Possible Role of Phosphoinositide-3-Kinase in Mx1 Protein Translation and Antiviral Activity of Interferon-Omega-Stimulated HeLa Cells

Background: Osteoarthritis (OA) is a disease characterized by progressive degeneration, joint hyperplasia, narrowing of joint spaces, and extracellular matrix metabolism. Recent studies have shown that the pathogenesis of OA may be related to non-coding RNA, and its pathological mechanism may be an effective way to reduce OA. Objective: The purpose of this review was to investigate the recent progress of miRNA, long noncoding RNA (lncRNA) and circular RNA (circRNA) in gene therapy of OA, discussing the effects of this RNA on gene expression, inflammatory reaction, apoptosis and extracellular matrix in OA. Methods: The following electronic databases were searched, including PubMed, EMBASE, Web of Science, and the Cochrane Library, for published studies involving the miRNA, lncRNA, and circRNA in OA. The outcomes included the gene expression, inflammatory reaction, apoptosis, and extracellular matrix. Results and Discussion: With the development of technology, miRNA, lncRNA, and circRNA have been found in many diseases. More importantly, recent studies have found that RNA interacts with RNA-binding proteins to regulate gene transcription and protein translation, and is involved in various pathological processes of OA, thus becoming a potential therapy for OA. Conclusion: In this paper, we briefly introduced the role of miRNA, lncRNA, and circRNA in the occurrence and development of OA and as a new target for gene therapy.

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Importance of Apolipoprotein A-I and A-II Composition in HDL and Its Potential for Studying COVID-19 and SARS-CoV-2

Medicines ◽

10.3390/medicines8070038 ◽

2021 ◽

Vol 8 (7) ◽

pp. 38

Author(s):

Kyung-Hyun Cho

Keyword(s):

Antiviral Activity ◽

High Density ◽

High Density Lipoproteins ◽

Potent Antiviral Activity ◽

Apolipoprotein A ◽

Putative Role

The composition and properties of apolipoprotein (apo) A-I and apoA-II in high-density lipoproteins (HDL) might be critical to SARS-CoV-2 infection via SR-BI and antiviral activity against COVID-19. HDL containing native apoA-I showed potent antiviral activity, while HDL containing glycated apoA-I or other apolipoproteins did not. However, there has been no report to elucidate the putative role of apoA-II in the antiviral activity of HDL.

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Possible role of tocopherols in the modulation of host microRNA with potential antiviral activity in patients with hepatitis B virus-related persistent infection: a systematic review

British Journal Of Nutrition ◽

10.1017/s0007114514002839 ◽

2014 ◽

Vol 112 (11) ◽

pp. 1751-1768 ◽

Cited By ~ 10

Author(s):

S. Fiorino ◽

L. Bacchi-Reggiani ◽

S. Sabbatani ◽

F. Grizzi ◽

L. di Tommaso ◽

...

Keyword(s):

Hepatitis B Virus ◽

Hepatitis B ◽

Antiviral Activity ◽

Hbv Infection ◽

Cochrane Library ◽

Viral Pathogen ◽

Increased Risk ◽

B Virus ◽

Chronic Hbv

Hepatitis B virus (HBV) infection represents a serious global health problem and persistent HBV infection is associated with an increased risk of cirrhosis, hepatocellular carcinoma and liver failure. Recently, the study of the role of microRNA (miRNA) in the pathogenesis of HBV has gained considerable interest as well as new treatments against this pathogen have been approved. A few studies have investigated the antiviral activity of vitamin E (VE) in chronic HBV carriers. Herein, we review the possible role of tocopherols in the modulation of host miRNA with potential anti-HBV activity. A systematic research of the scientific literature was performed by searching the MEDLINE, Cochrane Library and EMBASE databases. The keywords used were ‘HBV therapy’, ‘HBV treatment’, ‘VE antiviral effects’, ‘tocopherol antiviral activity’, ‘miRNA antiviral activity’ and ‘VE microRNA’. Reports describing the role of miRNA in the regulation of HBV life cycle,in vitroandin vivoavailable studies reporting the effects of VE on miRNA expression profiles and epigenetic networks, and clinical trials reporting the use of VE in patients with HBV-related chronic hepatitis were identified and examined. Based on the clinical results obtained in VE-treated chronic HBV carriers, we provide a reliable hypothesis for the possible role of this vitamin in the modulation of host miRNA profiles perturbed by this viral pathogen and in the regulation of some cellular miRNA with a suggested potential anti-HBV activity. This approach may contribute to the improvement of our understanding of pathogenetic mechanisms involved in HBV infection and increase the possibility of its management and treatment.

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Inhibitory role of oleanolic acid and esculetin in HeLa cells involve multiple signaling pathways

Gene ◽

10.1016/j.gene.2020.145370 ◽

2021 ◽

Vol 771 ◽

pp. 145370

Author(s):

Prajitha Mohandas Edathara ◽

Shivakanth Chintalapally ◽

Venkata Krishna Kanth Makani ◽

Chitrakshi Pant ◽

Suresh Yerramsetty ◽

...

Keyword(s):

Signaling Pathways ◽

Oleanolic Acid ◽

Hela Cells ◽

Inhibitory Role ◽

Multiple Signaling

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Signaling Pathways Regulating TC21-induced Tumorigenesis

Journal of Biological Chemistry ◽

10.1074/jbc.m703037200 ◽

2007 ◽

Vol 282 (38) ◽

pp. 27713-27720 ◽

Cited By ~ 26

Author(s):

Mete Erdogan ◽

Ambra Pozzi ◽

Neil Bhowmick ◽

Harold L Moses ◽

Roy Zent

Keyword(s):

P38 Mapk ◽

Cancer Progression ◽

Transforming Growth Factor ◽

Cellular Transformation ◽

Tumor Formation ◽

Transformed Cells ◽

Growth Inhibitory ◽

Phosphoinositide 3 Kinase

TC21(R-Ras2), a Ras-related GTPase with transforming potential similar to H-, K- and N-Ras, is implicated in the pathogenesis of human cancers. Transforming growth factor β (TGF-β), a cytokine that plays a significant role in modulating tumorigenesis, normally prevents uncontrolled cell proliferation but paradoxically induces proliferation in H-Ras-transformed cancer cells. Although TC21 activates some pathways that mediate cellular transformation by the classical Ras proteins, the mechanisms through which TC21 induces tumor formation and how TGF-β regulates TC21 transformed cells is not known. To better understand the role of TC21 in cancer progression, we overexpressed an activated G23V mutant of TC21 in a nontumorigenic murine mammary epithelial (EpH4) cell line. Mutant TC21-expressing cells were significantly more oncogenic than cells expressing activated G12V H-Ras both in vivo and in vitro. TC21-induced transformation and proliferation required activation of p38 MAPK, mTOR (the mammalian target of rapamycin), and phosphoinositide 3-kinase but not Akt/PKB. Transformation by TC21 rendered EpH4 cells insensitive to the growth inhibitory effects of TGF-β, and the soft agar growth of these cells was increased upon TGF-β stimulation. Despite losing responsiveness to TGF-β-mediated growth inhibition, both Smad-dependent and independent pathways remained intact in TC21-transformed cells. Thus, overexpression of active TC21 in EpH4 cells induces tumorigenicity through the phosphoinositide 3-kinase, p38 MAPK, and mTOR pathways, and these cells lose their sensitivity to the normal growth inhibitory role of TGF-β.

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An essential role of Cdc42-like GTPases in mitosis of HeLa cells

FEBS Letters ◽

10.1016/j.febslet.2006.05.009 ◽

2006 ◽

Vol 580 (14) ◽

pp. 3375-3380 ◽

Cited By ~ 19

Author(s):

Shingo Yasuda ◽

Hiroyuki Taniguchi ◽

Fabian Oceguera-Yanez ◽

Yoshikazu Ando ◽

Sadanori Watanabe ◽

...

Keyword(s):

Hela Cells ◽

Essential Role

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Akt isoforms differentially regulate neutrophil functions

Blood ◽

10.1182/blood-2009-11-255323 ◽

2010 ◽

Vol 115 (21) ◽

pp. 4237-4246 ◽

Cited By ~ 73

Author(s):

Jia Chen ◽

Haiyang Tang ◽

Nissim Hay ◽

Jingsong Xu ◽

Richard D. Ye

Keyword(s):

Kinase Inhibitor ◽

Nicotinamide Adenine Dinucleotide Phosphate ◽

Leading Edge ◽

Neutrophil Activation ◽

Enzyme Release ◽

Wild Type ◽

Akt Isoforms ◽

Phosphoinositide 3 Kinase ◽

O2 Production

In neutrophils, the phosphoinositide 3-kinase/Akt signaling cascade is involved in migration, degranulation, and O2− production. However, it is unclear whether the Akt kinase isoforms have distinct functions in neutrophil activation. Here we report functional differences between the 2 major Akt isoforms in neutrophil activation on the basis of studies in which we used individual Akt1 and Akt2 knockout mice. Akt2−/− neutrophils exhibited decreased cell migration, granule enzyme release, and O2− production compared with wild-type and Akt1−/− neutrophils. Surprisingly, Akt2 deficiency and pharmacologic inhibition of Akt also abrogated phorbol ester-induced O2− production, which was unaffected by treatment with the phosphoinositide 3-kinase inhibitor LY294002. The decreased O2− production in Akt2−/− neutrophils was accompanied by reduced p47phox phosphorylation and its membrane translocation, suggesting that Akt2 is important for the assembly of phagocyte nicotinamide adenine dinucleotide phosphate oxidase. In wild-type neutrophils, Akt2 but not Akt1 translocated to plasma membrane upon chemoattractant stimulation and to the leading edge in polarized neutrophils. In the absence of Akt2, chemoattractant-induced Akt protein phosphorylation was significantly reduced. These results demonstrate a predominant role of Akt2 in regulating neutrophil functions and provide evidence for differential activation of the 2 Akt isoforms in neutrophils.

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Impaired platelet responses to thrombin and collagen in AKT-1–deficient mice

Blood ◽

10.1182/blood-2003-10-3428 ◽

2004 ◽

Vol 104 (6) ◽

pp. 1703-1710 ◽

Cited By ~ 167

Author(s):

Juhua Chen ◽

Sarmishtha De ◽

Derek S. Damron ◽

William S. Chen ◽

Nissim Hay ◽

...

Keyword(s):

Platelet Aggregation ◽

Ex Vivo ◽

Dense Granules ◽

Fibrinogen Binding ◽

Downstream Effectors ◽

Low Concentrations ◽

Phosphoinositide 3 Kinase ◽

Deficient Mice ◽

Granule Release

Abstract We investigated the role of Akt-1, one of the major downstream effectors of phosphoinositide 3-kinase (PI3K), in platelet function using mice in which the gene for Akt-1 had been inactivated. Using ex vivo techniques, we showed that Akt-1-deficient mice exhibited impaired platelet aggregation and spreading in response to various agonists. These differences were most apparent in platelets activated with low concentrations of thrombin. Although Akt-1 is not the predominant Akt isoform in mouse platelets, its absence diminished the amount of total phospho-Akt and inhibited increases in intracellular Ca2+ concentration in response to thrombin. Moreover, thrombin-induced platelet α-granule release as well as release of adenosine triphosphate from dense granules was also defective in Akt-1-null platelets. Although the absence of Akt-1 did not influence expression of the major platelet receptors for thrombin and collagen, fibrinogen binding in response to these agonists was significantly reduced. As a consequence of impaired αIIbβ3 activation and platelet aggregation, Akt-1 null mice showed significantly longer bleeding times than wild-type mice. (Blood. 2004;104:1703-1710)

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The role of the membrane-spanning domain and stalk region of N-acetylglucosaminyltransferase I in retention, kin recognition and structural maintenance of the Golgi apparatus in HeLa cells

Journal of Cell Science ◽

10.1242/jcs.109.7.1975 ◽

1996 ◽

Vol 109 (7) ◽

pp. 1975-1989 ◽

Cited By ~ 4

Author(s):

T. Nilsson ◽

C. Rabouille ◽

N. Hui ◽

R. Watson ◽

G. Warren

Keyword(s):

Golgi Apparatus ◽

Cell Lines ◽

Hela Cells ◽

Kin Recognition ◽

Dramatic Effect ◽

Golgi Stack ◽

Stable Cell Lines ◽

Membrane Spanning ◽

Necessary And Sufficient

Using a series of chimeric and truncated N-acetylglucosaminyltransferase I (NAGT I) molecules we have shown that part of the lumenal stalk region is both necessary and sufficient for kin recognition of mannosidase II and retention in the Golgi stack. The membrane-spanning domain was not required for retention, but replacing part or all of this domain with leucine residues did have a dramatic effect on Golgi morphology. In stable cell lines, stacked cisternae were replaced by tubulo-vesicular clusters containing the mutated NAGT I. The loss of stacked cisternae was proportional to the number of leucines used to replace the membrane-spanning domain.

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