Abstract:1. TCs can accelerate the migration of MSCs from the intraperitoneal space into injured lung tissues through intercellular signals and/or cell-cell interaction. 2. Pre-activated MSCs and TCs with LPS show more efficient in cell-cell communication by OPN-or EGFR-dominated signal pathways
“… 27 OPN‐dominated molecular networks were also found to play an important role in lung tissue injury and repair and might be the decisive factor of therapeutic interaction between telocytes and stem cells. 28 During inflammation, OPN could increase leukocyte migration into inflammatory loci through multifactor regulations, for example, monocyte chemoattractant protein 1, β1 integrin, and PI3K. 29 The present study found that OPN gene overexpressed in three subtypes of NSCLC and was correlated with high metastasis and mortality rates of patients with NSCLC.…”
1. OPN can be a metastasis-associated or specific biomarker for lung cancer. 2. OPN over-expressed in lung cancer was correlated with cell movement, proliferation and the existence of EMT.3. OPN plays the decisive roles in lung cancer biological behaviors and EMT formation, through PI3K/Akt and MAPK/Erk1/2 pathways.
“… 27 OPN‐dominated molecular networks were also found to play an important role in lung tissue injury and repair and might be the decisive factor of therapeutic interaction between telocytes and stem cells. 28 During inflammation, OPN could increase leukocyte migration into inflammatory loci through multifactor regulations, for example, monocyte chemoattractant protein 1, β1 integrin, and PI3K. 29 The present study found that OPN gene overexpressed in three subtypes of NSCLC and was correlated with high metastasis and mortality rates of patients with NSCLC.…”
1. OPN can be a metastasis-associated or specific biomarker for lung cancer. 2. OPN over-expressed in lung cancer was correlated with cell movement, proliferation and the existence of EMT.3. OPN plays the decisive roles in lung cancer biological behaviors and EMT formation, through PI3K/Akt and MAPK/Erk1/2 pathways.
“… 1 , 2 During ALI, inflammatory response-activated neutrophils and macrophages can infiltrate into lung tissues and release cytokines, activating local pro-inflammatory reaction. 3 Innate immune signaling receptor NOD-like receptor family pyrin domain containing 3 (NLRP3) could be triggered by various danger signals including damage-related molecular patterns (DAMPs) and pathogen associated molecular patterns (PAMPs). 4 NLRP3 is the core assembly of inflammasome, the activation of which may give rise to caspase 1-mediated proteolytic activation of the interleukin-18 (IL-18) and IL-1β, and induce pyroptosis.…”
Scope
Mangiferin (MF) is a natural phytopolyphenol, which displays potential pharmacological properties involving antibacterial, anti-inflammation, antioxidant and anti-tumor. However, little is known about the roles of MF in lung injury. The aim of this study is to demonstrate the modulatory effects and molecular mechanisms by which MF operates in sepsis-induced lung injury.
Methods and Results
To examine the protective properties of MF, an in vivo model of lipopolysaccharide (LPS)-induced lung injury in mice and an in vitro model of LPS-treated J774A.1 cells were established, respectively. The results revealed that MF treatment significantly relieved LPS-induced pathological injury and inflammatory response in murine lung tissues. Meanwhile, MF treatment also inhibited nucleotide-binding oligomerization domain (NOD)-like receptor family, pyrin domain-containing protein 3 (NLRP3) inflammasome activation and pyroptosis induced by LPS. In macrophage-specific NLRP3 deficiency mice treated with LPS, MF showed little protective effects. NLRP3 overexpression by adenovirus could also offset the beneficial effects of MF in LPS-treated J774A.1 cells. Furthermore, we found that MF could suppress the expression of NLPR3 and pyroptosis of macrophages by inhibiting the nuclear translocation of the nuclear factor-κB (NF-κB) subunits P50 and P65.
Conclusion
MF protects against lung injury and inflammatory response by inhibiting NLRP3 inflammasome activation in a NF-κB-dependent manner in macrophages, which provides a promising therapeutic candidate for the treatment of lung injury.
“…Focusing on TCs in the respiratory system, Zhang et al established a rat model of acute lung injury and observed the effect of cotransplantation of TCs with mesenchymal stem cells. The results demonstrated that TCs had a synergic effect on the experimental lung injury's attenuation [69]. TCs were also previously implicated in the pathogenesis of a broad spectrum of chronic inflammatory and fibrotic diseases, including Crohn's disease, liver fibrosis, and psoriasis.…”
Section: Cardiac Telocytes In Cardiovascular Regenerative Medicine-recent Developmentsmentioning
The regeneration of a diseased heart is one of the principal challenges of modern cardiovascular medicine. There has been ongoing research on stem-cell-based therapeutic approaches. A cell population called telocytes (TCs) described only 16 years ago largely contributed to the research area of cardiovascular regeneration. TCs are cells with small bodies and extremely long cytoplasmic projections called telopodes, described in all layers of the heart wall. Their functions include cell-to-cell signaling, stem-cell nursing, mechanical support, and immunoregulation, to name but a few. The functional derangement or quantitative loss of TCs has been implicated in the pathogenesis of myocardial infarction, heart failure, arrhythmias, and many other conditions. The exact pathomechanisms are still unknown, but the loss of regulative, integrative, and nursing functions of TCs may provide important clues. Therefore, a viable avenue in the future modern management of these conditions is TC-based cell therapy. TCs have been previously transplanted into a mouse model of myocardial infarction with promising results. Tandem transplantation with stem cells may provide additional benefit; however, many underresearched areas need to be addressed in future research before routine application of TC-based cell therapy in human subjects. These include the standardization of protocols for isolation, cultivation, and transplantation, quantitative optimization of TC transplants, cost-effectivity analysis, and many others.
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