49

Song, Na, Hiroaki Wakimoto, Filippo Rossignoli, et al. "Mesenchymal stem cell immunomodulation: In pursuit of controlling COVID-19 related cytokine storm." Stem Cells 39, no. 6 (2021): 707–22. http://dx.doi.org/10.1002/stem.3354.

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Abstract The coronavirus disease 2019 (COVID-19) pandemic has grown to be a global public health crisis with no safe and effective treatments available yet. Recent findings suggest that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the coronavirus pathogen that causes COVID-19, could elicit a cytokine storm that drives edema, dysfunction of the airway exchange, and acute respiratory distress syndrome in the lung, followed by acute cardiac injury and thromboembolic events leading to multiorgan failure and death. Mesenchymal stem cells (MSCs), owing to their powerful immunomodulatory abilities, have the potential to attenuate the cytokine storm and have therefore been proposed as a potential therapeutic approach for which several clinical trials are underway. Given that intravenous infusion of MSCs results in a significant trapping in the lung, MSC therapy could directly mitigate inflammation, protect alveolar epithelial cells, and reverse lung dysfunction by normalizing the pulmonary microenvironment and preventing pulmonary fibrosis. In this review, we present an overview and perspectives of the SARS-CoV-2 induced inflammatory dysfunction and the potential of MSC immunomodulation for the prevention and treatment of COVID-19 related pulmonary disease.

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Shaykhiev, Renat, Rui Wang, Rachel K. Zwick, et al. "Airway basal cells of healthy smokers express an embryonic stem cell signature relevant to lung cancer." STEM CELLS 31, no. 9 (2013): 1992–2002. http://dx.doi.org/10.1002/stem.1459.

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