scholarly journals Transcription expression of gene encoding cathelicidin CATHL4 in Vietnam indigenous yellow cattle

2021 ◽  
Vol 43 (1) ◽  
Author(s):  
Do Thi Tuoi ◽  
Tran Thi Thuy Anh ◽  
Pham Doan Lan ◽  
Nguyen Thi Hoang Van
Keyword(s):  
Animal Experiments ◽  
Transgenic Animal ◽  
Host Defenses ◽  
Quantitative Real Time Pcr ◽  
Gene Encoding ◽  
Diverse Range ◽  
Yellow Cattle ◽  
Healthy Cattle ◽  
Transcription Expression

Cathelicidins, a family of host-defence peptides, are present in a diverse range of species, including fish, amphibians, birds, reptiles, and mammals. The evidence for the role of these cationic antimicrobial peptides in innate host defenses is convincing from the data of animal model and transgenic animal experiments as well as wildlife or domestic animals, indicating that the peptides protect against inflammatory and immune system after induction by bacterial infection. In this study, we present the assessment of transcription expression of CATHL4 gene which encodes indolicidin, a cathelicidin from indigenous yellow cattle of Vietnam. The research focused on RNA samples extracted from lung tissues and lymph node collected from diseased cattle which died of infectious respiratory symptoms and the healthy cattle which were slaughtered for food purposes. By quantitative real-time PCR, the relative expression of transcripts was determined and analyzed using the expression of YWHAZ gene as reference. The results showed that this gene was abundantly expressed at a higher level in tissues of the diseased cattle than in those of the healthy ones. In both infection and healthy states, the expression of CATHL4 in lymph nodes were higher than in lung tissues. This indicated that CATHL4 (indolicidin) may participate in functions against infectious pathogens.      

Exploring the role of identity fusion and group identification in predicting parochialism amongst Indonesian Islamic groups

2019 ◽  
Author(s):  
Christopher Michael Kavanagh ◽  
Susilo Wibisono ◽  
Rohan Kapitány ◽  
Whinda Yustisia ◽  
Idhamsyah Eka Putra ◽  
...  
Keyword(s):  
Group Identification ◽  
Control Sample ◽  
Theoretical Models ◽  
Religious Groups ◽  
Diverse Range ◽  
Beliefs And Practices ◽  
Identity Fusion ◽  
Beliefs And Practice ◽  
Fusion Theory

Indonesia is the most populous Islamic country and as such is host to a diverse range of Islamic beliefs and practices. Here we examine how the diversity of beliefs and practices among Indonesian Muslims relates to group bonding and parochialism. In particular, we examine the predictive power of two distinct types of group alignment, group identification and identity fusion, among individuals from three Sunni politico-religious groups - a fundamentalist group (PKS), a moderate group (NU), and a control sample of politically unaffiliated citizens. Fundamentalists were more fused to targets than moderates or citizens, but contrary to fusion theory, we found across all groups, that group identification (not fusion) better predicted parochialism, including willingness to carry out extreme pro-group actions. We discuss how religious beliefs and practice impact parochial attitudes, as well as the implications for theoretical models linking fusion to extreme behaviour.

Overexpression of Pygo2 Increases Differentiation of Human Umbilical Cord Mesenchymal Stem Cells into Cardiomyocyte-like Cells

2020 ◽  
Vol 20 (4) ◽  
pp. 318-324 ◽  
Author(s):  
Lei Yang ◽  
Shuoji Zhu ◽  
Yongqing Li ◽  
Jian Zhuang ◽  
Jimei Chen ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Umbilical Cord ◽  
Heart Function ◽  
Critical Role ◽  
Human Umbilical Cord ◽  
Stem Cell Markers ◽  
Quantitative Real Time Pcr ◽  
Qrt Pcr

Background: Our previous studies have shown that Pygo (Pygopus) in Drosophila plays a critical role in adult heart function that is likely conserved in mammals. However, its role in the differentiation of human umbilical cord mesenchymal stem cells (hUC-MSCs) into cardiomyocytes remains unknown. Objective: To investigate the role of pygo2 in the differentiation of hUC-MSCs into cardiomyocytes. Methods: Third passage hUC-MSCs were divided into two groups: a p+ group infected with the GV492-pygo2 virus and a p− group infected with the GV492 virus. After infection and 3 or 21 days of incubation, Quantitative real-time PCR (qRT-PCR) was performed to detect pluripotency markers, including OCT-4 and SOX2. Nkx2.5, Gata-4 and cTnT were detected by immunofluorescence at 7, 14 and 21 days post-infection, respectively. Expression of cardiac-related genes—including Nkx2.5, Gata-4, TNNT2, MEF2c, ISL-1, FOXH1, KDR, αMHC and α-Actin—were analyzed by qRT-PCR following transfection with the virus at one, two and three weeks. Results : After three days of incubation, there were no significant changes in the expression of the pluripotency stem cell markers OCT-4 and SOX2 in the p+ group hUC-MSCs relative to controls (OCT-4: 1.03 ± 0.096 VS 1, P > 0.05, SOX2: 1.071 ± 0.189 VS 1, P > 0.05); however, after 21 days, significant decreases were observed (OCT-4: 0.164 ± 0.098 VS 1, P < 0.01, SOX2: 0.209 ± 0.109 VS 1, P < 0.001). Seven days following incubation, expression of mesoderm specialisation markers, such as Nkx2.5, Gata-4, MEF2c and KDR, were increased; at 14 days following incubation, expression of cardiac genes, such as Nkx2.5, Gata-4, TNNT2, MEF2c, ISL-1, FOXH1, KDR, αMHC and α-Actin, were significantly upregulated in the p+ group relative to the p− group (P < 0.05). Taken together, these findings suggest that overexpression of pygo2 results in more hUCMSCs gradually differentiating into cardiomyocyte-like cells. Conclusion: We are the first to show that overexpression of pygo2 significantly enhances the expression of cardiac-genic genes, including Nkx2.5 and Gata-4, and promotes the differentiation of hUC-MSCs into cardiomyocyte-like cells.

scholarly journals New Insights on the Role of TRP Channels in Calcium Signalling and Immunomodulation: Review of Pathways and Implications for Clinical Practice

2021 ◽  
Author(s):  
Saied Froghi ◽  
Charlotte R. Grant ◽  
Radhika Tandon ◽  
Alberto Quaglia ◽  
Brian Davidson ◽  
...  
Keyword(s):  
Immune System ◽  
Calcium Release ◽  
Transient Receptor Potential ◽  
Trp Channels ◽  
Calcium Influx ◽  
Calcium Signalling ◽  
Chronic Fatigue ◽  
Diverse Range ◽  
Immune System Activation

AbstractCalcium is the most abundant mineral in the human body and is central to many physiological processes, including immune system activation and maintenance. Studies continue to reveal the intricacies of calcium signalling within the immune system. Perhaps the most well-understood mechanism of calcium influx into cells is store-operated calcium entry (SOCE), which occurs via calcium release-activated channels (CRACs). SOCE is central to the activation of immune system cells; however, more recent studies have demonstrated the crucial role of other calcium channels, including transient receptor potential (TRP) channels. In this review, we describe the expression and function of TRP channels within the immune system and outline associations with murine models of disease and human conditions. Therefore, highlighting the importance of TRP channels in disease and reviewing potential. The TRP channel family is significant, and its members have a continually growing number of cellular processes. Within the immune system, TRP channels are involved in a diverse range of functions including T and B cell receptor signalling and activation, antigen presentation by dendritic cells, neutrophil and macrophage bactericidal activity, and mast cell degranulation. Not surprisingly, these channels have been linked to many pathological conditions such as inflammatory bowel disease, chronic fatigue syndrome and myalgic encephalomyelitis, atherosclerosis, hypertension and atopy.

scholarly journals The Role of Mitochondria in Carcinogenesis

2021 ◽  
Vol 22 (10) ◽  
pp. 5100
Author(s):  
Paulina Kozakiewicz ◽  
Ludmiła Grzybowska-Szatkowska ◽  
Marzanna Ciesielka ◽  
Jolanta Rzymowska
Keyword(s):  
Prostate Cancer ◽  
Mitochondrial Dna ◽  
Nuclear Dna ◽  
Dna Polymorphisms ◽  
Gene Encoding ◽  
Dna Mutations ◽  
Nadh Ubiquinone Oxidoreductase ◽  
Gene Coi ◽  
The Impact

The mitochondria are essential for normal cell functioning. Changes in mitochondrial DNA (mtDNA) may affect the occurrence of some chronic diseases and cancer. This process is complex and not entirely understood. The assignment to a particular mitochondrial haplogroup may be a factor that either contributes to cancer development or reduces its likelihood. Mutations in mtDNA occurring via an increase in reactive oxygen species may favour the occurrence of further changes both in mitochondrial and nuclear DNA. Mitochondrial DNA mutations in postmitotic cells are not inherited, but may play a role both in initiation and progression of cancer. One of the first discovered polymorphisms associated with cancer was in the gene NADH-ubiquinone oxidoreductase chain 3 (mt-ND3) and it was typical of haplogroup N. In prostate cancer, these mutations and polymorphisms involve a gene encoding subunit I of respiratory complex IV cytochrome c oxidase subunit 1 gene (COI). At present, a growing number of studies also address the impact of mtDNA polymorphisms on prognosis in cancer patients. Some of the mitochondrial DNA polymorphisms occur in both chronic disease and cancer, for instance polymorphism G5913A characteristic of prostate cancer and hypertension.

Specialized, pro-resolving mediators as potential therapeutic agents for alleviating fibromyalgia symptomatology

Pain Medicine ◽  
2021 ◽  
Author(s):  
Gregory Livshits ◽  
Alexander Kalinkovich
Keyword(s):  
Animal Experiments ◽  
Therapeutic Agents ◽  
Treatment Modalities ◽  
Inflammatory Factors ◽  
Gut Dysbiosis ◽  
Unsuccessful Treatment ◽  
Pain Sensitization ◽  
Novel Strategy ◽  
Inflammation Resolution

Abstract Objective To present a hypothesis on a novel strategy in the treatment of fibromyalgia (FM). Design A narrative review. Setting FM as a disease remains a challenging concept for numerous reasons, including undefined etiopathogenesis, unclear triggers and unsuccessful treatment modalities. We hypothesize that the inflammatome, the entire set of molecules involved in inflammation, acting as a common pathophysiological instrument of gut dysbiosis, sarcopenia, and neuroinflammation, is one of the major mechanisms underlying FM pathogenesis. In this setup, dysbiosis is proposed as the primary trigger of the inflammatome, sarcopenia as the peripheral nociceptive source, and neuroinflammation as the central mechanism of pain sensitization, transmission and symptomatology of FM. Whereas neuroinflammation is highly-considered as a critical deleterious element in FM pathogenesis, the presumed pathogenic roles of sarcopenia and systemic inflammation remain controversial. Nevertheless, sarcopenia-associated processes and dysbiosis have been recently detected in FM individuals. The prevalence of pro-inflammatory factors in the cerebrospinal fluid and blood has been repeatedly observed in FM individuals, supporting an idea on the role of inflammatome in FM pathogenesis. As such, failed inflammation resolution might be one of the underlying pathogenic mechanisms. In accordance, the application of specialized, inflammation pro-resolving mediators (SPMs) seems most suitable for this goal. Conclusions The capability of various SPMs to prevent and attenuate pain has been repeatedly demonstrated in laboratory animal experiments. Since SPMs suppress inflammation in a manner that does not compromise host defense, they could be attractive and safe candidates for the alleviation of FM symptomatology, probably in combination with anti-dysbiotic medicine.

scholarly journals Controlled Transcription of Regulator Gene carS by Tet-on or by a Strong Promoter Confirms Its Role as a Repressor of Carotenoid Biosynthesis in Fusarium fujikuroi

2020 ◽  
Vol 9 (1) ◽  
pp. 71
Author(s):  
Julia Marente ◽  
Javier Avalos ◽  
M. Carmen Limón
Keyword(s):  
Wild Strain ◽  
Ring Finger ◽  
Carotenoid Biosynthesis ◽  
Negative Regulator ◽  
Fusarium Fujikuroi ◽  
Structural Genes ◽  
Gene Encoding ◽  
In The Wild ◽  
Set Up

Carotenoid biosynthesis is a frequent trait in fungi. In the ascomycete Fusarium fujikuroi, the synthesis of the carboxylic xanthophyll neurosporaxanthin (NX) is stimulated by light. However, the mutants of the carS gene, encoding a protein of the RING finger family, accumulate large NX amounts regardless of illumination, indicating the role of CarS as a negative regulator. To confirm CarS function, we used the Tet-on system to control carS expression in this fungus. The system was first set up with a reporter mluc gene, which showed a positive correlation between the inducer doxycycline and luminescence. Once the system was improved, the carS gene was expressed using Tet-on in the wild strain and in a carS mutant. In both cases, increased carS transcription provoked a downregulation of the structural genes of the pathway and albino phenotypes even under light. Similarly, when the carS gene was constitutively overexpressed under the control of a gpdA promoter, total downregulation of the NX pathway was observed. The results confirmed the role of CarS as a repressor of carotenogenesis in F. fujikuroi and revealed that its expression must be regulated in the wild strain to allow appropriate NX biosynthesis in response to illumination.

scholarly journals IL6 sensitizes prostate cancer to the antiproliferative effect of IFNα2 through IRF9

2013 ◽  
Vol 20 (5) ◽  
pp. 677-689 ◽  
Author(s):  
Holger H H Erb ◽  
Regina V Langlechner ◽  
Patrizia L Moser ◽  
Florian Handle ◽  
Tineke Casneuf ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Lines ◽  
Cellular Proliferation ◽  
Tissue Expression ◽  
Type I ◽  
Regulatory Factor ◽  
Quantitative Real Time Pcr ◽  
Antiproliferative Effects ◽  
Protein Levels

Development and progression of prostate cancer (PCa) are associated with chronic inflammation. The cytokine interleukin 6 (IL6) can influence progression, differentiation, survival, and angiogenesis of PCa. To identify novel pathways that are triggered by IL6, we performed a gene expression profiling of two PCa cell lines, LNCaP and MDA PCa 2b, treated with 5 ng/ml IL6. Interferon (IFN) regulatory factor 9 (IRF9) was identified as one of the most prevalent IL6-regulated genes in both cell lines. IRF9 is a mediator of type I IFN signaling and acts together with STAT1 and 2 to activate transcription of IFN-responsive genes. The IL6 regulation of IRF9 was confirmed at mRNA and protein levels by quantitative real-time PCR and western blot respectively in both cell lines and could be blocked by the anti-IL6 antibody Siltuximab. Three PCa cell lines, PC3, Du-145, and LNCaP-IL6+, with an autocrine IL6 loop displayed high expression of IRF9. A tissue microarray with 36 PCa tissues showed that IRF9 protein expression is moderately elevated in malignant areas and positively correlates with the tissue expression of IL6. Downregulation and overexpression of IRF9 provided evidence for an IFN-independent role of IRF9 in cellular proliferation of different PCa cell lines. Furthermore, expression of IRF9 was essential to mediate the antiproliferative effects of IFNα2. We concluded that IL6 is an inducer of IRF9 expression in PCa and a sensitizer for the antiproliferative effects of IFNα2.

scholarly journals Regulatory Role of the MisR/S Two-Component System in Hemoglobin Utilization in Neisseria meningitidis

2009 ◽  
Vol 78 (3) ◽  
pp. 1109-1122 ◽  
Author(s):  
Shuming Zhao ◽  
Grisselle E. Montanez ◽  
Pradeep Kumar ◽  
Soma Sannigrahi ◽  
Yih-Ling Tzeng
Keyword(s):  
Posttranscriptional Regulation ◽  
Regulatory Mechanisms ◽  
Two Component System ◽  
Gene Encoding ◽  
Positive Role ◽  
Upstream Gene ◽  
Component System ◽  
Two Component ◽  
Major Surface

ABSTRACT Outer membrane iron receptors are some of the major surface entities that are critical for meningococcal pathogenesis. The gene encoding the meningococcal hemoglobin receptor, HmbR, is both independently transcribed and transcriptionally linked to the upstream gene hemO, which encodes a heme oxygenase. The MisR/S two-component system was previously determined to regulate hmbR transcription, and its hemO and hmbR regulatory mechanisms were characterized further here. The expression of hemO and hmbR was downregulated in misR/S mutants under both iron-replete and iron-restricted conditions, and the downregulation could be reversed by complementation. No significant changes in expression of other iron receptors were detected, suggesting that the MisR/S system specifically regulates hmbR. When hemoglobin was the sole iron source, growth defects were detected in the mutants. Primer extension analysis identified a promoter upstream of the hemO-associated Correia element (CE) and another promoter at the proximal end of CE, and processed transcripts previously identified for other cotranscribed CEs were also detected, suggesting that there may be posttranscriptional regulation. MisR directly interacts with sequences upstream of the CE and upstream of the hmbR Fur binding site and thus independently regulates hemO and hmbR. Analysis of transcriptional reporters of hemO and hmbR further demonstrated the positive role of the MisR/S system and showed that the transcription of hmbR initiated from hemO was significantly reduced. A comparison of the effects of the misS mutation under iron-replete and iron-depleted conditions suggested that activation by the MisR/S system and iron-mediated repression by Fur act independently. Thus, the expression of hemO and hmbR is coordinately controlled by multiple independent regulatory mechanisms, including the MisR/S two-component system.

Platelet Glycoprotein Receptor IIIa Polymorphism PlA1/PlA2 and Coronary Risk: a Meta-Analysis

2001 ◽  
Vol 85 (04) ◽  
pp. 626-633 ◽  
Author(s):  
Augusto Di Castelnuovo ◽  
Giovanni de Gaetano ◽  
Maria Benedetta Donati ◽  
Licia Iacoviello
Keyword(s):  
Odds Ratio ◽  
Meta Analysis ◽  
Platelet Glycoprotein ◽  
Published Data ◽  
Coronary Risk ◽  
Gene Encoding ◽  
Glycoprotein Iiia ◽  
Artery Disease ◽  
Revascularization Procedures

SummaryMembrane glycoprotein IIb/IIIa plays a major role in platelet function. The gene encoding the glycoprotein IIIa shows a common polymorphism PlA1/PlA2 that was variably associated with vascular disease. To clarify the role of PlA1/PlA2 polymorphism in coronary risk, a meta-analysis of published data was conducted. Studies were identified both by MEDLINE searches, and hand searching of journals and abstract books.A total of 34 studies for coronary artery disease (CAD), and 6 for restenosis after revascularization were identified, for a total of 9,095 cases and 12,508 controls. In CAD, the overall odds ratio for carriers of the PlA2 allele was 1.10 (95% CI: 1.03 to 1.18), and it was 1.21 (95% CI: 1.05 to 1.38) in subjects younger than 60. Overall odds ratio was 1.31 (95% CI: 1.10 to 1.56) after revascularization procedures.The association of PlA2 status with overall cardiovascular disease in the general population is significant but weak; higher risk has been identified in less heterogeneous subgroups as in the younger cohorts and in the restenosis subset with stents.

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