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Secretion, Alveolar Processing, and Turnover of Pulmonary Surfactant
Published in Jacques R. Bourbon, Pulmonary Surfactant: Biochemical, Functional, Regulatory, and Clinical Concepts, 2019
Claypool et al.227,228 showed that the uptake of liposomal phospholipids was similarly enhanced by the natural lipophilic SP-C in the rat. A recent work by the same group,229 however, demonstrated that this apparent effect could in fact be due to phosphatidylglycerol (PG) co-isolated with the protein. PG exhibited a concentration-dependent enhancing activity on the uptake of PC liposomes by isolated type II pneumocytes. Phosphatidylethanolamine (PE) alone had no effect, but could inhibit the stimulating effect of PG. Surfactant protein C increased the cellular uptake of PC liposomes only when it presented a protein-to-phospholipid ratio superior to 1 and a PG-to-PE ratio over 2. Moreover, mixtures of PG and PE reflecting the phospholipid composition of the SP-C extract were able to reproduce the effects of the latter. The study therefore pointed out a new physiological function of PG which, along with the aforementioned action of PG upon alveolar phospholipase activities, represents a pertinent issue for the design of exogenous surfactant substitutes. In disagreement with these findings, however, another recent study230 indicated that synthetic SP-B and SP-C — therefore free of phospholipids — markedly stimulated the transfer of PC from liposomes to rat lung alveolar type II cells and Chinese hamster lung fibroblasts in a dose- and time-dependent fashion. Thus, these peptides could actually have a proper effect on readsorption of surfactant material.
Idiopathic pulmonary fibrosis: Epidemiology, natural history and pathophysiology
Published in Muhunthan Thillai, David R Moller, Keith C Meyer, Clinical Handbook of Interstitial Lung Disease, 2017
Zulma Yunt, Jeffrey J Swigris, Amy L Olson
Clues to the importance of a genetic component in the development of pulmonary fibrosis came from the recognition of familial disease and from specific known genetic disorders including dyskeratosis congenita and Hermansky–Pudlak syndrome. Dyskeratosis congenita is a rare, heritable condition characterized by bone marrow failure and mucocutaneous features, and is commonly complicated by pulmonary fibrosis (63,64). The disease is caused by genetic mutations in genes responsible for telomerase maintenance. This observation led to an examination of telomerase genes in familial forms of lung fibrosis not associated with dyskeratosis congenita. This identified an association between familial pulmonary fibrosis (FPF) and mutations in TERT and TERC (65,66). Similarly, other studies identified variants in genes encoding surfactant protein C (SFTPC), surfactant protein A2 (SFTPA2) (67–69). Together however, these mutations account for only a minority of cases of pulmonary fibrosis.
The Use of Placenta-Derived Cells in Inflammatory and Fibrotic Disorders
Published in Ornella Parolini, Antonietta Silini, Placenta, 2016
Euan M. Wallace, Anna Cargnoni, Rebecca Lim, Alex Hodge, William Sievert
In support of these early observations, more recently there has been much evidence supporting the role of macrophages in therapeutic effects of hAECs in lung injury. Murphy and collaborators used surfactant protein C–deficient (Sftpc-/-) mice, which are highly susceptible to pulmonary injury as a result of impairment of macrophage function, to show that the beneficial effects observed after hAEC treatment depend upon on macrophage recruitment and polarization (Murphy et al. 2012a). Specifically, hAEC treatment to bleomycin-injured Sftpc-/- mice did not mitigate the inflammatory and fibrotic injuries, and no preservation of lung function was observed. This was in stark contrast to hAEC-treated bleomycin-injured Sftpc+/+ mice where injury was prevented. Furthermore, they showed a lower neutrophil infiltration, but no effect was observed on lung macrophage levels, whereas in Sftpc+/+ mice hAEC administration was associated with increased polarization of macrophages toward alternatively activated (M2) phenotype. No hAECs were detected in the host lungs at day 7 posttransplantation (Murphy et al. 2012a).
Effect of epithelial-specific MyD88 signaling pathway on airway inflammatory response to organic dust exposure
Published in Journal of Immunotoxicology, 2023
Amber N. Johnson, John Dickinson, Amy Nelson, Rohit Gaurav, Katrina Kudrna, Scott E. Evans, Katherine Janike, Todd A. Wyatt, Jill A. Poole
Targeted deletion of alleles can be achieved using Cre/Lox technology, wherein LoxP sites are inserted flanking an exon of interest and Cre recombinase is expressed under the control of cell-specific promoter (Wang 2009). This approach circumvents potential confounding issues of conventional gene-targeting approaches, including the unknown impact that global gene deletion may have on numerous cell and tissue types outside the area of study, and the possibility of overexpression in global transgenic approaches. The major lung epithelial cell types include ciliated cells, secretory cells, serous cells, and basal cells in the airways, and Type I and Type II pneumocytes in the alveoli (Singh and Katyal 2000). Although expression of surfactant protein C protein (SPC) is a marker Type II pneumocytes in postnatal mice, when under control of the Sftpc promoter, Cre recombinase is expressed in all these cell types during embryogenesis, allowing deletion of alleles (i.e. alleles that are floxed) throughout the lung epithelium. In comparison, the club cell-specific protein (CCSP) Cre mouse targets secretory epithelial cells diffusely expressed throughout the airways (Rawlins et al. 2009). Thus, using genetically engineered mouse lines, MyD88 deficiency can be localized to airway epithelial cells such that studies could then be undertaken to inform the specific roles of airway epithelial cells throughout the lung compartments.
DLC1 inhibits lung adenocarcinoma cell proliferation, migration and invasion via regulating MAPK signaling pathway
Published in Experimental Lung Research, 2021
Niu Niu, Xingjie Ma, Haitao Liu, Junjie Zhao, Chao Lu, Fan Yang, Weibo Qi
For the development of targeted therapy against LUAD, effective target genes are emerging to be vital significant. Numerous studies proved that mRNA is closely associated with the diagnosis and prognosis of LUAD and plays a regulatory role in tumor malignant progression. Koh YW et al.8 found that high expression of aldehyde dehydrogenase-1 (ALDH1) improves the prognosis of LUAD. Li B et al.9 reported that low expression of surfactant protein C (SFTPC) is associated with poor overall survival of LUAD patients, and overexpression of SFTPC can inhibit tumor cell proliferation. Recent studies show that Deleted in Liver Cancer 1 (DLC1) has received increasing attention as a metastasis suppressor gene in various cancers including lung cancer.10 DLC1 was initially identified as a deleted or down-regulated gene in primary hepatocellular carcinoma (HCC), and it exerts its tumor suppressive role mainly through the Rho-GTPase-activating protein (RhoGAP) domain.11,12 Yang X et al.13 discovered that DLC1 can inhibit in vitro migration, invasion, colony formation and anchorage-independent growth of aggressive lung cancer cells by interacting with S100A10. Besides, DLC1 expression is significantly associated with the prognosis of patients with LUAD.14 Collectively, these findings suggest that DLC1 may play a role in malignant progression of LUAD, thereby to make an effect on the prognosis of patients.
MiR-629-3p-induced downregulation of SFTPC promotes cell proliferation and predicts poor survival in lung adenocarcinoma
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Bin Li, Yu-Qi Meng, Zheng Li, Ci Yin, Jun-Ping Lin, Duo-Jie Zhu, Shao-Bo Zhang
In this study, we observed that surfactant protein C (SFTPC) expression was downregulated in human lung adenocarcinoma tissues and cell lines, and low SFTPC expression correlated with poor overall survival of lung adenocarcinoma patients. Moreover, we found that overexpression of SFTPC could inhibit lung cancer cell proliferation in vitro and in vivo, but downregulation of SFTPC showed the opposite results. Besides, it was observed that miR-629-3p expression was upregulated in human lung adenocarcinoma tissues and cell lines. More importantly, we found that miR-629-3p could downregulate SFTPC expression by directly binding to the SFTPC 3'-UTR, and inhibit the regulatory effect of SFTPC on lung adenocarcinoma cell proliferation. Thus, it could be hypothesized that miR-629-3p-mediated downregulation of SFTPC could contribute to lung adenocarcinoma progression.