scholarly journals Differential expression of selected microRNA and putative target genes in peripheral blood cells as early markers of severe forms of dengue

2019 ◽  
Author(s):  
Harsha Hapugaswatta ◽  
Pubudu Amarasena ◽  
Ranjan Premaratna ◽  
Kapila N. Seneviratne ◽  
Nimanthi Jayathilaka
Keyword(s):  
Differential Expression ◽  
Dengue Fever ◽  
Peripheral Blood ◽  
Blood Cells ◽  
Target Genes ◽  
Severe Dengue ◽  
Peripheral Blood Cells ◽  
Early Stages ◽  
Putative Target ◽  
Life Threatening

AbstractBackgroundDengue presents a wide clinical spectrum including asymptomatic dengue fever (DF) or severe forms, such as dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). Early symptoms of DHF are similar to those of non-life-threatening DF. Severe symptoms manifest after 3-5 days of fever, which can be life threatening due to lack of proper medications and inability to distinguish severe cases during the early stages. Early prediction of severe dengue in patients with no warning signs who may later develop severe infection is very important for proper disease management to alleviate DHF related complications and mortality. Due to the role in post-transcriptional regulation of gene expression and remarkable stability of microRNA, altered expression of microRNA was evaluated to explore clinically relevant biomarkers.Methodology/Principal findingsThe relative expression of microRNA hsa-let-7e, hsa-miR-30b-5p, hsa-miR-30e-3p, hsa-miR-33a, and hsa-miR-150-5p and several putative target genes in peripheral blood cells (PBC) collected from 20 DF and 20 DHF positive patients within four days from fever onset was evaluated by qRT-PCR. hsa-miR-150-5p showed significant (P<0.05) up regulation in PBC of DHF patients compared to DF patients during the acute phase of infection. Expression of enhancer of zeste homolog 2 (EZH2) was significantly (P<0.05) down regulated indicating that genes involved in epigenetic regulation are also differentially expressed in DHF patients during the early stage of infection.Conclusions/SignificanceDifferential expression of microRNA miR-150-5p and the putative target gene EZH2 may serve as reliable biomarkers of disease severity during early stages of dengue infection.Author summarySevere dengue cannot be distinguished from dengue fever during the early stages of infection based on the clinical symptoms. A diagnosis is only made after the patient is presented with severe manifestations such as plasma leakage and hemorrhage. During a dengue outbreak, this leads to high occupancy of hospital beds. However, only a small percentage of patients present with severe symptoms and the others do not require medical care at a hospital. Therefore, early prognosis of severe manifestations could reduce dengue related mortality by identifying the patients who will benefit from hospitalization and early intervention. We demonstrate that severe dengue in Sri Lankan patients is associated with increased expression of miRNA miR150 and decreased expression of EZH2 during the early stages of infection when none of the patients showed symptoms of developing severe manifestations at later stages of infection.

Differential expression of wild-type and mutant NMMHC-IIA polypeptides in blood cells suggests cell-specific regulation mechanisms in MYH9 disorders

Blood ◽  
2008 ◽  
Vol 111 (6) ◽  
pp. 3015-3023 ◽  
Author(s):  
Shinji Kunishima ◽  
Motohiro Hamaguchi ◽  
Hidehiko Saito
Keyword(s):  
Differential Expression ◽  
Peripheral Blood ◽  
Blood Cells ◽  
Inclusion Bodies ◽  
Peripheral Blood Cells ◽  
Wild Type ◽  
Normal Peripheral Blood ◽  
Peripheral Blood Cd34 ◽  
Regulation Mechanisms ◽  
Specific Regulation

Abstract MYH9 disorders such as May-Hegglin anomaly are characterized by macrothrombocytopenia and cytoplasmic granulocyte inclusion bodies that result from mutations in MYH9, the gene for nonmuscle myosin heavy chain-IIA (NMMHC-IIA). We examined the expression of mutant NMMHC-IIA polypeptide in peripheral blood cells from patients with MYH9 5770delG and 5818delG mutations. A specific antibody to mutant NMMHC-IIA (NT629) was raised against the abnormal carboxyl-terminal residues generated by 5818delG. NT629 reacted to recombinant 5818delG NMMHC-IIA but not to wild-type NMMHC-IIA, and did not recognize any cellular components of normal peripheral blood cells. Immunofluorescence and immunoblotting revealed that mutant NMMHC-IIA was present and sequestrated only in inclusion bodies within neutrophils, diffusely distributed throughout lymphocyte cytoplasm, sparsely localized on a diffuse cytoplasmic background in monocytes, and uniformly distributed at diminished levels only in large platelets. Mutant NMMHC-IIA did not translocate to lamellipodia in surface activated platelets. Wild-type NMMHC-IIA was homogeneously distributed among megakaryocytes derived from the peripheral blood CD34+ cells of patients, but coarse mutant NMMHC-IIA was heterogeneously scattered without abnormal aggregates in the cytoplasm. We show the differential expression of mutant NMMHC-IIA and postulate that cell-specific regulation mechanisms function in MYH9 disorders.

scholarly journals Inflammatory Responses Induced by the Rupture of Intracranial Aneurysms Are Modulated by miRNAs

2019 ◽  
Vol 57 (2) ◽  
pp. 988-996 ◽  
Author(s):  
Michal Korostynski ◽  
Rafal Morga ◽  
Marcin Piechota ◽  
Dzesika Hoinkis ◽  
Slawomir Golda ◽  
...  
Keyword(s):  
Peripheral Blood ◽  
Blood Cells ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Immune Cell ◽  
Inflammatory Responses ◽  
Chronic Phase ◽  
Mature Mirnas ◽  
Inflammatory Factors ◽  
Peripheral Blood Cells

Abstract Influence of an intracranial aneurysm (IA) rupture on the expression of miRNAs and the potential significance of the resulting changes remains poorly understood. We aimed to characterize the response to the IA rupture through the analysis of miRNAs in peripheral blood cells. Expression of small RNAs was investigated using deep transcriptome sequencing in patients in the acute phase of an IA rupture (first 72 h), in the chronic phase (3–15 months), and controls. A functional analysis and the potential interactions between miRNAs and target genes were investigated. We also measured the levels of proteins that were influenced by regulated miRNAs. We found that 106 mature miRNAs and 90 miRNA precursors were differentially expressed among the groups. The regulated miRNAs were involved in a variety of pathways, and the top pathway involved cytokine-cytokine receptor interactions. The identified miRNAs targeted the inflammatory factors HMGB1 and FASLG. Changes in their expression were detected at the mRNA and protein levels. IA rupture strongly influences the transcription profiles in peripheral blood cells. The regulated miRNAs were involved in the control of immune cell homeostasis. In summary, these results may aid in the elucidation of the molecular mechanisms that orchestrate the inflammatory response to IA rupture.

Receptor Mediated Binding of the Fibrinolytic Components, Plasminogen and Urokinase, to Peripheral Blood Cells

1987 ◽  
Vol 58 (03) ◽  
pp. 936-942 ◽  
Author(s):  
Lindsey A Miles ◽  
Edward F Plow
Keyword(s):  
T Cells ◽  
B Cell ◽  
Peripheral Blood ◽  
Binding Sites ◽  
Blood Cells ◽  
High Capacity ◽  
Red Cells ◽  
Peripheral Blood Cells ◽  
Cellular Functions ◽  
Fibrinolytic Proteins

SummaryGlu-plasminogen binds to platelets; the monocytoid line, U937, and the human fetal fibroblast line, GM1380 bind both plasminogen and its activator, urokinase. This study assesses the interaction of these fibrinolytic proteins with circulating human blood cells. Plasminogen bound minimally to red cells but bound saturably and reversibly to monocytes, granulocytes and lymphocytes with apparent Kd values of 0.9-1.4 μM. The interactions were of high capacity with 1.6 to 49 × 105 sites/cell and involved the lysine binding sites of plasminogen. Both T cells and non-rosetting lymphocytes and two B cell lines saturably bound plasminogen. Urokinase bound saturably to gianulocytes, monocytes, non-rosetting lymphocytes and a B cell line, but minimally to T cells, platelets and red cells. Therefore, plasminogen binding sites of high capacity, of similar affinities, and with common recognition specificities are expressed by many peripheral blood cells. Urokinase receptors are also widely distributed, but less so than plasminogen binding sites. The binding ol plasminogen and/ or urokinase to these cells may lead to generation of cell- associated proteolytic activity which contributes to a variety of cellular functions.

scholarly journals RNA Sequencing of Human Peripheral Blood Cells Indicates Upregulation of Immune-Related Genes in Huntington's Disease

2020 ◽  
Vol 11 ◽  
Author(s):  
Miguel A. Andrade-Navarro ◽  
Katja Mühlenberg ◽  
Eike J. Spruth ◽  
Nancy Mah ◽  
Adrián González-López ◽  
...  
Keyword(s):  
Gene Expression ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Peripheral Blood ◽  
Blood Cells ◽  
Trinucleotide Repeat ◽  
Neurodegenerative Disorder ◽  
Gene Expression Signature ◽  
Interferon Response ◽  
Peripheral Blood Cells

Huntington's disease (HD) is an autosomal dominantly inherited neurodegenerative disorder caused by a trinucleotide repeat expansion in the Huntingtin gene. As disease-modifying therapies for HD are being developed, peripheral blood cells may be used to indicate disease progression and to monitor treatment response. In order to investigate whether gene expression changes can be found in the blood of individuals with HD that distinguish them from healthy controls, we performed transcriptome analysis by next-generation sequencing (RNA-seq). We detected a gene expression signature consistent with dysregulation of immune-related functions and inflammatory response in peripheral blood from HD cases vs. controls, including induction of the interferon response genes, IFITM3, IFI6 and IRF7. Our results suggest that it is possible to detect gene expression changes in blood samples from individuals with HD, which may reflect the immune pathology associated with the disease.

Transplantation of Bone Marrow as Compared with Peripheral-Blood Cells from HLA-Identical Relatives in Patients with Hematologic Cancers

2001 ◽  
Vol 344 (3) ◽  
pp. 175-181 ◽  
Author(s):  
William I. Bensinger ◽  
Paul J. Martin ◽  
Barry Storer ◽  
Reginald Clift ◽  
Steven J. Forman ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Peripheral Blood ◽  
Blood Cells ◽  
Peripheral Blood Cells
Sign in / Sign up

Export Citation Format

Share Document