scholarly journals Mesenchymal Stem Cell Therapy For COVID-19; Is A New Challenge Review

2021 ◽  
Vol 25 (1) ◽  
pp. 258
Author(s):  
Maged Naser ◽  
Mohamed MN ◽  
Lamia H. Shehata
Keyword(s):  
Stem Cell ◽  
Infection Type ◽  
Large Population ◽  
Alveolar Epithelial Cells ◽  
First Century ◽  
Mesenchymal Stem Cell Therapy ◽  
Alveolar Epithelial ◽  
Lung Dysfunction ◽  
Immunological Reactions ◽  
Severe Respiratory Infection

"Coronavirus" is the word that absolutely isn't forgotten by everybody who lives in the first half of the twenty-first century. COVID19, as a pandemic, has driven numerous researchers from various biomedical fields to discover arrangements or therapies to deal with the pandemic. Nonetheless, no standard treatment for this infection has been found to date. Presumably, preventing the acute severe respiratory   infection type of COVID-19 as the most risky period of this disease can be useful for the therapy and decrease of the death rate. In such manner, mesenchymal stem cells (MSCs)-based immunomodulation treatment has been proposed as a reasonable restorative methodology and a several clinical studies have started. Recently, MSCs as indicated by their immunomodulatory and regenerative properties stand out in clinical trials. After the intravenous transplantation of MSCs, a large population of cells gathers in the lung, which they close by immunomodulatory impact could protect alveolar epithelial cells, recover the respiratory microenvironment, prevent pneumonic fibrosis, and cure lung dysfunction. Given the vulnerabilities here, we checked on detailed clinical preliminaries and theories to give helpful data to scientists and those keen on stem cell therapy.In this study, we considered this new way to deal with improve patient's immunological reactions to COVID-19 utilizing MSCs and talked about the parts of this proposed treatment. Nonetheless, right now, there are no affirmed MSC-based methodologies for the anticipation or potentially treatment of COVID-19 patients however clinical preliminaries progressing.  

Human induced pluripotent stem cell–derived lung progenitor and alveolar epithelial cells attenuate hyperoxia-induced lung injury

Cytotherapy ◽  
2018 ◽  
Vol 20 (1) ◽  
pp. 108-125 ◽  
Author(s):  
Mehdi Shafa ◽  
Lavinia Iuliana Ionescu ◽  
Arul Vadivel ◽  
Jennifer J.P. Collins ◽  
Liqun Xu ◽  
...  
Keyword(s):  
Stem Cell ◽  
Epithelial Cells ◽  
Lung Injury ◽  
Pluripotent Stem Cell ◽  
Induced Pluripotent Stem Cell ◽  
Alveolar Epithelial Cells ◽  
Alveolar Epithelial ◽  
Induced Pluripotent ◽  
Lung Progenitor

scholarly journals Telomere dysfunction causes alveolar stem cell failure

2015 ◽  
Vol 112 (16) ◽  
pp. 5099-5104 ◽  
Author(s):  
Jonathan K. Alder ◽  
Christina E. Barkauskas ◽  
Nathachit Limjunyawong ◽  
Susan E. Stanley ◽  
Frant Kembou ◽  
...  
Keyword(s):  
Stem Cell ◽  
Lung Disease ◽  
Inflammatory Responses ◽  
Alveolar Epithelial Cells ◽  
Cytokine Signaling ◽  
Telomere Dysfunction ◽  
Alveolar Epithelial ◽  
Conditional Deletion ◽  
Telomere Function ◽  
Underlying Mechanisms

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.

scholarly journals Wnt signaling regulates trans-differentiation of stem cell like type 2 alveolar epithelial cells to type 1 epithelial cells

2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Elhusseiny Mohamed Mahmud Abdelwahab ◽  
Judit Rapp ◽  
Diana Feller ◽  
Veronika Csongei ◽  
Szilard Pal ◽  
...  
Keyword(s):  
Stem Cell ◽  
Epithelial Cells ◽  
Wnt Signaling ◽  
Alveolar Epithelial Cells ◽  
Alveolar Epithelial

scholarly journals Hypoxia-induced alveolar epithelial-mesenchymal transition requires mitochondrial ROS and hypoxia-inducible factor 1

2009 ◽  
Vol 297 (6) ◽  
pp. L1120-L1130 ◽  
Author(s):  
Guofei Zhou ◽  
Laura A. Dada ◽  
Minghua Wu ◽  
Aileen Kelly ◽  
Humberto Trejo ◽  
...  
Keyword(s):  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Hypoxia Inducible Factor ◽  
Alveolar Epithelial Cells ◽  
Type I ◽  
Mesenchymal Transition ◽  
Alveolar Epithelial ◽  
Mitochondrial Ros ◽  
Lung Dysfunction ◽  
Tgf Β1

Patients with acute lung injury develop hypoxia, which may lead to lung dysfunction and aberrant tissue repair. Recent studies have suggested that epithelial-mesenchymal transition (EMT) contributes to pulmonary fibrosis. We sought to determine whether hypoxia induces EMT in alveolar epithelial cells (AEC). We found that hypoxia induced the expression of α-smooth muscle actin (α-SMA) and vimentin and decreased the expression of E-cadherin in transformed and primary human, rat, and mouse AEC, suggesting that hypoxia induces EMT in AEC. Both severe hypoxia and moderate hypoxia induced EMT. The reactive oxygen species (ROS) scavenger Euk-134 prevented hypoxia-induced EMT. Moreover, hypoxia-induced expression of α-SMA and vimentin was prevented in mitochondria-deficient ρ0 cells, which are incapable of ROS production during hypoxia. CoCl2 and dimethyloxaloylglycine, two compounds that stabilize hypoxia-inducible factor (HIF)-α under normoxia, failed to induce α-SMA expression in AEC. Furthermore, overexpression of constitutively active HIF-1α did not induce α-SMA. However, loss of HIF-1α or HIF-2α abolished induction of α-SMA mRNA during hypoxia. Hypoxia increased the levels of transforming growth factor (TGF)-β1, and preincubation of AEC with SB431542, an inhibitor of the TGF-β1 type I receptor kinase, prevented the hypoxia-induced EMT, suggesting that the process was TGF-β1 dependent. Furthermore, both ROS and HIF-α were necessary for hypoxia-induced TGF-β1 upregulation. Accordingly, we have provided evidence that hypoxia induces EMT of AEC through mitochondrial ROS, HIF, and endogenous TGF-β1 signaling.

Reversibility of lung inflammation caused by SP-B deficiency

2005 ◽  
Vol 289 (6) ◽  
pp. L962-L970 ◽  
Author(s):  
Machiko Ikegami ◽  
Jeffrey A. Whitsett ◽  
Prithy C. Martis ◽  
Timothy E. Weaver
Keyword(s):  
Lung Inflammation ◽  
Pulmonary Inflammation ◽  
Surfactant Protein ◽  
Alveolar Epithelial Cells ◽  
Lung Mechanics ◽  
Phospholipid Content ◽  
Alveolar Epithelial ◽  
Adult Mice ◽  
Lung Dysfunction

Whereas decreased concentrations of surfactant protein (SP)-B are associated with lung injury and respiratory distress, potential causal relationships between SP-B deficiency and lung inflammation remain unclear. A transgenic mouse in which human SP-B expression was placed under conditional control of doxycycline via the CCSP promoter was utilized to determine the role of SP-B in the initiation of pulmonary inflammation. Adult mice, made SP-B deficient by removal of doxycycline, developed severe respiratory failure within 4 days. Deficiency of SP-B was associated with increased minimal surface tension of the surfactant and perturbed lung mechanics. Four days of SP-B deficiency did not alter SP-C content or surfactant phospholipid content or composition. SP-B deficiency was associated with lung inflammation and increased soluble L-selectin, STAT-3, and phosphorylated STAT-3 in alveolar macrophages and alveolar epithelial cells. Alveolar IL-6, IL-1β, and macrophage inflammatory protein-2 concentrations were increased after removal of doxycycline, indicating pulmonary inflammation. Restoration of SP-B expression following administration of doxycycline rapidly reversed SP-B-dependent abnormalities in lung mechanics and inflammation. SP-B deficiency is sufficient to cause lung dysfunction and inflammation in adult mice. SP-B reversed inflammation and maintained lung function in vivo, indicating its potential utility for the prevention and treatment of pulmonary injury and surfactant deficiency.

scholarly journals Mesenchymal Stem Cell Conditioned Medium Promotes Proliferation and Migration of Alveolar Epithelial Cells under Septic Conditions In Vitro via the JNK-P38 Signaling Pathway

2015 ◽  
Vol 37 (5) ◽  
pp. 1830-1846 ◽  
Author(s):  
Jie Chen ◽  
Yanqin Li ◽  
Haojie Hao ◽  
Chonghui Li ◽  
Yu Du ◽  
...  
Keyword(s):  
Stem Cell ◽  
Botulinum Toxin ◽  
Epithelial Cells ◽  
Mesenchymal Stem Cell ◽  
Conditioned Medium ◽  
Alveolar Epithelial Cells ◽  
Receptor Type ◽  
Alveolar Epithelial ◽  
And Migration ◽  
Proliferation And Migration

Background/Aims: Mesenchymal stem cell (MSC) based therapies may be useful for treating acute respiratory distress syndrome (ARDS), but the underlying mechanisms are incompletely understood. We investigated the impact of human umbilical cord Wharton's jelly-derived MSC (hUC-MSC) secreted factors on alveolar epithelial cells under septic conditions and determined the relevant intracellular signaling pathways. Methods: Human alveolar epithelial cells (AEC) and primary human small airway epithelial cells (SAEC) were subjected to lipopolysaccharide (LPS) with or without the presence of hUC-MSC-conditioned medium (CM). Proliferation and migration of AEC and SAEC were determined via an MTT assay, a wound healing assay and a transwell migration assay (only for AEC). Protein phosphorylation was determined by western blot and the experiments were repeated in presence of small-molecule inhibitors. The hMSC-secretory proteins were identified by LC-MS/MS mass spectrometry. Results: MSC-CM enhanced proliferation and migration. Activation of JNK and P38, but not ERK, was required for the proliferation and migration of AEC and SAEC. Pretreatment of AEC or SAEC with SP600125, an inhibitor of JNK1 or SB200358, an inhibitor of P38, significantly reduced cell proliferation and migration. An array of proteins including TGF-beta receptor type-1, TGF-beta receptor type-2, Ras-related C3 botulinum toxin substrate 1 and Ras-related C3 botulinum toxin substrate 2 which influencing the proliferation and migration of AEC and SAEC were detected in MSC-CM. Conclusion: Our data suggest MSC promote epithelial cell repair through releasing a repertoire of paracrine factors via activation of JNK and P38 MAPK.

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