scholarly journals Cross-Talk Between Nitrosative Stress, Inflammation and Hypoxia-Inducible Factor in Patients with Adrenal Masses

2021 ◽  
Vol Volume 14 ◽  
pp. 6317-6330
Author(s):  
Barbara Choromańska ◽  
Piotr Myśliwiec ◽  
Tomasz Kozłowski ◽  
Magdalena Łuba ◽  
Piotr Wojskowicz ◽  
...  
Keyword(s):  
Cross Talk ◽  
Nitrosative Stress ◽  
Hypoxia Inducible Factor ◽  
Adrenal Masses

scholarly journals Hypoxia-Inducible Factor 1 Regulation through Cross Talk between mTOR and MT1-MMP

2013 ◽  
Vol 34 (1) ◽  
pp. 30-42 ◽  
Author(s):  
T. Sakamoto ◽  
J. S. Weng ◽  
T. Hara ◽  
S. Yoshino ◽  
H. Kozuka-Hata ◽  
...  
Keyword(s):  
Cross Talk ◽  
Hypoxia Inducible Factor ◽  
Hypoxia Inducible Factor 1

scholarly journals Tip110 Regulates the Cross Talk between p53 and Hypoxia-Inducible Factor 1α under Hypoxia and Promotes Survival of Cancer Cells

2015 ◽  
Vol 35 (13) ◽  
pp. 2254-2264 ◽  
Author(s):  
Khalid Amine Timani ◽  
Ying Liu ◽  
Yan Fan ◽  
Khalid S. Mohammad ◽  
Johnny J. He
Keyword(s):  
Cross Talk ◽  
Hypoxia Inducible Factor ◽  
Ubiquitin Proteasome System ◽  
Metastatic Progression ◽  
Hypoxia Inducible Factor 1Α ◽  
Important Mediator ◽  
P300 Binding ◽  
Ubiquitin Proteasome ◽  
The Cross ◽  
Hypoxic Region

Hypoxia often occurs under various physiological and pathophysiological conditions, including solid tumors; it is linked to malignant transformation, metastatic progression, and treatment failure or resistance. Tip110 protein plays important roles in several known physiological and pathophysiological processes, including cancers. Thus, in the present study we investigated the regulation of Tip110 expression under hypoxia. Hypoxia led to Tip110 protein degradation through the ubiquitin-proteasome system. Under hypoxia, Tip110 stabilized p53, which in return destabilized Tip110. In addition, Tip110 regulated hypoxia-inducible factor 1α (HIF-1α), likely through enhancement of its protein stability. Furthermore, Tip110 upregulated p300, a known coactivator for both p53 and HIF-1α. Expression of a p53(22/23) mutant deficient in p300 binding accelerated Tip110 degradation under hypoxia. Tip110 knockdown resulted in the inhibition of cell proliferation and cell death in the presence of p53. Finally, significantly less Tip110, p53, and HIF-1α was detected in the hypoxic region of bone metastasis tumors in a mouse model of human melanoma cells. Taken together, these results suggest Tip110 is an important mediator in the cross talk between p53 and HIF-1α in response to hypoxic stress.

Cross-talk between the Ras GTPase and the Hog1 survival pathways in response to nitrosative stress in Paracoccidioides brasiliensis

Nitric Oxide ◽  
2019 ◽  
Vol 86 ◽  
pp. 1-11 ◽  
Author(s):  
Palloma Mendes Conceição ◽  
Alison Felipe Alencar Chaves ◽  
Marina Valente Navarro ◽  
Daniele Gonçalves Castilho ◽  
Juliana Cristina P. Calado ◽  
...  
Keyword(s):  
Cross Talk ◽  
Nitrosative Stress ◽  
Paracoccidioides Brasiliensis ◽  
Ras Gtpase ◽  
Survival Pathways

scholarly journals Cross-Talk between Mitochondrial Dysfunction-Provoked Oxidative Stress and Aberrant Noncoding RNA Expression in the Pathogenesis and Pathophysiology of SLE

2019 ◽  
Vol 20 (20) ◽  
pp. 5183 ◽  
Author(s):  
Chang-Youh Tsai ◽  
Song-Chou Hsieh ◽  
Cheng-Shiun Lu ◽  
Tsai-Hung Wu ◽  
Hsien-Tzung Liao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Cross Talk ◽  
Noncoding Rna ◽  
Nitrosative Stress ◽  
Noncoding Rnas ◽  
The Body ◽  
Rna Expression ◽  
Epigenetic Regulations ◽  
The Cross

Systemic lupus erythematosus (SLE) is a prototype of systemic autoimmune disease involving almost every organ. Polygenic predisposition and complicated epigenetic regulations are the upstream factors to elicit its development. Mitochondrial dysfunction-provoked oxidative stress may also play a crucial role in it. Classical epigenetic regulations of gene expression may include DNA methylation/acetylation and histone modification. Recent investigations have revealed that intracellular and extracellular (exosomal) noncoding RNAs (ncRNAs), including microRNAs (miRs), and long noncoding RNAs (lncRNAs), are the key molecules for post-transcriptional regulation of messenger (m)RNA expression. Oxidative and nitrosative stresses originating from mitochondrial dysfunctions could become the pathological biosignatures for increased cell apoptosis/necrosis, nonhyperglycemic metabolic syndrome, multiple neoantigen formation, and immune dysregulation in patients with SLE. Recently, many authors noted that the cross-talk between oxidative stress and ncRNAs can trigger and perpetuate autoimmune reactions in patients with SLE. Intracellular interactions between miR and lncRNAs as well as extracellular exosomal ncRNA communication to and fro between remote cells/tissues via plasma or other body fluids also occur in the body. The urinary exosomal ncRNAs can now represent biosignatures for lupus nephritis. Herein, we’ll briefly review and discuss the cross-talk between excessive oxidative/nitrosative stress induced by mitochondrial dysfunction in tissues/cells and ncRNAs, as well as the prospect of antioxidant therapy in patients with SLE.

scholarly journals Nitric Oxide-Dependent Pathways as Critical Factors in the Consequences and Recovery after Brain Ischemic Hypoxia

Biomolecules ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 1097
Author(s):  
Joanna M Wierońska ◽  
Paulina Cieślik ◽  
Leszek Kalinowski
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Nitrosative Stress ◽  
Neuronal Damage ◽  
Hypoxia Inducible Factor ◽  
Inflammatory Cells ◽  
Reactive Astrocytes ◽  
Ischemic Hypoxia ◽  
Inflammatory Proteins ◽  
Brain Tissue Damage

Brain ischemia is one of the leading causes of disability and mortality worldwide. Nitric oxide (NO•), a molecule that is involved in the regulation of proper blood flow, vasodilation, neuronal and glial activity constitutes the crucial factor that contributes to the development of pathological changes after stroke. One of the early consequences of a sudden interruption in the cerebral blood flow is the massive production of reactive oxygen and nitrogen species (ROS/RNS) in neurons due to NO• synthase uncoupling, which leads to neurotoxicity. Progression of apoptotic or necrotic neuronal damage activates reactive astrocytes and attracts microglia or lymphocytes to migrate to place of inflammation. Those inflammatory cells start to produce large amounts of inflammatory proteins, including pathological, inducible form of NOS (iNOS), which generates nitrosative stress that further contributes to brain tissue damage, forming vicious circle of detrimental processes in the late stage of ischemia. S-nitrosylation, hypoxia-inducible factor 1α (HIF-1α) and HIF-1α-dependent genes activated in reactive astrocytes play essential roles in this process. The review summarizes the roles of NO•-dependent pathways in the early and late aftermath of stroke and treatments based on the stimulation or inhibition of particular NO• synthases and the stabilization of HIF-1α activity.

scholarly journals Glucocorticoid-Dependent Mechanisms of Brain Tolerance to Hypoxia

2021 ◽  
Vol 22 (15) ◽  
pp. 7982
Author(s):  
Elena Rybnikova ◽  
Natalia Nalivaeva
Keyword(s):  
Cross Talk ◽  
Glucocorticoid Receptors ◽  
Molecular Mechanisms ◽  
Hypoxia Inducible Factor ◽  
Later Life ◽  
Adaptation To Hypoxia ◽  
Hypoxic Injury ◽  
Hypoxic Tolerance ◽  
Resistance To Stress ◽  
The Brain

Adaptation of organisms to stressors is coordinated by the hypothalamic-pituitary-adrenal axis (HPA), which involves glucocorticoids (GCs) and glucocorticoid receptors (GRs). Although the effects of GCs are well characterized, their impact on brain adaptation to hypoxia/ischemia is still understudied. The brain is not only the most susceptible to hypoxic injury, but also vulnerable to GC-induced damage, which makes studying the mechanisms of brain hypoxic tolerance and resistance to stress-related elevation of GCs of great importance. Cross-talk between the molecular mechanisms activated in neuronal cells by hypoxia and GCs provides a platform for developing the most effective and safe means for prevention and treatment of hypoxia-induced brain damage, including hypoxic pre- and post-conditioning. Taking into account that hypoxia- and GC-induced reprogramming significantly affects the development of organisms during embryogenesis, studies of the effects of prenatal and neonatal hypoxia on health in later life are of particular interest. This mini review discusses the accumulated data on the dynamics of the HPA activation in injurious and non-injurious hypoxia, the role of the brain GRs in these processes, interaction of GCs and hypoxia-inducible factor HIF-1, as well as cross-talk between GC and hypoxic signaling. It also identifies underdeveloped areas and suggests directions for further prospective studies.

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