scholarly journals Peroxiredoxin6 in Endothelial Signaling

Antioxidants ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 63 ◽  
Author(s):  
Priyal Patel ◽  
Shampa Chatterjee
Keyword(s):  
Peroxidase Activity ◽  
Vascular Diseases ◽  
Catalytic Triad ◽  
Cysteine Residue ◽  
Pla2 Activity ◽  
Redox Equilibrium ◽  
Cellular Redox ◽  
Peroxiredoxin 6 ◽  
Injury And Repair

Peroxiredoxins (Prdx) are a ubiquitous family of highly conserved antioxidant enzymes with a cysteine residue that participate in the reduction of peroxides. This family comprises members Prdx1–6, of which Peroxiredoxin 6 (Prdx6) is unique in that it is multifunctional with the ability to neutralize peroxides (peroxidase activity) and to produce reactive oxygen species (ROS) via its phospholipase (PLA2) activity that drives assembly of NADPH oxidase (NOX2). From the crystal structure, a C47 residue is responsible for peroxidase activity while a catalytic triad (S32, H26, and D140) has been identified as the active site for its PLA2 activity. This paradox of being an antioxidant as well as an oxidant generator implies that Prdx6 is a regulator of cellular redox equilibrium (graphical abstract). It also indicates that a fine-tuned regulation of Prdx6 expression and activity is crucial to cellular homeostasis. This is specifically important in the endothelium, where ROS production and signaling are critical players in inflammation, injury, and repair, that collectively signal the onset of vascular diseases. Here we review the role of Prdx6 as a regulator of redox signaling, specifically in the endothelium and in mediating various pathologies.

Role of Emotional Processes in Cardio-vascular Diseases

2012 ◽  
Author(s):  
Suman Balhara ◽  
Nov Rattan Sharma ◽  
Amrita Yadav
Keyword(s):  
Vascular Diseases ◽  
Emotional Processes ◽  
Cardio Vascular

An ESR study of the peroxidase reaction catalyzed by human methaemoglobin and methaemoglobin-haptoglobin complex

1991 ◽  
Vol 56 (4) ◽  
pp. 923-932
Author(s):  
Jana Stejskalová ◽  
Pavel Stopka ◽  
Zdeněk Pavlíček
Keyword(s):  
Hydrogen Peroxide ◽  
Ascorbic Acid ◽  
Amino Acid ◽  
Peroxidase Activity ◽  
Amino Acid Analysis ◽  
Superoxide Radical ◽  
Esr Spectra ◽  
The Other ◽  
Delocalized Electron

The ESR spectra of peroxidase systems of methaemoglobin-ascorbic acid-hydrogen peroxide and methaemoglobin-haptoglobin complex-ascorbic acid-hydrogen peroxide have been measured in the acetate buffer of pH 4.5. For the system with methaemoglobin an asymmetrical signal with g ~ 2 has been observed which is interpreted as the perpendicular region of anisotropic spectrum of superoxide radical. On the other hand, for the system with methaemoglobin-haptoglobin complex the observed signal with g ~ 2 is symmetrical and is interpreted as a signal of delocalized electron. After realization of three repeatedly induced peroxidase processes the ESR signal of the perpendicular part of anisotropic spectrum of superoxide radical is distinctly diminished, whereas the signal of delocalized electron remains practically unchanged. An amino acid analysis of methaemoglobin along with results of the ESR measurements make it possible to derive a hypothesis about the role of haptoglobin in increasing of the peroxidase activity of methaemoglobin.

scholarly journals Thromboses and Hemostasis Disorders Associated with Coronavirus Disease 2019: The Possible Causal Role of Cross-Reactivity and Immunological Imprinting

2021 ◽  
Author(s):  
Darja Kanduc
Keyword(s):  
Immune System ◽  
Severe Acute Respiratory Syndrome ◽  
Natural Infection ◽  
Vascular Diseases ◽  
Cross Reactivity ◽  
Active Immunization ◽  
Thromboembolic Complications ◽  
Human Proteins ◽  
Almost All

AbstractBy examining the issue of the thromboses and hemostasis disorders associated with severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) through the lens of cross-reactivity, it was found that 60 pentapeptides are shared by SARS-CoV-2 spike glycoprotein (gp) and human proteins that— when altered, mutated, deficient or, however, improperly functioning— cause vascular diseases, thromboembolic complications, venous thrombosis, thrombocytopenia, coagulopathies, and bleeding, inter alia. The peptide commonality has a relevant immunological potential as almost all of the shared sequences are present in experimentally validated SARS-CoV-2 spike gp-derived epitopes, thus supporting the possibility of cross-reactions between the viral gp and the thromboses-related human proteins. Moreover, many of the shared peptide sequences are also present in pathogens to which individuals have previously been exposed following natural infection or vaccinal routes, and of which the immune system has stored imprint. Such an immunological memory might rapidly trigger anamnestic secondary cross-reactive responses of extreme affinity and avidity, in this way explaining the thromboembolic adverse events that can associate with SARS-CoV-2 infection or active immunization.

scholarly journals Genome-Wide Expression Patterns of Rhoptry Kinases during the Eimeria tenella Life-Cycle

2021 ◽  
Vol 9 (8) ◽  
pp. 1621
Author(s):  
Adeline Ribeiro E Silva ◽  
Alix Sausset ◽  
Françoise I. Bussière ◽  
Fabrice Laurent ◽  
Sonia Lacroix-Lamandé ◽  
...  
Keyword(s):  
Life Cycle ◽  
Expression Patterns ◽  
Housekeeping Genes ◽  
Catalytic Triad ◽  
Eimeria Tenella ◽  
Apicomplexan Parasites ◽  
Genome Wide ◽  
Infected Cells ◽  
First And Second Generation

Kinome from apicomplexan parasites is composed of eukaryotic protein kinases and Apicomplexa specific kinases, such as rhoptry kinases (ROPK). Ropk is a gene family that is known to play important roles in host–pathogen interaction in Toxoplasma gondii but is still poorly described in Eimeria tenella, the parasite responsible for avian coccidiosis worldwide. In the E. tenella genome, 28 ropk genes are predicted and could be classified as active (n = 7), inactive (incomplete catalytic triad, n = 12), and non-canonical kinases (active kinase with a modified catalytic triad, n = 9). We characterized the ropk gene expression patterns by real-time quantitative RT-PCR, normalized by parasite housekeeping genes, during the E. tenella life-cycle. Analyzed stages were: non-sporulated oocysts, sporulated oocysts, extracellular and intracellular sporozoites, immature and mature schizonts I, first- and second-generation merozoites, and gametes. Transcription of all those predicted ropk was confirmed. The mean intensity of transcription was higher in extracellular stages and 7–9 ropk were specifically transcribed in merozoites in comparison with sporozoites. Transcriptional profiles of intracellular stages were closely related to each other, suggesting a probable common role of ROPKs in hijacking signaling pathways and immune responses in infected cells. These results provide a solid basis for future functional analysis of ROPK from E. tenella.

scholarly journals Differential Expression of Peroxisomal Proteins in Distinct Types of Parotid Gland Tumors

2021 ◽  
Vol 22 (15) ◽  
pp. 7872
Author(s):  
Malin Tordis Meyer ◽  
Christoph Watermann ◽  
Thomas Dreyer ◽  
Steffen Wagner ◽  
Claus Wittekindt ◽  
...  
Keyword(s):  
Redox Balance ◽  
Matrix Proteins ◽  
Parotid Tumor ◽  
Gene Expressions ◽  
Tissue Samples ◽  
Cellular Redox ◽  
Tumor Subtypes ◽  
Parotid Tumors ◽  
Aggressive Tumors

Salivary gland cancers are rare but aggressive tumors that have poor prognosis and lack effective cure. Of those, parotid tumors constitute the majority. Functioning as metabolic machinery contributing to cellular redox balance, peroxisomes have emerged as crucial players in tumorigenesis. Studies on murine and human cells have examined the role of peroxisomes in carcinogenesis with conflicting results. These studies either examined the consequences of altered peroxisomal proliferators or compared their expression in healthy and neoplastic tissues. None, however, examined such differences exclusively in human parotid tissue or extended comparison to peroxisomal proteins and their associated gene expressions. Therefore, we examined differences in peroxisomal dynamics in parotid tumors of different morphologies. Using immunofluorescence and quantitative PCR, we compared the expression levels of key peroxisomal enzymes and proliferators in healthy and neoplastic parotid tissue samples. Three parotid tumor subtypes were examined: pleomorphic adenoma, mucoepidermoid carcinoma and acinic cell carcinoma. We observed higher expression of peroxisomal matrix proteins in neoplastic samples with exceptional down regulation of certain enzymes; however, the degree of expression varied between tumor subtypes. Our findings confirm previous experimental results on other organ tissues and suggest peroxisomes as possible therapeutic targets or markers in all or certain subtypes of parotid neoplasms.

scholarly journals SUMOylation Negatively Regulates Angiogenesis by Targeting Endothelial NOTCH Signaling

2017 ◽  
Vol 121 (6) ◽  
pp. 636-649 ◽  
Author(s):  
Xiaolong Zhu ◽  
Sha Ding ◽  
Cong Qiu ◽  
Yanna Shi ◽  
Lin Song ◽  
...  
Keyword(s):  
Notch Signaling ◽  
Cell Fate ◽  
Developmental Disorders ◽  
Interaction Mechanism ◽  
Growth Factor Receptor ◽  
Vascular Diseases ◽  
Cell Interaction ◽  
Protein Signaling

Rationale: The highly conserved NOTCH (neurogenic locus notch homolog protein) signaling pathway functions as a key cell–cell interaction mechanism controlling cell fate and tissue patterning, whereas its dysregulation is implicated in a variety of developmental disorders and cancers. The pivotal role of endothelial NOTCH in regulation of angiogenesis is widely appreciated; however, little is known about what controls its signal transduction. Our previous study indicated the potential role of post-translational SUMO (small ubiquitin-like modifier) modification (SUMOylation) in vascular disorders. Objective: The aim of this study was to investigate the role of SUMOylation in endothelial NOTCH signaling and angiogenesis. Methods and Results: Endothelial SENP1 (sentrin-specific protease 1) deletion, in newly generated endothelial SENP1 (the major protease of the SUMO system)–deficient mice, significantly delayed retinal vascularization by maintaining prolonged NOTCH1 signaling, as confirmed in cultured endothelial cells. An in vitro SUMOylation assay and immunoprecipitation revealed that when SENP1 associated with N1ICD (NOTCH1 intracellular domain), it functions as a deSUMOylase of N1ICD SUMOylation on conserved lysines. Immunoblot and immunoprecipitation analyses and dual-luciferase assays of natural and SUMO-conjugated/nonconjugated NOTCH1 forms demonstrated that SUMO conjugation facilitated NOTCH1 cleavage. This released N1ICD from the membrane and stabilized it for translocation to the nucleus where it functions as a cotranscriptional factor. Functionally, SENP1-mediated NOTCH1 deSUMOylation was required for NOTCH signal activation in response to DLL4 (Delta-like 4) stimulation. This in turn suppressed VEGF (vascular endothelial growth factor) receptor signaling and angiogenesis, as evidenced by immunoblotted signaling molecules and in vitro angiogenesis assays. Conclusions: These results establish reversible NOTCH1 SUMOylation as a regulatory mechanism in coordinating endothelial angiogenic signaling; SENP1 acts as a critical intrinsic mediator of this process. These findings may apply to NOTCH-regulated biological events in nonvascular tissues and provide a novel therapeutic strategy for vascular diseases and tumors.

The role of the ultrasound dopplerography in diagnosis of vascular diseases

1998 ◽  
Vol 7 ◽  
pp. S49
Author(s):  
M.V. Isaeva ◽  
M.I. Pylkov ◽  
A.R. Zubarev ◽  
A.V. Bystrov ◽  
O.Y. Izotova ◽  
...  
Keyword(s):  
Vascular Diseases

Role of the Catalytic Triad and Oxyanion Hole in Acetylcholinesterase Catalysis:  An ab initio QM/MM Study

2002 ◽  
Vol 124 (35) ◽  
pp. 10572-10577 ◽  
Author(s):  
Yingkai Zhang ◽  
Jeremy Kua ◽  
J. Andrew McCammon
Keyword(s):  
Ab Initio ◽  
Catalytic Triad ◽  
Oxyanion Hole
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