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15 results on '"Chandel, N.S."'

8. Mitochondrial reactive oxygen species trigger hypoxia-induced transcription

Author

Chandel, N.S., Maltepe, E., Goldwasser, E., Mathieu, C.E., Simon, M.C., and Schumacker, P.T.

Subjects
Hypoxia -- Research, Genetic transcription -- Research, Mitochondria -- Research, Oxygen -- Research, Science and technology
Abstract

Transcriptional activation of erythropoietin, glycolytic enzymes, and vascular endothelial growth factor occurs during hypoxia or in response to cobalt chloride (Co[Cl.sub.2]) in Hep3B cells. However, neither the mechanism of cellular [O.sub.2] sensing nor that of cobalt is fully understood. We tested whether mitochondria act as [O.sub.2] sensors during hypoxia and whether hypoxia and cobalt activate transcription by increasing generation of reactive oxygen species (ROS). Results show (i) wild-type Hep3B cells increase ROS generation during hypoxia (1.5% [O.sub.2]) or Co[Cl.sub.2] incubation, (ii) Hep3B cells depleted of mitochondrial DNA ([[Rho].sup.0] cells) fail to respire, fail to activate mRNA for erythropoietin, glycolytic enzymes, or vascular endothelial growth factor during hypoxia, and fail to increase ROS generation during hypoxia; (iii) [[Rho].sup.0] cells increase ROS generation in response to Co[Cl.sub.2] and retain the ability to induce expression of these genes; and (iv) the antioxidants pyrrolidine dithiocarbamate and ebselen abolish transcriptional activation of these genes during hypoxia or Co[Cl.sub.2] in wild-type cells, and abolish the response to Co[Cl.sub.2] in [[Rho].sup.[convolution]] cells. Thus, hypoxia activates transcription via a mitochondria-dependent signaling process involving increased ROS, whereas CO[C.sub.12] activates transcription by stimulating ROS generation via a mitochondria-independent mechanism.

Published
1998

10. A Multi-Omics Survey of the Age-Related Susceptibility to Influenza

Author

Stoeger, T., primary, Grant, R.A., additional, Reyfman, P.A., additional, Loguercio, S., additional, Hutt, D.M., additional, Amaral, L.A.N., additional, Sznajder, J.I., additional, Chandel, N.S., additional, Balch, W.E., additional, Morimoto, R., additional, Misharin, A., additional, and Budinger, G.S., additional

Published
2019
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12. Role of MRI in delineation of internal derangement of knee in trauma patients

Author

Gupta R, Chandel N.S, and Vyas Mm

Subjects
musculoskeletal diseases, medicine.medical_specialty, business.industry, Joint effusion, Knee Joint, medicine.disease, ACL injury, Mr imaging, Conventional radiography, Derangement, Soft tissue contrast, Medicine, Radiology, medicine.symptom, business, Pathological
Abstract

Introduction: Knee joint is one of the most commonly injured joints, as an isolated injury or a frequent component in a multiple trauma patient. Knee joint injury is a significant cause of morbidity in young and active individuals especially amongst sports person, laborers, soldiers and military recruits. Multiple imaging modalities are currently being used to evaluate various pathological conditions of the knee including conventional radiography, CT scan, sonography , nuclear medicine and MR Imaging. Multi planar imaging and excellent soft tissue contrast has made the MRI an ideal modality for imaging of complex anatomy of knee joint in trauma patient. Objective: To study the diagnostic accuracy & efficacy of MRI in evaluation of internal derangement of knee joint in trauma patient. Material & Method: 44 cases with history of trauma were evaluated by Siemens magnetom vision plus 1.5 tesla MRI machine. Results: Mean age of patient - 32.2 years. Count of male patients exceeded the count of female patients. ACL injury was observed in 81.8%, PCL injury in 6.8%, MCl in 11.3%, LCL in 2.3%, medial meniscal tear in 45.5%, joint effusion in 95%. Conclusion: MRI emerged as a front line investigation for the assessment of internal derangement of knee joint in trauma patient.

Published
2015
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13. TCA Cycle and Mitochondrial Membrane Potential Are Necessary for Diverse Biological Functions

Author

Martínez-Reyes, I., Diebold, L.P., Kong, H., Schieber, M., Huang, H., Hensley, C.T., Mehta, M.M., Wang, T., Santos, J.H., Woychik, R., Dufour, E., Spelbrink, J.N., Weinberg, S.E., Zhao, Y., DeBerardinis, R.J., Chandel, N.S., Martínez-Reyes, I., Diebold, L.P., Kong, H., Schieber, M., Huang, H., Hensley, C.T., Mehta, M.M., Wang, T., Santos, J.H., Woychik, R., Dufour, E., Spelbrink, J.N., Weinberg, S.E., Zhao, Y., DeBerardinis, R.J., and Chandel, N.S.

Abstract

Item does not contain fulltext

Published
2016

15. Cells depleted of mitochondrial DNA (@r^0) yield insight into physiological mechanisms

Author

Chandel, N.S. and Schumacker, P.T.

Abstract

A resurgence of interest in mitochondrial physiology has recently developed as a result of new experimental data demonstrating that mitochondria function as important participants in a diverse collection of novel intracellular signaling pathways. Cells depleted of mitochondrial DNA, or @r^0 cells, lack critical respiratory chain catalytic subunits that are encoded in the mitochondrial genome. Although @r^0 cells contain petit mitochondria, they cannot support normal oxidative phosphorylation and must survive and replicate using ATP derived solely from glycolysis. Without a functional electron transport chain, @r^0 cells cannot normally regulate redox potential and their mitochondria appear to be incapable of generating reactive oxygen species. Emerging evidence suggests that these signals are important components in a number of mitochondria-initiated signaling pathways. The present article focuses on how @r^0 cells have contributed to an understanding of the role that mitochondria play in distinct physiological pathways involved with apoptosis, glucose-induced insulin secretion, and oxygen sensing.

Published
1999
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