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Book ; Online ; E-Book: Diagnostics to pathogenomics of sexually transmitted infections

Singh, Sunit K.

2019

Author's details	edited by, Sunit K. Singh
Keywords	Sexually Transmitted Diseases ; Sexually transmitted diseases
Subject code	616.951
Language	English
Size	1 Online-Ressource (XXI, 392 Seiten, [9 Blätter])
Publisher	Wiley Blackwell
Publishing place	Hoboken, NJ
Publishing country	United States
Document type	Book ; Online ; E-Book
Remark	Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
HBZ-ID	HT019851390
ISBN	9781119380955 ; 9781119380900 ; 9781119380849 ; 1119380952 ; 1119380901 ; 1119380847
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Article ; Online: Zika virus NS1 suppresses VE-cadherin via hsa-miR-29b-3p/DNMT3b/MMP-9 pathway in human brain microvascular endothelial cells.

Bhardwaj, Utkarsh / Singh, Sunit K

Cellular signalling

2023 Volume 106, Page(s) 110659

Abstract: Zika virus infection has been reported to cause microcephaly in newborns. ZIKV exploits various strategies to cross the blood-brain barrier. ZIKV NS1 may compromise the barrier integrity of endothelial cells by regulating expression of junctional ... ...

Abstract	Zika virus infection has been reported to cause microcephaly in newborns. ZIKV exploits various strategies to cross the blood-brain barrier. ZIKV NS1 may compromise the barrier integrity of endothelial cells by regulating expression of junctional proteins. MicroRNAs play an important role in post-transcriptional gene regulations. We demonstrated that ZIKV-NS1 affected the adherence junction protein in human brain microvascular endothelial cells via hsa-miR-29b-3p/DNMT3b/MMP-9 pathway. The hCMEC/D3 cells were exposed to ZIKV-NS1 with different doses (500 ng/mL and 1000 ng/mL) for 24 h. The expression pattern of DNTM3b, MMP-9, and VE-cadherin were studied using immunoblotting and the distribution of DNMT3b and MMP-9 were studied using immunofluorescence. The quantification of hsa-miR-29b-3p was done through qRT-PCR. Direct regulation of DNMT3b by hsa-miR-29b-3p was demonstrated by overexpression of hsa-miR-29b-3p using hsa-miR-29b-3p mimic, and knockdown of hsa-miR-29b-3p by using hsa-miR-29b-3p inhibitors. The ZIKV-NS1 affected the barrier function of endothelial cells through the increased expression of hsa-miR29b-3p, which suppressed the DNMT3b, thus enhanced expression of MMP-9, which finally suppressed the expression of VE-cadherin. These findings suggested that ZIKV-NS1 alters the expression of Adherens Junction protein in human brain microvascular endothelial cells through hsa-miR-29b-3p/DNMT3b/MMP-9 pathway, which compromised the barrier function of human brain microvascular endothelial cells.
MeSH term(s)	Infant, Newborn ; Humans ; Zika Virus/genetics ; Zika Virus/metabolism ; Endothelial Cells/metabolism ; Matrix Metalloproteinase 9/metabolism ; Zika Virus Infection/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Brain/metabolism
Chemical Substances	MIRN29B1 microRNA, human ; cadherin 5 ; Matrix Metalloproteinase 9 (EC 3.4.24.35) ; MicroRNAs
Language	English
Publishing date	2023-03-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1002702-6
ISSN	1873-3913 ; 0898-6568
ISSN (online)	1873-3913
ISSN	0898-6568
DOI	10.1016/j.cellsig.2023.110659
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 2579: Show issues

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Article ; Online: Direct antimicrobial effects of chemokines on Cryptococcus spp, with special emphasis on a 'CXC' chemokine.

Singh, Arpita / Singh, Sunit K

Journal de mycologie medicale

2023 Volume 33, Issue 4, Page(s) 101415

Abstract: Cryptococcus species are ingenious human pathogens that are widespread globally. They continue to cause over 200,000 deaths per year. Presently due to the rise in resistance and therapy failure, it is necessary to shift the focus to an alternate ... ...

Abstract	Cryptococcus species are ingenious human pathogens that are widespread globally. They continue to cause over 200,000 deaths per year. Presently due to the rise in resistance and therapy failure, it is necessary to shift the focus to an alternate therapeutic strategy against this pathogen. One promising approach is to emphasize the host defense system in order to develop more precise and customized treatment strategies. In this regard, research has revealed that interferon-γ-inducible CXCL10 chemokine, amongst other chemokines spanning both CXC and CC categories, has a direct killing effect in vitro against Cryptococcus neoformans and Cryptococcus gattii, with a significantly greater microbicidal effect against the former. Moreover, when CXCL10 is used in combination with CCL5, there is a significant reduction in the survival of C. gattii at normal-serum level concentration, indicating a previously unreported synergistic effect of these two chemokines. Confocal and STED microscopic studies have demonstrated that CXCL10 has both cell wall/membrane and intracellular targets against this fungus. These findings present new possibilities for developing chemokine-derived small molecule antifungals and may represent a step forward in creating precision medicine tailored to each patient.
MeSH term(s)	Humans ; Chemokine CXCL10/pharmacology ; Cryptococcus neoformans ; Interferon-gamma ; Cryptococcosis/drug therapy ; Cryptococcosis/microbiology ; Cryptococcus gattii ; Anti-Infective Agents/pharmacology
Chemical Substances	Chemokine CXCL10 ; Interferon-gamma (82115-62-6) ; Anti-Infective Agents
Language	English
Publishing date	2023-07-21
Publishing country	France
Document type	Journal Article
ZDB-ID	1067006-3
ISSN	1773-0449 ; 1156-5233
ISSN (online)	1773-0449
ISSN	1156-5233
DOI	10.1016/j.mycmed.2023.101415
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Zs.A 3148: Show issues

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Article ; Online: MicroRNA-155 triggers a cellular antiviral immune response against Chandipura virus in human microglial cells.

Pandey, Neha / Singh, Sunit K

Microbes and infection

2023 Volume 25, Issue 7, Page(s) 105173

Abstract: Chandipura virus (CHPV) belongs to the family Rhabdoviridae and has a single-stranded RNA genome that causes encephalitis among children in India's tropical states. Activation of the antiviral immune response upon viral infection is important for the ... ...

Abstract	Chandipura virus (CHPV) belongs to the family Rhabdoviridae and has a single-stranded RNA genome that causes encephalitis among children in India's tropical states. Activation of the antiviral immune response upon viral infection is important for the host's defense. In response to CHPV infection, the brain resident macrophages (microglial cells) control the pathogenic insults. The microRNAs (miRNAs) are 22 nts non-coding RNAs that serve as delicate regulators of their target genes at the post-transcriptional level. In this study, we explored miR-155 mediated antiviral response in CHPV infected human microglial cells. The gene and protein expression patterns were studied through quantitative real-time PCR (qPCR) and immunoblotting, respectively. Additionally, miRNA target validation was done by overexpression and knockdown of miR-155. We observed an increased expression of miR-155 in CHPV infected human microglial cells. The upregulated miR-155 suppresses the Suppressor of Cytokine Signalling 1 (SOCS1). Reduced SOCS1, in turn, led to enhanced phosphorylation of Signal Transducer and Activator of Transcription 1 (STAT1) and induction of Interferon-β (IFN-β), which promoted the expression of IFN-stimulated gene 54 (ISG54) and IFN-stimulated gene 56 (ISG56). In this study, miR-155 positively modulated the cellular antiviral response by enhancing type I IFN signalling through inhibition of SOCS1 in CHPV infected microglial cells.
MeSH term(s)	Child ; Humans ; Vesiculovirus/genetics ; Microglia ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Signal Transduction ; Immunity
Chemical Substances	MicroRNAs ; MIRN155 microRNA, human
Language	English
Publishing date	2023-06-15
Publishing country	France
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1465093-9
ISSN	1769-714X ; 1286-4579
ISSN (online)	1769-714X
ISSN	1286-4579
DOI	10.1016/j.micinf.2023.105173
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Zs.A 5014: Show issues

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Article ; Online: ORF3a of SARS-CoV-2 modulates PI3K/AKT signaling in human lung epithelial cells via hsa-miR-155-5p.

Ahmad, Faiyaz / Keshri, Vishal / Singh, Sunit K

International journal of biological macromolecules

2024 Volume 268, Issue Pt 1, Page(s) 131734

Abstract: SARS-CoV-2 infection results in cytokine burst, leading to proinflammatory responses in lungs of COVID-19 patients. SARS-CoV-2 ORF3a triggers the generation of proinflammatory cytokines. However, the underlying mechanism of dysregulation of ... ...

Abstract	SARS-CoV-2 infection results in cytokine burst, leading to proinflammatory responses in lungs of COVID-19 patients. SARS-CoV-2 ORF3a triggers the generation of proinflammatory cytokines. However, the underlying mechanism of dysregulation of proinflammatory responses is not well understood. We studied the role of microRNA in the generation of proinflammatory responses as a bystander effect of SARS-CoV-2 ORF3a in human lung epithelial cells. We observed upregulation of hsa-miR-155-5p in SARS-CoV-2 ORF3a transfected human lung epithelial cells, which led to the reduced expression of SHIP1. This resulted in phosphorylation of AKT and NF-κB, which further led to the increased expression of the proinflammatory cytokines IL-6 and TNF-α. Additionally, overexpression and knockdown studies of hsa-miR-155-5p were performed to confirm the role of hsa-miR-155-5p in the regulation of the SHIP1. We demonstrated that hsa-miR-155-5p modulates the proinflammatory response by activating the PI3K/AKT pathway through the inhibition of SHIP1 in SARS-CoV-2 ORF3a transfected human lung epithelial cells.
Language	English
Publishing date	2024-04-21
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	282732-3
ISSN	1879-0003 ; 0141-8130
ISSN (online)	1879-0003
ISSN	0141-8130
DOI	10.1016/j.ijbiomac.2024.131734
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Zs.B 2374: Show issues

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Article ; Online: Zika Virus NS1 Suppresses VE-Cadherin and Claudin-5 via hsa-miR-101-3p in Human Brain Microvascular Endothelial Cells.

Bhardwaj, Utkarsh / Singh, Sunit K

Molecular neurobiology

2021 Volume 58, Issue 12, Page(s) 6290–6303

Abstract: Zika virus (ZIKV) is a neurotropic virus that causes microcephaly in newborns and Guillain-Barré syndrome (GBS) in adults. ZIKV is known to transmigrate through the blood-brain barrier (BBB) by utilizing different strategies. NS1 is a conserved ... ...

Abstract	Zika virus (ZIKV) is a neurotropic virus that causes microcephaly in newborns and Guillain-Barré syndrome (GBS) in adults. ZIKV is known to transmigrate through the blood-brain barrier (BBB) by utilizing different strategies. NS1 is a conserved flavivirus protein, which is secreted extracellularly. ZIKV-NS1 has been shown to target adherens junctions (AJs) and tight junctions (TJs) to disrupt the endothelial barrier integrity. The microRNAs are short non-coding RNAs, which post-transcriptionally regulate the gene expression by binding to 3' UTR of the target gene. In the present study, we studied the ZIKV-NS1-mediated effect through hsa-miR-101-3p on the junctional barrier integrity in human brain microvascular endothelial cells. We exposed hBMVECs and hCMEC/D3 cells with ZIKV-NS1 at different time points (12 h and 24 h) with the doses 500 ng/mL and 1000 ng/mL. The change in the expression of VE-cadherin and claudin-5 was quantified using immunoblotting. The expression of the hsa-miR-101-3p was quantified using qRT-PCR. To prove the targeting of hsa-miR-101-3p to VE-cadherin, we transfected hsa-miR-101-3p mimic, scramble, hsa-miR-101-3p inhibitor, and Cy3 in the ZIKV-NS1-exposed hCMEC/D3 cells. The distribution and expression of the VE-cadherin and claudin-5 were observed using immunofluorescence and immunoblotting. The ZIKV-NS1 compromises the endothelial barrier integrity by disrupting the VE-cadherin and claudin-5 protein expression via hsa-miR-101-3p. The findings of this study suggest that ZIKV-NS1 dysregulates the adherens junction and tight junction proteins through hsa-miR-101-3p, which compromises the barrier integrity of human brain microvascular endothelial cells.
MeSH term(s)	Adherens Junctions/metabolism ; Antigens, CD/metabolism ; Brain/metabolism ; Brain/virology ; Cadherins/metabolism ; Claudin-5/metabolism ; Endothelial Cells/metabolism ; Endothelial Cells/virology ; Humans ; MicroRNAs/metabolism ; Tight Junctions/metabolism ; Zika Virus
Chemical Substances	Antigens, CD ; Cadherins ; Claudin-5 ; MicroRNAs ; cadherin 5
Language	English
Publishing date	2021-09-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	645020-9
ISSN	1559-1182 ; 0893-7648
ISSN (online)	1559-1182
ISSN	0893-7648
DOI	10.1007/s12035-021-02548-x
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 2411: Show issues

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Article ; Online: Hypoxia-Induced miR-101 Impairs Endothelial Barrier Integrity Through Altering VE-Cadherin and Claudin-5.

Shukla, Astha / Bhardwaj, Utkarsh / Apoorva / Seth, Pankaj / Singh, Sunit K

Molecular neurobiology

2023 Volume 61, Issue 3, Page(s) 1807–1817

Abstract: Stroke is a life-threatening medical condition across the world that adversely affects the integrity of the blood-brain barrier (BBB). The brain microvascular endothelial cells are the important constituent of the BBB. These cells line the blood vessels ... ...

Abstract	Stroke is a life-threatening medical condition across the world that adversely affects the integrity of the blood-brain barrier (BBB). The brain microvascular endothelial cells are the important constituent of the BBB. These cells line the blood vessels and form a semipermeable barrier. Disruptions in adherens junction and tight junction proteins of brain microvascular endothelial cells compromise the integrity of BBB. The Vascular Endothelial (VE)-cadherin is an integral adherens junction protein required for the establishment and maintenance of the endothelial barrier integrity. This study aims to investigate the role of miRNA in hypoxia-induced endothelial barrier disruption. In this study, brain endothelial cells were exposed to hypoxic conditions for different time points. Western blotting, overexpression and knockdown of miRNA, real-time PCR, TEER, and sodium fluorescein assay were used to examine the effect of hypoxic conditions on brain endothelial cells. Hypoxic exposure was validated using HIF-1α protein. Exposure to hypoxic conditions resulted to a significant decrease in endothelial barrier resistance and an increase in sodium fluorescein migration across the endothelial barrier. Reduction in endothelial barrier resistance demonstrated compromised barrier integrity, whereas the increase in migration of sodium fluorescein across the barrier indicated the increase in barrier permeability. The present study revealed microRNA-101 decreases the expression of VE-cadherin and claudin-5 in brain endothelial cells exposed to the hypoxic conditions.
MeSH term(s)	Humans ; Endothelial Cells/metabolism ; Claudin-5/genetics ; Claudin-5/metabolism ; Fluorescein/metabolism ; Fluorescein/pharmacology ; Cadherins/genetics ; Cadherins/metabolism ; Blood-Brain Barrier/metabolism ; Hypoxia/metabolism ; MicroRNAs/metabolism ; Antigens, CD
Chemical Substances	cadherin 5 ; Claudin-5 ; Fluorescein (TPY09G7XIR) ; Cadherins ; MicroRNAs ; MIRN101 microRNA, human ; Antigens, CD
Language	English
Publishing date	2023-09-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	645020-9
ISSN	1559-1182 ; 0893-7648
ISSN (online)	1559-1182
ISSN	0893-7648
DOI	10.1007/s12035-023-03662-8
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Zika virus NS1 affects the junctional integrity of human brain microvascular endothelial cells.

Rastogi, Meghana / Singh, Sunit K

Biochimie

2020 Volume 176, Page(s) 52–61

Abstract: Zika virus (ZIKV) infection leads to microcephaly in newborns. Flaviviruses are known to secrete NS1 protein extracellularly and its concentration in serum directly co-relate to disease severity. The presence of ZIKV-NS1 near the brain microvascular ... ...

Abstract	Zika virus (ZIKV) infection leads to microcephaly in newborns. Flaviviruses are known to secrete NS1 protein extracellularly and its concentration in serum directly co-relate to disease severity. The presence of ZIKV-NS1 near the brain microvascular endothelial cells (BMVECs) affects blood-brain-barrier, which is composed of tight junctions (TJs) and adherens junctions (AJs). Viruses utilize different strategies to circumvent this barrier to enter in brain. The present study demonstrated the mechanism of junctional integrity disruption in BMVECs by ZIKV-NS1 protein exposure. The Transendothelial Electrical Resistance and sodium fluorescein migration assays revealed the endothelial barrier disruption in BMVECs exposed to ZIKV-NS1 at different time (12hr and 24hr) and doses (500 ng/mL, 1000 ng/mL and 1500 ng/mL). The exposure of ZIKV-NS1 on BMVECs led to the phosphorylation of AJs and suppression of TJs through secreted ZIKV-NS1 in a bystander fashion. The activation of NADPH dependent reactive oxygen species activity and redox sensitive tyrosine kinase further increased the phosphorylation of AJs. The reduced expression of the phosphatase led to the increased phosphorylation of the AJs. The treatment with Diphenyleneiodonium chloride rescued the phosphatase and TJs expression and suppressed the expression of kinase and AJs in BMVECs exposed to ZIKV-NS1.
MeSH term(s)	Adherens Junctions/metabolism ; Brain/metabolism ; Endothelial Cells/metabolism ; Humans ; Microvessels/metabolism ; Tight Junctions/metabolism ; Viral Nonstructural Proteins/metabolism ; Viral Nonstructural Proteins/pharmacology ; Zika Virus/metabolism
Chemical Substances	NS1 protein, zika virus ; Viral Nonstructural Proteins
Language	English
Publishing date	2020-07-05
Publishing country	France
Document type	Journal Article
ZDB-ID	120345-9
ISSN	1638-6183 ; 0300-9084
ISSN (online)	1638-6183
ISSN	0300-9084
DOI	10.1016/j.biochi.2020.06.011
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Article: Zika virus NS1 affects the junctional integrity of human brain microvascular endothelial cells

Rastogi, Meghana / Singh, Sunit K

Biochimie. 2020 Sept., v. 176

2020

Abstract	Zika virus (ZIKV) infection leads to microcephaly in newborns. Flaviviruses are known to secrete NS1 protein extracellularly and its concentration in serum directly co-relate to disease severity. The presence of ZIKV-NS1 near the brain microvascular endothelial cells (BMVECs) affects blood-brain-barrier, which is composed of tight junctions (TJs) and adherens junctions (AJs). Viruses utilize different strategies to circumvent this barrier to enter in brain. The present study demonstrated the mechanism of junctional integrity disruption in BMVECs by ZIKV-NS1 protein exposure. The Transendothelial Electrical Resistance and sodium fluorescein migration assays revealed the endothelial barrier disruption in BMVECs exposed to ZIKV-NS1 at different time (12hr and 24hr) and doses (500 ng/mL, 1000 ng/mL and 1500 ng/mL). The exposure of ZIKV-NS1 on BMVECs led to the phosphorylation of AJs and suppression of TJs through secreted ZIKV-NS1 in a bystander fashion. The activation of NADPH dependent reactive oxygen species activity and redox sensitive tyrosine kinase further increased the phosphorylation of AJs. The reduced expression of the phosphatase led to the increased phosphorylation of the AJs. The treatment with Diphenyleneiodonium chloride rescued the phosphatase and TJs expression and suppressed the expression of kinase and AJs in BMVECs exposed to ZIKV-NS1.
Keywords	Zika virus ; blood serum ; blood-brain barrier ; brain ; chlorides ; disease severity ; electrical resistance ; fluorescein ; humans ; phosphorylation ; reactive oxygen species ; tyrosine
Language	English
Dates of publication	2020-09
Size	p. 52-61.
Publishing place	Elsevier B.V.
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	120345-9
ISSN	0300-9084
ISSN	0300-9084
DOI	10.1016/j.biochi.2020.06.011
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Article ; Online: Middle East Respiratory Syndrome Virus Pathogenesis.

Singh, Sunit K

Seminars in respiratory and critical care medicine

2016 Volume 37, Issue 4, Page(s) 572–577

Abstract: Coronaviruses (CoVs) are enveloped RNA viruses that infect birds, mammals, and humans. Infections caused by human coronaviruses (hCoVs) are mostly associated with the respiratory, enteric, and nervous systems. The hCoVs only occasionally induce lower ... ...

Abstract	Coronaviruses (CoVs) are enveloped RNA viruses that infect birds, mammals, and humans. Infections caused by human coronaviruses (hCoVs) are mostly associated with the respiratory, enteric, and nervous systems. The hCoVs only occasionally induce lower respiratory tract disease, including bronchitis, bronchiolitis, and pneumonia. In 2002 to 2003, a global outbreak of severe acute respiratory syndrome (SARS) was the seminal detection of a novel CoV (SARS-CoV). A decade later (June 2012), another novel CoV was implicated as the cause of Middle East respiratory syndrome (MERS) in Saudi Arabia. Although bats might serve as a reservoir of MERS-CoV, it is unlikely that they are the direct source for most human cases. Severe lines of evidence suggest that dromedary camels have been the major cause of transmission to humans. The emergence of MERS-CoV has triggered serious concerns about the potential for a widespread outbreak. All MERS cases were linked directly or indirectly to the Middle East region including Saudi Arabia, Jordan, Qatar, Oman, Kuwait, and UAE. MERS cases have also been reported in the later phases in the United Kingdom, France, Germany, Italy, Spain, and Tunisia. Most of these MERS cases were linked with the Middle East. The high mortality rates in family-based and hospital-based outbreaks were reported among patients with comorbidities such as diabetes and renal failure. MERS-CoV causes an acute, highly lethal pneumonia and renal dysfunction. The major complications reported in fatal cases are hyperkalemia with associated ventricular tachycardia, disseminated intravascular coagulation, pericarditis, and multiorgan failure. The case-fatality rate seems to be higher for MERS-CoV (around 30%) than for SARS-CoV (9.6%). The combination regimen of type 1 interferon + lopinavir/ritonavir is considered as the first-line therapy for MERS. Antiviral treatment is generally recommended for 10 to 14 days in patients with MERS-CoV infection. Convalescent plasma therapy has shown some efficacy among patients refractory to antiviral drugs if administered within 2 weeks of the onset of the disease.
MeSH term(s)	Animals ; Camelus/virology ; Coronavirus Infections/complications ; Coronavirus Infections/transmission ; Coronavirus Infections/virology ; Humans ; Middle East Respiratory Syndrome Coronavirus ; SARS Virus ; Severe Acute Respiratory Syndrome/complications ; Severe Acute Respiratory Syndrome/transmission ; Severe Acute Respiratory Syndrome/virology
Keywords	covid19
Language	English
Publishing date	2016-08-03
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1183617-9
ISSN	1098-9048 ; 1069-3424
ISSN (online)	1098-9048
ISSN	1069-3424
DOI	10.1055/s-0036-1584796
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