Melatonin regulates PARP1 to control the senescence-associated secretory phenotype (SASP) in human fetal lung fibroblast cells

2017 ◽  
Vol 63 (1) ◽  
pp. e12405 ◽  
Author(s):  
Songtao Yu ◽  
Xiaojiao Wang ◽  
Peiliang Geng ◽  
Xudong Tang ◽  
Lisha Xiang ◽  
...  
Keyword(s):  
Fetal Lung ◽  
Lung Fibroblast ◽  
Fibroblast Cells ◽  
Secretory Phenotype ◽  
Human Fetal Lung ◽  
Human Fetal Lung Fibroblast

scholarly journals THE ROLE OF THE IGF AXIS IN THE REGULATION OF HUMAN FETAL LUNG FIBROBLAST CELL GROWTH. † 504

1996 ◽  
Vol 39 ◽  
pp. 86-86
Author(s):  
Paulo Collett-Solberg ◽  
Roopmathy Rajah ◽  
Ruzheng Oian ◽  
Pinchas Cohen
Keyword(s):  
Cell Growth ◽  
Fetal Lung ◽  
Fibroblast Cell ◽  
Lung Fibroblast ◽  
Human Fetal Lung ◽  
Human Fetal Lung Fibroblast

PDE4 inhibitors roflumilast and rolipram augment PGE2 inhibition of TGF-β1-stimulated fibroblasts

2009 ◽  
Vol 296 (6) ◽  
pp. L959-L969 ◽  
Author(s):  
Shinsaku Togo ◽  
Xiangde Liu ◽  
Xingqi Wang ◽  
Hisatoshi Sugiura ◽  
Koichiro Kamio ◽  
...  
Keyword(s):  
Transforming Growth Factor ◽  
Three Dimensional ◽  
Fetal Lung ◽  
Independent Effect ◽  
Collagen Gels ◽  
Fibrotic Diseases ◽  
Human Fetal Lung ◽  
Human Fetal Lung Fibroblast ◽  
Adult Human Lung ◽  
Tgf Β1

Fibrotic diseases are characterized by the accumulation of extracellular matrix together with distortion and disruption of tissue architecture. Phosphodiesterase (PDE)4 inhibitors, by preventing the breakdown of cAMP, can inhibit fibroblast functions and may be able to mitigate tissue remodeling. Transforming growth factor (TGF)-β1, a mediator of fibrosis, can potentially modulate cAMP by altering PGE2 metabolism. The present study assessed whether PDE4 inhibitors functionally antagonize the profibrotic activity of fibroblasts stimulated by TGF-β1. The PDE4 inhibitors roflumilast and rolipram both inhibited fibroblast-mediated contraction of three-dimensional collagen gels and fibroblast chemotaxis toward fibronectin in the widely studied human fetal lung fibroblast strain HFL-1 and several strains of fibroblasts from adult human lung. Roflumilast was ∼10-fold more potent than rolipram. There was a trend for PDE4 inhibitors to inhibit more in the presence of TGF-β1 (0.05 < P < 0.08). The effect of the PDE4 inhibitors was mediated through cAMP-stimulated protein kinase A (PKA), although a PKA-independent effect on gel contraction was also observed. The effect of PDE4 inhibitors depended on fibroblast production of PGE2 and TGF-β1-induced PGE2 production. PDE4 inhibitors together with TGF-β1 resulted in augmented PGE2 production together with increased expression of COX mRNA and protein. The present study supports the concept that PDE4 inhibitors may attenuate fibroblast activities that can lead to fibrosis and that PDE4 inhibitors may be particularly effective in the presence of TGF-β1-induced fibroblast stimulation.

scholarly journals MicroRNA-377-3p released by mesenchymal stem cell exosomes ameliorates lipopolysaccharide-induced acute lung injury by targeting RPTOR to induce autophagy

2020 ◽  
Vol 11 (8) ◽  
Author(s):  
Xuxia Wei ◽  
Xiaomeng Yi ◽  
Haijin Lv ◽  
Xin Sui ◽  
Pinglan Lu ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Fetal Lung ◽  
Lung Damage ◽  
Inflammatory Factors ◽  
Human Umbilical Cord ◽  
Human Fetal Lung ◽  
Human Fetal Lung Fibroblast

Abstract Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are the severe lung damage and respiratory failure without effective therapy. However, there was a lack of understanding of the mechanism by which exosomes regulate autophagy during ALI/ARDS. Here, we found lipopolysaccharide (LPS) significantly increased inflammatory factors, administration of exosomes released by human umbilical cord mesenchymal stem cells (hucMSCs) successfully improved lung morphometry. Further studies showed that miR-377-3p in the exosomes played a pivotal role in regulating autophagy, leading to protect LPS induced ALI. Compared to exosomes released by human fetal lung fibroblast cells (HFL-1), hucMSCs-exosomes overexpressing miR-377-3p more effectively suppressed the bronchoalveolar lavage (BALF) and inflammatory factors and induced autophagy, causing recoveration of ALI. Administration of miR-377-3p expressing hucMSCs-exosomes or its target regulatory-associated protein of mTOR (RPTOR) knockdown significantly reduced ALI. In summary, miR-377-3p released by hucMSCs-exosomes ameliorated Lipopolysaccharide-induced acute lung injury by targeting RPTOR to induce autophagy in vivo and in vitro.

scholarly journals Synthesis, Optimization, Antifungal Activity, Selectivity, and CYP51 Binding of New 2-Aryl-3-azolyl-1-indolyl-propan-2-ols

2020 ◽  
Vol 13 (8) ◽  
pp. 186
Author(s):  
Nicolas Lebouvier ◽  
Fabrice Pagniez ◽  
Young Min Na ◽  
Da Shi ◽  
Patricia Pinson ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Absolute Configuration ◽  
Fetal Lung ◽  
X Ray Diffraction ◽  
X Ray ◽  
Access Channel ◽  
Docking Calculations ◽  
Dynamics Simulations ◽  
Human Fetal Lung ◽  
Human Fetal Lung Fibroblast

A series of 2-aryl-3-azolyl-1-indolyl-propan-2-ols was designed as new analogs of fluconazole (FLC) by replacing one of its two triazole moieties by an indole scaffold. Two different chemical approaches were then developed. The first one, in seven steps, involved the synthesis of the key intermediate 1-(1H-benzotriazol-1-yl)methyl-1H-indole and the final opening of oxiranes by imidazole or 1H-1,2,4-triazole. The second route allowed access to the target compounds in only three steps, this time with the ring opening by indole and analogs. Twenty azole derivatives were tested against Candida albicans and other Candida species. The enantiomers of the best anti-Candida compound, 2-(2,4-dichlorophenyl)-3-(1H-indol-1-yl)-1-(1H-1,2,4-triazol-1-yl)-propan-2-ol (8g), were analyzed by X-ray diffraction to determine their absolute configuration. The (−)-8g enantiomer (Minimum inhibitory concentration (MIC) = IC80 = 0.000256 µg/mL on C. albicans CA98001) was found with the S-absolute configuration. In contrast the (+)-8g enantiomer was found with the R-absolute configuration (MIC = 0.023 µg/mL on C. albicans CA98001). By comparison, the MIC value for FLC was determined as 0.020 µg/mL for the same clinical isolate. Additionally, molecular docking calculations and molecular dynamics simulations were carried out using a crystal structure of Candida albicans lanosterol 14α-demethylase (CaCYP51). The (−)-(S)-8g enantiomer aligned with the positioning of posaconazole within both the heme and access channel binding sites, which was consistent with its biological results. All target compounds have been also studied against human fetal lung fibroblast (MRC-5) cells. Finally, the selectivity of four compounds on a panel of human P450-dependent enzymes (CYP19, CYP17, CYP26A1, CYP11B1, and CYP11B2) was investigated.

scholarly journals Toxicity mechanism in fetal lung fibroblast cells for multi-walled carbon nanotubes defined by chemical impurities and dispersibility

2016 ◽  
Vol 5 (1) ◽  
pp. 248-258 ◽  
Author(s):  
Aparna Shinde ◽  
Candace S. J. Tsai
Keyword(s):  
Carbon Nanotubes ◽  
Human Health ◽  
Fetal Lung ◽  
Lung Fibroblast ◽  
Fibroblast Cells ◽  
Chemical Impurities ◽  
Wide Range ◽  
Multi Walled Carbon Nanotubes ◽  
Nano Medicine ◽  
Walled Carbon Nanotubes

Multi-walled carbon nanotubes (MWCNTs) are beneficial in a wide range of applications in fields such as electronics, optics and nano-medicine, so knowledge concerning their effect on human health is important.

Collagen secretion mediated by NMDR activation in human fetal lung fibroblasts

2010 ◽  
Vol 34 (8) ◽  
pp. S70-S70
Author(s):  
MingJie WANG ◽  
ZiQiang LUO ◽  
Mei LU ◽  
LiHong SHANG ◽  
ShaoJie YUE
Keyword(s):  
Fetal Lung ◽  
Lung Fibroblasts ◽  
Collagen Secretion ◽  
Human Fetal Lung

Design of Arylsulfonylhydrazones as Potential FabH Inhibitors: Synthesis, Antimicrobial Evaluation and Molecular Docking

2019 ◽  
Vol 15 ◽  
Author(s):  
Thais Batista Fernandes ◽  
Natanael Dante Segretti ◽  
Felipe Rebello Lourenço ◽  
Thalita Marcílio Cândido ◽  
André Rolim Baby ◽  
...  
Keyword(s):  
Antioxidant Activity ◽  
Molecular Docking ◽  
Antimicrobial Agents ◽  
Acyl Carrier Protein ◽  
Condensation Reaction ◽  
Lung Fibroblast ◽  
Fibroblast Cells ◽  
Human Lung Fibroblast ◽  
Persistent Problem ◽  
E Coli

Background: Antimicrobial resistance is a persistent problem about infections treatment and carries needing for develop new antimicrobial agents. Inhibiting of bacterial β-ketoacyl acyl carrier protein synthase III (FabH), which catalyzes the condensation reaction between a CoA-attached acetyl group and an ACP-attached malonyl group in bacteria is an interesting strategy to find new antibacterial agents. Objective: The aim of this work was to design and synthesize arylsulfonylhydrazones potentially FabH inhibitors and evaluate their antimicrobial activity. Methods: MIC50 of sulfonylhydrazones against E. coli and S. aureus was determined. Antioxidant activity was evaluated by DPPH (1-1’-diphenyl-2-picrylhydrazyl) assay and cytotoxicity against LL24 lung fibroblast cells was verified by MTT method. Principal component analysis (PCA) was performed in order to suggest a structure-activity relationship. Molecular docking allowed to propose sulfonylhydrazones interactions with FabH. Results: The most active compound showed activity against S. aureus and E. coli, with MIC50 = 0.21 and 0.44 µM, respectively. PCA studies correlated better activity to lipophilicity and molecular docking indicated that sulfonylhydrazone moiety is important to hydrogen-bond with FabH while methylcatechol ring performs π-π stacking interaction. The DPPH assay revealed that some sulfonylhydrazones derived from the methylcatechol series had antioxidant activity. None of the evaluated compounds was cytotoxic to human lung fibroblast cells, suggesting that the compounds might be considered safe at the tested concentration. Conclusion: Arylsufonylhydrazones is a promising scaffold to be explored for design of new antimicrobial agents.

Sign in / Sign up

Export Citation Format

Share Document