scholarly journals Mitochondrial Impairment Mechanism in D-galactose-induced Senescence in Experimental Fibroblast Cell Model

2016 ◽  
Author(s):  
Wei Ye ◽  
Jian-Ming Cao ◽  
Xiao-Jun Tang ◽  
Chu Liu ◽  
Dong-Jie Hao ◽  
...  
Keyword(s):  
Cell Model ◽  
Fibroblast Cell ◽  
Mitochondrial Impairment

scholarly journals Flower Infusions From Cornus mas and Cornus kousa Inhibit Aldose Reductase Enzyme, Without Any Effects on Lipotoxicity

2020 ◽  
Vol 15 (3) ◽  
pp. 1934578X2091286
Author(s):  
Vladimír Forman ◽  
Ivana Šušaníková ◽  
Ľubica Kukurová ◽  
Emil Švajdlenka ◽  
Milan Nagy ◽  
...  
Keyword(s):  
Aldose Reductase ◽  
Cell Model ◽  
Enzyme Reaction ◽  
Fibroblast Cell ◽  
Protective Role ◽  
Blood Levels ◽  
Cytotoxic Action ◽  
Cornus Mas ◽  
Cornus Kousa

Aldose reductase inhibitors are considered to be potential therapeutic agents for chronic diabetic complications. Diabetes mellitus can be accompanied by elevated blood levels of free fatty acids, which can cause lipotoxicity. Herbal extracts and their constituents are promising agents which have the potential for alleviating these complications. Our study was focused on the influence on these effects by flower infusions from Cornus mas L. and Cornus kousa F.Buerger ex Hance. Initially, phenolic compounds were quantified in the dried flowers. Next, we studied the ability of flower infusions from both plants to inhibit aldose reductase in vitro, the protective role in the cell model of lipotoxicity, and the cytotoxic action on fibroblast cell line NIH-3T3 by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2 H-tetrazolium bromide assay. Both species are rich in phenolics; C. kousa flowers contain slightly higher amounts of phenolic acids (20.8%) and flavonoids (56.1%) than C. mas (20.2%) and (47.4%), respectively. Both extracts showed effective inhibition, expressed as half-maximal inhibitory concentration (IC50) (the concentration of inhibitor required to exhibit 50% inhibition of the enzyme reaction), of aldose reductase in non-toxic low concentrations (IC50 = 3.06 μg/mL for C. mas and IC50 = 2.49 μg/mL for C. kousa, respectively). In contrast, these concentrations of both extracts had almost no effects in the lipotoxicity cell model. To our knowledge, this study is the first report on C. mas and C. kousa flowers’ aldose reductase inhibitory activity and influence upon lipotoxicity.

scholarly journals Mitochondrial Impairment Upregulates MICOS Expression in a Human Microglial Cell Model

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Alejandra Bargues Carot ◽  
Emir Malovic ◽  
Huajun Jin ◽  
Vellareddy Anantharam ◽  
Arthi Kanthasamy ◽  
...  
Keyword(s):  
Microglial Cell ◽  
Cell Model ◽  
Mitochondrial Impairment

scholarly journals Heat-Killed Lactobacilli Preparations Promote Healing in the Experimental Cutaneous Wounds

Cells ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 3264
Author(s):  
Wan-Hua Tsai ◽  
Chia-Hsuan Chou ◽  
Tsuei-Yin Huang ◽  
Hui-Ling Wang ◽  
Peng-Ju Chien ◽  
...  
Keyword(s):  
Wound Repair ◽  
Therapeutic Potential ◽  
Cell Model ◽  
Fibroblast Cell ◽  
Lipoteichoic Acid ◽  
Skin Wound ◽  
Cutaneous Wounds ◽  
Alternative Approach ◽  
Skin Healing ◽  
Systemic Infections

Probiotics are defined as microorganisms with beneficial health effects when consumed by humans, being applied mainly to improve allergic or intestinal diseases. Due to the increasing resistance of pathogens to antibiotics, the abuse of antibiotics becomes inefficient in the skin and in systemic infections, and probiotics may also provide the protective effect for repairing the healing of infected cutaneous wounds. Here we selected two Lactobacillus strains, L. plantarum GMNL-6 and L. paracasei GMNL-653, in heat-killed format to examine the beneficial effect in skin wound repair through the selection by promoting collagen synthesis in Hs68 fibroblast cells. The coverage of gels containing heat-killed GMNL-6 or GMNL-653 on the mouse tail with experimental wounds displayed healing promoting effects with promoting of metalloproteinase-1 expression at the early phase and reduced excessive fibrosis accumulation and deposition in the later tail-skin recovery stage. More importantly, lipoteichoic acid, the major component of Lactobacillus cell wall, from GMNL-6/GMNL-653 could achieve the anti-fibrogenic benefit similar to the heat-killed bacteria cells in the TGF-β stimulated Hs68 fibroblast cell model. Our study offers a new therapeutic potential of the heat-killed format of Lactobacillus as an alternative approach to treating skin healing disorders.

A Mouse Fibroblast Cell Model to Study Human Papillomavirus-Associated Tumorigenesis

2000 ◽  
Vol 270 (1) ◽  
pp. 119-124 ◽  
Author(s):  
Patricia Hernández ◽  
Nelson Merino ◽  
Omar Lopez-Ocejo ◽  
Manuel de Jesus Araña
Keyword(s):  
Human Papillomavirus ◽  
Cell Model ◽  
Fibroblast Cell ◽  
Mouse Fibroblast ◽  
Mouse Fibroblast Cell

Protein Glycosylation in a Heat-Resistant Rat Fibroblast Cell Model Expressing Human HSP70

1997 ◽  
Vol 232 (1) ◽  
pp. 26-32 ◽  
Author(s):  
Kurt J. Henle ◽  
Sunita M. Jethmalani ◽  
Ligeng Li ◽  
Gloria C. Li
Keyword(s):  
Cell Model ◽  
Fibroblast Cell ◽  
Protein Glycosylation ◽  
Heat Resistant ◽  
Human Hsp70

A model of human p210bcr/ABL-mediated chronic myelogenous leukemia by transduction of primary normal human CD34+ cells with a BCR/ABL-containing retroviral vector

Blood ◽  
2001 ◽  
Vol 97 (8) ◽  
pp. 2406-2412 ◽  
Author(s):  
Robert C. Zhao ◽  
Yuehua Jiang ◽  
Catherine M. Verfaillie
Keyword(s):  
Cell Lines ◽  
Chronic Myelogenous Leukemia ◽  
Molecular Mechanisms ◽  
Cell Model ◽  
Fibroblast Cell ◽  
Myelogenous Leukemia ◽  
Hematopoietic Progenitor Cell ◽  
Hematopoietic Progenitor ◽  
Human Cd34 ◽  
Cd34 Cells

Abstract Most insights into the molecular mechanisms underlying transformation by the p210BCR/ABL oncoprotein are derived from studies in which BCR/ABL cDNA was introduced into hematopoietic or fibroblast cell lines. However, such cell line models may not represent all the features of chronic myelogenous leukemia (CML) caused by additional genetic abnormalities and differences in the biology of cell lines compared with primary hematopoietic progenitor and stem cells. A primary human hematopoietic progenitor cell model for CML was developed by the transduction of b3a2 BCR/ABL cDNA in normal CD34+cells. Adhesion of BCR/ABL-transduced CD34+ cells to fibronectin was decreased, but migration over fibronectin was enhanced compared with that of mock-transduced CD34+ cells. Adhesion to fibronectin did not decrease the proliferation of BCR/ABL-transduced CD34+ cells but decreased the proliferation of mock-transduced CD34+ cells. This was associated with elevated levels of p27Kip in p210BCR/ABL-expressing CD34+ cells. In addition, the presence of p210BCR/ABLdelayed apoptosis after the withdrawal of cytokines and serum. Finally, significantly more and larger myeloid colony-forming units grew from BCR/ABL than from mock-transduced CD34+ cells. Thus, the transduction of CD34+ cells with the b3a2-BCR/ABL cDNA recreates most, if not all, phenotypic abnormalities seen in primary CML CD34+ cells. This model should prove useful for the study of molecular mechanisms associated with the presence of p210BCR/ABL in CML.

Scanning electron microscopic study of collagen fibrillogenesis and extracellular compartmentalization in the chick embryo tendon

1986 ◽  
Vol 44 ◽  
pp. 208-209
Author(s):  
Grace C.H. Yang
Keyword(s):  
Chick Embryo ◽  
Extracellular Space ◽  
Fibroblast Cell ◽  
Collagen Fibrils ◽  
Electron Microscopic ◽  
Voltage Electron ◽  
Scanning Electron Microscopic Study ◽  
Microscopic Studies ◽  
And Function

The size and organization of collagen fibrils in the extracellular matrix is an important determinant of tissue structure and function. The synthesis and deposition of collagen involves multiple steps which begin within the cell and continue in the extracellular space. High-voltage electron microscopic studies of the chick embryo cornea and tendon suggested that the extracellular space is compartmentalized by the fibroblasts for the regulation of collagen fibril, bundle, and tissue specific macroaggregate formation. The purpose of this study is to gather direct evidence regarding the association of the fibroblast cell surface with newly formed collagen fibrils, and to define the role of the fibroblast in the control and the precise positioning of collagen fibrils, bundles, and macroaggregates during chick tendon development.

Endogenous hydrogen sulfide sulfhydrates IKKβ at cysteine 179 to control pulmonary artery endothelial cell inflammation

2019 ◽  
Vol 133 (20) ◽  
pp. 2045-2059 ◽  
Author(s):  
Da Zhang ◽  
Xiuli Wang ◽  
Siyao Chen ◽  
Selena Chen ◽  
Wen Yu ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Endothelial Cell ◽  
Pulmonary Artery ◽  
Cell Model ◽  
Site Directed Mutagenesis ◽  
Critical Event ◽  
Hypertensive Rats ◽  
Pulmonary Artery Endothelial Cell

Abstract Background: Pulmonary artery endothelial cell (PAEC) inflammation is a critical event in the development of pulmonary arterial hypertension (PAH). However, the pathogenesis of PAEC inflammation remains unclear. Methods: Purified recombinant human inhibitor of κB kinase subunit β (IKKβ) protein, human PAECs and monocrotaline-induced pulmonary hypertensive rats were employed in the study. Site-directed mutagenesis, gene knockdown or overexpression were conducted to manipulate the expression or activity of a target protein. Results: We showed that hydrogen sulfide (H2S) inhibited IKKβ activation in the cell model of human PAEC inflammation induced by monocrotaline pyrrole-stimulation or knockdown of cystathionine γ-lyase (CSE), an H2S generating enzyme. Mechanistically, H2S was proved to inhibit IKKβ activity directly via sulfhydrating IKKβ at cysteinyl residue 179 (C179) in purified recombinant IKKβ protein in vitro, whereas thiol reductant dithiothreitol (DTT) reversed H2S-induced IKKβ inactivation. Furthermore, to demonstrate the significance of IKKβ sulfhydration by H2S in the development of PAEC inflammation, we mutated C179 to serine (C179S) in IKKβ. In purified IKKβ protein, C179S mutation of IKKβ abolished H2S-induced IKKβ sulfhydration and the subsequent IKKβ inactivation. In human PAECs, C179S mutation of IKKβ blocked H2S-inhibited IKKβ activation and PAEC inflammatory response. In pulmonary hypertensive rats, C179S mutation of IKKβ abolished the inhibitory effect of H2S on IKKβ activation and pulmonary vascular inflammation and remodeling. Conclusion: Collectively, our in vivo and in vitro findings demonstrated, for the first time, that endogenous H2S directly inactivated IKKβ via sulfhydrating IKKβ at Cys179 to inhibit nuclear factor-κB (NF-κB) pathway activation and thereby control PAEC inflammation in PAH.

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