scholarly journals Role of Capsaicin in the Repair of Cellular Activity in Mice Liver

2021 ◽  
Vol 13 (6s) ◽  
pp. 1573-1576
Author(s):  
Mohammad Sukmanadi ◽  
Mustofa Helmi Effendi ◽  
Faisal Fikri ◽  
Muhammad Thohawi El Purnama
Keyword(s):  
Cellular Activity ◽  
Mice Liver

The role of the physicochemical environment in determining disc cell behaviour

2002 ◽  
Vol 30 (6) ◽  
pp. 858-863 ◽  
Author(s):  
J. P. G. Urban
Keyword(s):  
Extracellular Matrix ◽  
Ionic Composition ◽  
Cell Types ◽  
Mechanical Forces ◽  
Dense Matrix ◽  
Cellular Activity ◽  
High Concentration ◽  
Cell Behaviour ◽  
Disc Cells

The cells of the intervertebral disc exist in an unusual environment. They are embedded in a dense matrix containing a high concentration of aggrecan whose fixed negative charges regulate the extracellular ionic composition and osmolarity; both extracellular cation concentrations and osmolarity are considerably higher than those experienced by most cell types. The disc also is avascular. Oxygen levels in the centre of the nucleus, where cells may be 6–8 mm from the blood supply, are very low. Since metabolism is mainly by glycolysis, lactic acid is produced at high rates and hence the pH is acidic. Finally, the disc is subjected to mechanical forces at all times; these vary with posture and activity. In particular, because the disc is under low loads during rest and high loads during the day's activities, it loses and regains around 25% of its fluid over a diurnal cycle with consequent changes to the concentrations of extracellular matrix macromolecules and ions and hence extracellular osmolality. Here we will briefly review these factors and discuss the influence of changes in the physicochemical environment on cellular activity, in particular on the rate at which disc cells synthesize and degrade matrix macro-molecules.

scholarly journals C57BL/6 and A/J Mice Have Different Inflammatory Response and Liver Lipid Profile in Experimental Alcoholic Liver Disease

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Lorena Bavia ◽  
Íris Arantes de Castro ◽  
Lourdes Isaac
Keyword(s):  
Liver Disease ◽  
Alcoholic Liver Disease ◽  
Genetic Background ◽  
Inflammatory Responses ◽  
Liver Lipid ◽  
Liver Steatosis ◽  
Public Health Issue ◽  
Mouse Strains ◽  
Mice Liver

Alcoholic liver disease (ALD) is an important worldwide public health issue characterized by liver steatosis, inflammation, necrosis, and apoptosis of hepatocytes with eventual development of fibrosis and cirrhosis. Comparison of murine models with different inflammatory responses for ALD is important for an evaluation of the importance of genetic background in the interpretation of ethanol-induced phenotypes. Here, we investigated the role of inflammation and genetic background for the establishment of ALD using two different mouse strains: C57BL/6 (B6) and A/J. B6 and A/J mice were treated with a high fat diet containing ethanol (HFDE) and compared to the controls for 10 weeks. Hepatomegaly and steatohepatitis were similar in B6 and A/J mice, but only A/J mice were resistant to weight gain. On the other hand, HFDE-fed B6 accumulated more triglycerides (TG) and cholesterol and presented more intense cellular infiltrate in the liver when compared to HFDM-fed mice. Liver inflammatory environment was distinct in these two mouse strains. While HFDE-fed B6 produced more liver IL-12, A/J mice increased the TNF-αproduction. We concluded that mouse genetic background could dictate the intensity of the HFDE-induced liver injury.

scholarly journals Effects of Chromeceptin on Insulin-like Growth Factor II in Human Osteoblastic and Osteosarcoma Cells

2018 ◽  
Vol 4 (1) ◽  
pp. 59-67
Author(s):  
Rosemary Dziak ◽  
Dalia Nourah ◽  
That AlHousami ◽  
Dinh Nguyen
Keyword(s):  
Growth Factor ◽  
Regulatory System ◽  
Cellular Systems ◽  
Insulin Like Growth Factor ◽  
Cellular Activity ◽  
Osteosarcoma Cells ◽  
Skeletal Tissue ◽  
Surface Receptors ◽  
Insulin Growth Factor

The insulin-like growth factor system is a complex regulatory system of insulin-like growth factors I and II (IGF-I and IGF-II) as well as their cell surface receptors and a family of insulin growth factor binding proteins (IGF-BPs). Despite extensive research on the IGF system in skeletal tissue, there is still not a complete understanding particularly of the role of IGF-II in the regulation of normal and pathological osseous cells in human skeletal biology. The purpose of this study was to further delineate the possible involvement of IGF-II in the regulation of human normal calvarial osteoblasts and G292 human osteosarcoma cellular activity using exogenously added IGF-II as well as a drug, Chromeceptin that has been shown in some other cellular systems to down regulate endogenous IGF-II levels.The results presented here show a similar dose dependent effect of Chromeceptin on inhibition of endogenous IGF-II levels (measured with an immunoassay) and cellular activity (measured with the MTT assay) in both the normal and osteosarcoma cells while small significant increases in activity with exogenously added IGF-II were observed only in the osteosarcoma cells. Moreover, IGF-BP1 levels (measured with an immunoassay) were shown to significantly increase in the G292 cells in a similar manner previously reported in other cell systems with only minor non-significant effects of exogenously added IGF-BP1 in the osteosarcoma cells studied here. These studies suggest that endogenous IGF-II is a critical regulator of activity in both normal and osteosarcoma cells and Chromeceptin can be an effective pharmacological agent for further studies on the role of the growth factor in human skeletal systems.

scholarly journals Malaria parasite CelTOS targets the inner leaflet of cell membranes for pore-dependent disruption

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
John R Jimah ◽  
Nichole D Salinas ◽  
Monica Sala-Rabanal ◽  
Nathaniel G Jones ◽  
L David Sibley ◽  
...  
Keyword(s):  
Phosphatidic Acid ◽  
Malaria Parasite ◽  
Plasma Membranes ◽  
Sequence Similarity ◽  
Membrane Damage ◽  
Mammalian Host ◽  
Cellular Activity ◽  
Apicomplexan Parasites ◽  
Insight Into

Apicomplexan parasites contain a conserved protein CelTOS that, in malaria parasites, is essential for traversal of cells within the mammalian host and arthropod vector. However, the molecular role of CelTOS is unknown because it lacks sequence similarity to proteins of known function. Here, we determined the crystal structure of CelTOS and discovered CelTOS resembles proteins that bind to and disrupt membranes. In contrast to known membrane disruptors, CelTOS has a distinct architecture, specifically binds phosphatidic acid commonly present within the inner leaflet of plasma membranes, and potently disrupts liposomes composed of phosphatidic acid by forming pores. Microinjection of CelTOS into cells resulted in observable membrane damage. Therefore, CelTOS is unique as it achieves nearly universal inner leaflet cellular activity to enable the exit of parasites from cells during traversal. By providing novel molecular insight into cell traversal by apicomplexan parasites, our work facilitates the design of therapeutics against global pathogens.

scholarly journals Cardioprotective Role of SIRT5 in Response to Acute Ischemia Through a Novel Liver-Cardiac Crosstalk Mechanism

2021 ◽  
Vol 9 ◽  
Author(s):  
Boda Zhou ◽  
Min Xiao ◽  
Hao Hu ◽  
Xiaoxia Pei ◽  
Yajun Xue ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Fibrosis ◽  
Posttranslational Modifications ◽  
Tricarboxylic Acid Cycle ◽  
Liver Mitochondria ◽  
Experimental Myocardial Infarction ◽  
Fibroblast Growth Factor 21 ◽  
Acute Ischemia ◽  
Mice Liver

Protein posttranslational modifications play important roles in cardiovascular diseases. The authors’ previous report showed that the abundance of succinylated and glutarylated proteins was significantly lower in the serum of patients with acute myocardial infarction (AMI) than in that of healthy volunteers, suggesting a potential relationship between protein acylation and AMI. Sirtuin 5 (SIRT5) facilitates the removal of malonyl, succinyl, and glutaryl modification; however, its effects on AMI remain unknown. In this study, the levels of SIRT5 in AMI mouse model was compared. Results showed elevated hepatic SIRT5 after myocardial infarction. Hepatocyte-specific SIRT5 overexpressing mice (liver SIRT5 OE) were generated to address the possible involvement of hepatic SIRT5 in AMI. The areas of myocardial infarction, myocardial fibrosis, and cardiac function in a model of experimental myocardial infarction were compared between liver SIRT5 OE mice and wild-type (WT) mice. The liver SIRT5 OE mice showed a significantly smaller area of myocardial infarction and myocardial fibrosis than the WT mice. The fibroblast growth factor 21 (FGF21) in the blood and myocardium of liver SIRT5 OE mice after AMI was markedly elevated compared with that in WT mice. The results of mass spectrometry showed increased levels of proteins regulating tricarboxylic acid cycle, oxidative phosphorylation, and fatty acid β-oxidation pathways in the liver mitochondria of liver SIRT5 OE mice. These findings showed that SIRT5 may exhibit a cardioprotective effect in response to acute ischemia through a liver-cardiac crosstalk mechanism, probably by increasing the secretion of FGF21 and the improvement of energy metabolism.

scholarly journals Continued dysregulation of the B cell lineage promotes multiple sclerosis activity despite disease modifying therapies

F1000Research ◽  
2021 ◽  
Vol 10 ◽  
pp. 1305
Author(s):  
Ana C. Londoño ◽  
Carlos A. Mora
Keyword(s):  
Multiple Sclerosis ◽  
B Cells ◽  
B Cell ◽  
Cell Lineage ◽  
Clear Understanding ◽  
Cellular Activity ◽  
Regulatory B Cells ◽  
Disease Modifying Therapies

A clear understanding of the origin and role of the different subtypes of the B cell lineage involved in the activity or remission of multiple sclerosis (MS) is important for the treatment and follow-up of patients living with this disease. B cells, however, are dynamic and can play an anti-inflammatory or pro-inflammatory role, depending on their milieu. Depletion of B cells has been effective in controlling the progression of MS, but it can have adverse side effects. A better understanding of the role of the B cell subtypes, through the use of surface biomarkers of cellular activity with special attention to the function of memory and regulatory B cells (Bregs), will be necessary in order to offer specific treatments without inducing undesirable effects.

scholarly journals Upregulation of miR-34a by Inhibition of IRE1α Has Protective Effect against Aβ-Induced Injury in SH-SY5Y Cells by Targeting Caspase-2

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Qianqian Li ◽  
Tingjiao Liu ◽  
Shanshan Yang ◽  
Zhongling Zhang
Keyword(s):  
Protective Effects ◽  
Cellular Activity ◽  
Activity Assay ◽  
Quantitative Real Time Pcr ◽  
Rt Pcr ◽  
Human Neuroblastoma ◽  
Expression Levels ◽  
Xbp1 Mrna ◽  
Caspase 2

Background. Neurotoxicity induced by the amyloid-β (Aβ) peptide is one of the most important pathological mechanisms of Alzheimer’s disease (AD). Based on accumulating evidence in AD research, both endoplasmic reticulum stress (ER stress) and alterations in the microRNA (miRNA) network contribute to the pathogenesis of the disease, making them potential therapeutic targets for AD. The present study was performed to investigate whether miR-34a and the inositol-requiring enzyme 1 (IRE1) are involved in the regulation of Aβ-induced cytotoxicity. Methods. Human neuroblastoma SH-SY5Y cells were treated with Aβ1-40. Cell viability was assessed by the MTT assay. The integrity of the plasma membrane was assessed by LDH release. The expression levels of XBP1s, IRE1α, p-IRE1α, and Caspase-2 were detected by Western blot analysis. Spliced-XBP1 mRNA and miR-34a were detected by reverse transcription- (RT-) PCR and quantitative real-time PCR, respectively. Caspase-2 activity was measured using the Caspase-2 cellular activity assay kit. The IRE1 inhibitor (STF-083010) was used to determine the role of IRE1α on miR-34a expression. SH-SY5Y cells were transfected with miR-34a mimics to assess the role of miR-34a on the activation of Caspase-2 and the viability of Aβ-exposed SH-SY5Y cells. Results. We showed that Aβ caused concentration- and duration-dependent death of SH-SY5Y cells. The expression levels of XBP1s, p-IRE1α, and Caspase-2 were increased, along with a corresponding decrease in the miR-34a levels in Aβ-exposed SH-SY5Y cells. The IRE1 inhibitor (STF-083010) upregulated the expression of miR-34a and suppressed the activation of Caspase-2, effectively alleviating the Aβ-induced death of SH-SY5Y cells. Transfection studies show that miR-34a mimics inhibit the expression of Caspase-2 and restore the viability of Aβ-exposed SH-SY5Y cells. Conclusion. Aβ peptide induced downregulation of miR-34a through the activation of IRE1α, which may induce cytotoxicity by targeting Caspase-2. Upregulation of miR-34a by inhibition of IRE1α has protective effects against Aβ-induced injury in SH-SY5Y cells.

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