Salidroside attenuates CoCl2-simulated hypoxia injury in PC12 cells partly by mitochondrial protection

2021 ◽  
pp. 174617
Author(s):  
Yan Tang ◽  
Ya Hou ◽  
Yong Zeng ◽  
Yao Hu ◽  
Yi Zhang ◽  
...  
Keyword(s):  
Simulated Hypoxia

Inhibition of Migration and Invasion of Hepatocarcinoma HepG2 Cells by Dietary Saponins via Targeting HIF-1α

2018 ◽  
Vol 18 (7) ◽  
pp. 1025-1031
Author(s):  
Cheng Luo ◽  
Di Wu ◽  
Meiling Chen ◽  
Wenhua Miao ◽  
Changfeng Xue ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Confocal Microscopy ◽  
Protein Expression ◽  
Mtt Assay ◽  
Hepg2 Cells ◽  
Molecular Mechanisms ◽  
Migration And Invasion ◽  
Rt Pcr ◽  
Gene And Protein Expression ◽  
Simulated Hypoxia

Background: Different saponins from herbs have been used as tonic or functional foods, and for treatment of various diseases including cancers. Although clinical data has supported the function of these saponins, their underlying molecular mechanisms have not been well defined. Methods: With the simulated hypoxia created by 8 hours of Cu++ exposure and following 24 hour incubation with different concentration of saponins in HepG2 cells for MTT assay, migration and invasion assays, and for RT-PCR, and with each group of cells for immunofluorescence observation by confocal microscopy. Results： ZC-4 had the highest rate of inhibition of cell proliferation by MTT assay, and the highest inhibition of migration rate by in vitro scratch assay, while ZC-3 had the highest inhibition of invasion ratio by transwell assay. Under the same simulated hypoxia, the molecular mechanism of saponin function was conducted by measuring the gene expression of Hypoxia Inducible Factor (HIF)-1α through RT-PCR, in which ZC-3 showed a potent inhibition of gene HIF-1α. For the protein expression by immunofluorescence staining with confocal microscopy, HIF-1α was also inhibited by saponins, with the most potent one being ZC-4 after eight hours’ relatively hypoxia incubation. Conclusion: Saponins ZC-4 and ZC-3 have the potential to reduce HepG2 cell proliferation, migration and invasion caused by hypoxia through effectively inhibiting the gene and protein expression of HIF-1α directly and as antioxidant indirectly

Sessional work-rate does not affect the magnitude to which simulated hypoxia can augment acute physiological responses during resistance exercise

2020 ◽  
Vol 120 (10) ◽  
pp. 2159-2169
Author(s):  
Thomas P. Walden ◽  
Olivier Girard ◽  
Andrew M. Jonson ◽  
Alasdair R. Dempsey ◽  
Kieran J. Marston ◽  
...  
Keyword(s):  
Resistance Exercise ◽  
Physiological Responses ◽  
Work Rate ◽  
Simulated Hypoxia

scholarly journals Metabolic and functional consequences of cytosolic 5′-nucleotidase-IA overexpression in neonatal rat cardiomyocytes

2003 ◽  
Vol 285 (3) ◽  
pp. H991-H998 ◽  
Author(s):  
Graciela B. Sala-Newby ◽  
Nicola V. E. Freeman ◽  
Maria A. Curto ◽  
Andrew C. Newby
Keyword(s):  
Neonatal Rat ◽  
Nucleoside Transporter ◽  
Chronotropic Effect ◽  
Rat Cardiomyocytes ◽  
Adenosine Receptor Antagonist ◽  
Neonatal Rat Cardiomyocytes ◽  
Functional Consequences ◽  
Chronotropic Effects ◽  
Simulated Hypoxia ◽  
Positive Chronotropic Effect

Adenosine exerts a spectrum of energy-preserving actions on the heart negative chronotropic effects. The pathways leading to adenosine formation have remained controversial. In particular, although cytosolic 5′-nucleotidases can catalyze adenosine formation in cardiomyocytes, their contribution to the actions of adenosine has not been documented previously. We recently cloned two closely related AMP-preferring cytosolic 5′-nucleotidases (cN-IA and -IB); the A form predominates in the heart. In this study, we overexpressed pigeon cN-IA in neonatal rat cardiomyocytes using an adenovirus. cN-IA overexpression increased adenosine formation and release into the medium caused by simulated hypoxia and by isoproterenol in the absence and presence of inhibitors of adenosine metabolism. Adenosine release was not affected by an ecto-5′-nucleotidase inhibitor, α,β-methylene-ADP, but was affected by a nucleoside transporter, dipyridamole. The positive chronotropic effect of isoproterenol (130 ±3 vs. 100 ±4 beats/min) was inhibited (107 ±3 vs. 94 ±3 beats/min) in cells overexpressing cN-IA, and this was reversed by the addition of the adenosine receptor antagonist 8-( p-sulfophenyl)theophilline (120 ± 3 vs. 90 ± 4 beats/min). Our results demonstrate that overexpressed cN-IA can be sufficiently active in cardiomyocytes to generate physiologically effective concentrations of adenosine at its receptors.

Abstract 257: Calreticulin Regulates Acetylation in Cardiac Cells During Endoplasmic Reticulum Stress

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Janet R Manning
Keyword(s):  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Cardiac Tissue ◽  
Stress Proteins ◽  
Cardiac Cells ◽  
Tunel Staining ◽  
Signaling Proteins ◽  
Cell Mortality ◽  
Simulated Hypoxia

Background: Myocardial infarction (MI) is exacerbated by endoplasmic reticulum (ER) stress, which contributes to apoptosis signaling and tissue death in cardiomyocytes. Although the calcium-handing protein calreticulin is upregulated during MI, the role of calreticulin in the progression of ER stress remains controversial. We hypothesized that calreticulin expression accelerates ER stress via regulation of the acetylation status of ER proteins, and knockdown reduces pro-apoptotic ER stress. Methods: We examined the expression of calreticulin in human cardiac cells in response to ischemia or thapsigargin-mediated ER stress. To test the effect of calreticulin modulation on cell mortality, we generated a stable partial calreticulin knockdown line in proliferating human cardiomyocyte-derived cells. We further examined the induction and acetylation of ER stress signaling proteins, including proteins in each of the three major pathways that account for ER-stress mediated cell death. Results and Conclusions: Calreticulin is upregulated in human ischemic heart failure cardiac tissue, as well as simulated hypoxia and reoxygenation and thapsigargin-mediated ER stress. It was found that partial knockdown protects against the expression of caspase 12, CHOP, and reduces thapsigargin-driven TUNEL staining. In addition, significant changes in the acetylation of ER stress proteins and the expression of the deacetylase SIRT1 were observed. These data shed light on the role that calreticulin plays in apoptosis signaling during ER stress in cardiac cells.

Exogenously Applied Spermidine Alleviates Hypoxia Stress in Phyllostachys Praecox Seedlings Via Changes in Endogenous Hormones and Gene Expression

2021 ◽  
Author(s):  
JS Gao ◽  
Shunyao Zhuang ◽  
YH Zhang ◽  
ZZ Qian
Keyword(s):  
Lipid Peroxidation ◽  
Higher Plants ◽  
Cell Damage ◽  
Acc Oxidase ◽  
Membrane Lipid ◽  
Hypoxia Stress ◽  
Adenosylmethionine Decarboxylase ◽  
Aba Content ◽  
Phyllostachys Praecox ◽  
Simulated Hypoxia

Abstract PurposeHypoxia stress is thought to be one of the major abiotic stresses that inhibits the growth and development of higher plants. Phyllostachys pracecox is sensitive to oxygen and suffers soil hypoxia during cultivation; however, the corresponding measures to mitigate this stress are still limited in practice. In this study, a simulated hypoxia stress with flooding was conducted to investigate the regulatory effect of Spermidine (Spd) on P. praecox seedlings. MethodsIndicators including growth, membrane lipid peroxidation, S-adenosylmethionine decarboxylase (SAMDC), ACC oxidase (ACO) and ACC synthetase (ACS) activities, indole-3-acetic acid (IAA) and abscisic acid (ABA) content, and expression of hormone-related genes in P. praecox were measured. ResultsApplication of 1 mM and 2 mM Spd could alleviate plant growth inhibition and reduce oxidative damage from hypoxia stress. Exogenous Spd significantly (P<0.05) increased SAMDC activity, enhanced ABA and IAA content, and reduced ACO and ACS activities to protect membranes from lipid peroxidation. Moreover, exogenous Spd up-regulated the expression of auxin-related genes auxin responsive factor1 (ARF1), auxin1 protein (AUX1), auxin2 protein (AUX2), auxin3 protein (AUX3) and auxin4 protein (AUX4), and down-regulated the expression of ethylene-related ACO and ACS genes during flooding. ConclusionThe results indicated that exogenous Spd altered hormone concentrations and the expression of hormone-related genes, thereby protecting the bamboo growth. Our data suggest that Spd can be used to reduce hypoxia-induced cell damage and improve the adaptability of P. praecox to flooding stress.

scholarly journals Intermittent simulated hypoxia for pre-acclimatization

2009 ◽  
Vol 14 (3) ◽  
pp. 185-186 ◽  
Author(s):  
Markus Tannheimer
Keyword(s):  
Simulated Hypoxia

The Potential Role of Galectin-1 in Hypoxia Induced AML Cell Differentiation through C/EBPαa Transcription Regulation.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 3120-3120
Author(s):  
Meng Zhao ◽  
Xu-Yun Zhao ◽  
Shi-Hua Liao ◽  
Ke-Wen Zhao ◽  
Li-Shun Wang ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Conflicts Of Interest ◽  
Hypoxia Inducible Factor ◽  
Luciferase Assay ◽  
Hypoxia Inducible Factor 1 ◽  
Morphological Criteria ◽  
Interfering Rna ◽  
Simulated Hypoxia ◽  
Mild Hypoxia

Abstract Abstract 3120 Poster Board III-57 Recently we reported that cobalt chloride-simulated hypoxia and mild hypoxia could induce the differentiation of human acute myeloid leukemic (AML) cells probably through hypoxia inducible factor-1 alpha (HIF-1αa) independent of its transcription activity. In this study, we used differential gel electrophoresis to compare the HIF-1αa regulated proteins between conditional induction and absence of HIF-1αa protein in U937T cells. Among all the up-regulated proteins indentified, the mRNA and protein level of galectin-1 was most remarkably changed. Knockdown of galectin-1 partially blocked the differentiation induced by HIF-1αa overexpression in U937T cells as assessed by morphological criteria and differentiation associated-antigens. Notably, reduced expression of C/EBPαa, a critical transcription factor for granulocyte differentiation, could inhibit the up-regulation of galectin-1 induced by HIF-1αa, and inducible expression of C/EBPαa in U937T cells also increased galectin-1 expression. Furthermore, by using the luciferase assay and chromatin immunoprecipitation we localized the binding site of C/EBPαa in the promoter of galectin-1. Finally the role of galectin-1 during chloride-simulated hypoxia and mild hypoxia was addressed by decreasing the expression of galectin-1 with small interfering RNA. Taken together, these results conclude that galectin-1 is required for hypoxia triggered C/EBPαa dependent AML cell differentiation. Disclosures No relevant conflicts of interest to declare.

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