• Filter By:
• Specialty
• Source
• Condition
• Cancer
• Infectious Disease
• Drug
• Training
• Management
• Procedure
• Therapy
• Vaccine
• Nutrition
• Country

Survival Motor Neuron (SMN) Protein Insufficiency Exacerbates Renal Ischemia/Reperfusion Injury
The survival of motor neuron (SMN) protein is ubiquitously involved in spliceosome assembly and ribonucleoprotein biogenesis. SMN protein is expressed in kidney and can affect cell death processes. However, the role of SMN in acute kidney injury is largely unknown. In the current study, we found that the expression of SMN in the kidney was significantly reduced in both clinical ischemic acute kidney injury (AKI) and a mouse model of renal ischemia-reperfusion injury (IRI). We then used SMN heterozygous knockout (SMN+/-) mice and found that the declines in renal function, tubular injury, and tubular cell apoptosis after exp...
Source: Frontiers in Physiology - May 13, 2019 Category: Physiology Source Type: research

BNIP3-mediated autophagy induced inflammatory response and inhibited VEGF expression in cultured retinal pigment epithelium cells under hypoxia.
Conclusion: BNIP3-mediated autophagy induced by hypoxia may regulate inflammatory response and VEGF expression, which can affect the cell viability of RPE under hypoxia. PMID: 31072291 [PubMed - as supplied by publisher]
Source: Current Molecular Medicine - May 7, 2019 Category: Molecular Biology Authors: Chen Y, Yan Q, Xu Y, Ye F, Sun X, Zhu H, Wang H Tags: Curr Mol Med Source Type: research

TonEBP Suppresses the HO-1 Gene by Blocking Recruitment of Nrf2 to Its Promoter
Discussion Dynamic changes in the functional phenotype of macrophages are associated with pathogenesis of inflammatory diseases (5–7). TonEBP primes macrophages toward an M1 phenotype, which has pro-inflammatory properties. TonEBP does this by promoting expression of pro-inflammatory genes via interaction with NF-κB (36) and by binding directly to the promoter (37, 64). In addition, TonEBP suppresses expression of the anti-inflammatory cytokine IL-10 by limiting chromatin access to the promoter (37). The pro-inflammatory function of TonEBP suggests that inhibiting its expression or activation could suppres...
Source: Frontiers in Immunology - April 17, 2019 Category: Allergy & Immunology Source Type: research

Periprosthetic hypoxia as consequence of TRPM7 mediated cobalt influx in osteoblasts
This study shows that chemical hypoxia originating from HIF‐1α upregulation within the periprosthetic tissue is related to cobalt wear debris and highlights TRPM7 as an important key mediator in this context. © 2018 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 00B: 0 00–000, 2018.
Source: Journal of Biomedical Materials Research Part B: Applied Biomaterials - December 3, 2018 Category: Materials Science Authors: Constantin R ömmelt, Thomas Munsch, Andreas Drynda, Volkmar Lessmann, Christoph H. Lohmann, Jessica Bertrand Tags: Original Research Reports Source Type: research

The long non-coding RNA MALAT1 is increased in renal ischemia-reperfusion injury and inhibits hypoxia-induced inflammation.
CONCLUSION: The expression of MALAT1 is increased in renal ischemia-reperfusion injury. It is likely that MALAT1 inhibits the hypoxia-induced inflammatory response through the NF-κB pathway. PMID: 30277425 [PubMed - in process]
Source: Renal Failure - October 3, 2018 Category: Urology & Nephrology Tags: Ren Fail Source Type: research

Interleukin 17 under hypoxia mimetic condition augments osteoclast mediated bone erosion and expression of HIF-1 α and MMP-9.
In conclusion, IL-17 synergizes with CoCl2 induced hypoxic condition to augment osteoclast mediated bone erosion and synovial macrophages mediated RA pathogenesis. PMID: 30029761 [PubMed - as supplied by publisher]
Source: Cellular Immunology - July 17, 2018 Category: Allergy & Immunology Authors: Samarpita S, Doss HM, Ganesan R, Rasool M Tags: Cell Immunol Source Type: research

Notch signaling molecule is involved in the invasion of MiaPaCa2 cells induced by CoCl2 via regulating epithelial ‑mesenchymal transition.
Notch signaling molecule is involved in the invasion of MiaPaCa2 cells induced by CoCl2 via regulating epithelial‑mesenchymal transition. Mol Med Rep. 2018 Jan 26;: Authors: Chen DW, Wang H, Bao YF, Xie K Abstract Pancreatic cancer exhibits a high mortality rate resulting from metastasis and there is currently no effective treatment strategy. Hypoxia serves an important role in cancer cells, where cellular metabolic rate is high. The underlying mechanisms that trigger hypoxia and the invasion of pancreatic cancer cells remain unknown. Investigation of the importance of hypoxia in the invasion of panc...
Source: Molecular Medicine Reports - February 4, 2018 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

Silencing the autophagy-specific gene Beclin-1 contributes to attenuated hypoxia-induced vasculogenic mimicry formation in glioma.
CONCLUSION: Silencing Beclin-1 can attenuate hypoxia-induced VM formation and the metastatic ability of U87MG cells and is a potential target for VM inhibition in glioma. PMID: 29278874 [PubMed - as supplied by publisher]
Source: Cancer Biomarkers : Section A of Disease Markers - December 15, 2017 Category: Cancer & Oncology Authors: Duan S Tags: Cancer Biomark Source Type: research

Astaxanthin mitigates cobalt cytotoxicity in the MG-63 cells by modulating the oxidative stress.
CONCLUSIONS: ASX mitigated cobalt cytotoxicity in the MG-63 cells by modulating the oxidative stress. And ASX could be a promising therapy against cobalt toxicity in the hip articulation surgery. PMID: 28738843 [PubMed - in process]
Source: BMC Pharmacology and Toxicology - July 27, 2017 Category: Drugs & Pharmacology Tags: BMC Pharmacol Toxicol Source Type: research

Cobalt Chloride Attenuates Oxidative Stress and Inflammation through NF-κB Inhibition in Human Renal Proximal Tubular Epithelial Cells.
Abstract We evaluated the effect of cobalt chloride (CoCl2) on TNF-α and IFN-γ-induced-inflammation and reactive oxygen species (ROS) in renal tubular epithelial cells (HK-2 cells). We treated HK-2 cells with CoCl2 before the administration of TNF-α/IFN-γ. To regulate hemeoxygenase-1 (HO-1) expression, the cells were treated CoCl2 or HO-1 siRNA. CoCl2 reduced the generation of ROS induced by TNF-α/IFN-γ. TNF-α/IFN-γ-treated-cells showed an increase in the nuclear translocation of phosphorylated NF-κBp65 protein, the DNA-binding activity of NF-κBp50 and NF-κB transcriptional activity and a decrease in I�...
Source: J Korean Med Sci - September 1, 2014 Category: Journals (General) Authors: Oh SW, Lee YM, Kim S, Chin HJ, Chae DW, Na KY Tags: J Korean Med Sci Source Type: research

Pages: 1  2