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Article ; Online: Aberrant Post-Transcriptional Regulation of Protein Expression in the Development of Chronic Obstructive Pulmonary Disease.

Aloufi, Noof / Alluli, Aeshah / Eidelman, David H / Baglole, Carolyn J

International journal of molecular sciences

2021 Volume 22, Issue 21

Abstract: Chronic obstructive pulmonary disease (COPD) is an incurable and prevalent respiratory disorder that is characterized by chronic inflammation and emphysema. COPD is primarily caused by cigarette smoke (CS). CS alters numerous cellular processes, ... ...

Abstract	Chronic obstructive pulmonary disease (COPD) is an incurable and prevalent respiratory disorder that is characterized by chronic inflammation and emphysema. COPD is primarily caused by cigarette smoke (CS). CS alters numerous cellular processes, including the post-transcriptional regulation of mRNAs. The identification of RNA-binding proteins (RBPs), microRNAs (miRNAs), and long non-coding RNAs (lncRNAs) as main factors engaged in the regulation of RNA biology opens the door to understanding their role in coordinating physiological cellular processes. Dysregulation of post-transcriptional regulation by foreign particles in CS may lead to the development of diseases such as COPD. Here we review current knowledge about post-transcriptional events that may be involved in the pathogenesis of COPD.
MeSH term(s)	Animals ; Gene Expression Regulation ; Humans ; Pulmonary Disease, Chronic Obstructive/genetics ; Pulmonary Disease, Chronic Obstructive/pathology ; RNA Processing, Post-Transcriptional
Language	English
Publishing date	2021-11-04
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms222111963
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Aberrant Post-Transcriptional Regulation of Protein Expression in the Development of Chronic Obstructive Pulmonary Disease

Noof Aloufi / Aeshah Alluli / David H. Eidelman / Carolyn J. Baglole

International Journal of Molecular Sciences, Vol 22, Iss 11963, p

2021 Volume 11963

Abstract	Chronic obstructive pulmonary disease (COPD) is an incurable and prevalent respiratory disorder that is characterized by chronic inflammation and emphysema. COPD is primarily caused by cigarette smoke (CS). CS alters numerous cellular processes, including the post-transcriptional regulation of mRNAs. The identification of RNA-binding proteins (RBPs), microRNAs (miRNAs), and long non-coding RNAs (lncRNAs) as main factors engaged in the regulation of RNA biology opens the door to understanding their role in coordinating physiological cellular processes. Dysregulation of post-transcriptional regulation by foreign particles in CS may lead to the development of diseases such as COPD. Here we review current knowledge about post-transcriptional events that may be involved in the pathogenesis of COPD.
Keywords	post-transcriptional regulation ; RNA binding proteins ; miRNAs ; COPD ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	570
Language	English
Publishing date	2021-11-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Endogenous regulation of the Akt pathway by the aryl hydrocarbon receptor (AhR) in lung fibroblasts.

Shi, Fangyi / Aloufi, Noof / Traboulsi, Hussein / Trempe, Jean-François / Eidelman, David H / Baglole, Carolyn J

Scientific reports

2021 Volume 11, Issue 1, Page(s) 23189

Abstract: The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor known to mediate toxic responses to dioxin. However, the role of the AhR in the regulation of cellular physiology has only recently been appreciated, including its ability to ... ...

Abstract	The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor known to mediate toxic responses to dioxin. However, the role of the AhR in the regulation of cellular physiology has only recently been appreciated, including its ability to control cell cycle progression and apoptosis by unknown mechanisms. We hypothesized that the AhR enhances the activation of the AKT serine/threonine kinase (Akt) pathway to promote cell survival. Utilizing AhR knock-out (Ahr
MeSH term(s)	Animals ; Cell Survival ; Cells, Cultured ; Cytoskeleton ; Fibroblasts/metabolism ; Gene Expression Regulation ; Homeostasis ; Intercellular Signaling Peptides and Proteins ; Lung/metabolism ; Mass Spectrometry ; Mice ; Phosphorylation ; Proteomics/methods ; Proto-Oncogene Proteins c-akt/biosynthesis ; Receptors, Aryl Hydrocarbon/metabolism ; Smoke ; Tetrazolium Salts/pharmacology ; Thiazoles/pharmacology ; Tobacco Products
Chemical Substances	Intercellular Signaling Peptides and Proteins ; Receptors, Aryl Hydrocarbon ; Smoke ; Tetrazolium Salts ; Thiazoles ; Akt1 protein, mouse (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; thiazolyl blue (EUY85H477I)
Language	English
Publishing date	2021-11-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-02339-3
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Article: The Prevalence of Acceptance Between General Anesthesia and Spinal Anesthesia Among Pregnant Women Undergoing Elective Caesarean Sections in Saudi Arabia.

Tawfeeq, Nasser A / Hilal, Faisal / Alharbi, Noof M / Alowid, Fay / Almaghrabi, Rana Y / Alsubhi, Rahaf / Alharbi, Shahd F / Fallatah, Amal / Aloufi, Leenah M / Alsaleh, Noor A

Cureus

2023 Volume 15, Issue 9, Page(s) e44972

Abstract: Background The choice of anesthesia for an elective cesarean section should be based on an individual benefit-risk assessment, considering the pregnant woman's preferences, concerns, and the available medical expertise. This study aimed to determine the ... ...

Abstract	Background The choice of anesthesia for an elective cesarean section should be based on an individual benefit-risk assessment, considering the pregnant woman's preferences, concerns, and the available medical expertise. This study aimed to determine the preferences for general and spinal anesthesia among women undergoing elective cesarean sections and the factors affecting their choice. Methods The study design is a cross-sectional study, and it was conducted on pregnant women to measure the acceptance of general anesthesia and spinal anesthesia in patients with elective cesarean sections in Saudi Arabia. Random pregnant women were invited to participate in this study across Saudi Arabia after fulfilling the inclusion criteria. A digital questionnaire was distributed across Saudi Arabia to be filled out by female residents. A Microsoft Excel (Microsoft Corporation, Redmond, Washington, USA
Language	English
Publishing date	2023-09-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	2747273-5
ISSN	2168-8184
ISSN	2168-8184
DOI	10.7759/cureus.44972
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Article: Standardized Cannabis Smoke Extract Induces Inflammation in Human Lung Fibroblasts.

Aloufi, Noof / Namkung, Yoon / Traboulsi, Hussein / Wilson, Emily T / Laporte, Stephane A / Kaplan, Barbara L F / Ross, Matthew K / Nair, Parameswaran / Eidelman, David H / Baglole, Carolyn J

Frontiers in pharmacology

2022 Volume 13, Page(s) 852029

Abstract: Cannabis (marijuana) is the most commonly used illicit product in the world and is the second most smoked plant after tobacco. There has been a rapid increase in the number of countries legalizing cannabis for both recreational and medicinal purposes. ... ...

Abstract	Cannabis (marijuana) is the most commonly used illicit product in the world and is the second most smoked plant after tobacco. There has been a rapid increase in the number of countries legalizing cannabis for both recreational and medicinal purposes. Smoking cannabis in the form of a joint is the most common mode of cannabis consumption. Combustion of cannabis smoke generates many of the same chemicals as tobacco smoke. Although the impact of tobacco smoke on respiratory health is well-known, the consequence of cannabis smoke on the respiratory system and, in particular, the inflammatory response is unclear. Besides the combustion products present in cannabis smoke, cannabis also contains cannabinoids including Δ
Language	English
Publishing date	2022-03-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2022.852029
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Article ; Online: HuR drives lung fibroblast differentiation but not metabolic reprogramming in response to TGF-β and hypoxia.

Trivlidis, Joshua / Aloufi, Noof / Al-Habeeb, Fatmah / Nair, Parameswaran / Azuelos, Ilan / Eidelman, David H / Baglole, Carolyn J

Respiratory research

2021 Volume 22, Issue 1, Page(s) 323

Abstract: Background: Pulmonary fibrosis is thought to be driven by recurrent alveolar epithelial injury which leads to the differentiation of fibroblasts into α-smooth muscle actin (α-SMA)-expressing myofibroblasts and subsequent deposition of extracellular ... ...

Abstract	Background: Pulmonary fibrosis is thought to be driven by recurrent alveolar epithelial injury which leads to the differentiation of fibroblasts into α-smooth muscle actin (α-SMA)-expressing myofibroblasts and subsequent deposition of extracellular matrix (ECM). Transforming growth factor beta-1 (TGF-β1) plays a key role in fibroblast differentiation, which we have recently shown involves human antigen R (HuR). HuR is an RNA binding protein that also increases the translation of hypoxia inducible factor (HIF-1α) mRNA, a transcription factor critical for inducing a metabolic shift from oxidative phosphorylation towards glycolysis. This metabolic shift may cause fibroblast differentiation. We hypothesized that under hypoxic conditions, HuR controls myofibroblast differentiation and glycolytic reprogramming in human lung fibroblasts (HLFs). Methods: Primary HLFs were cultured in the presence (or absence) of TGF-β1 (5 ng/ml) under hypoxic (1% O Results: Hypoxia alone had no significant effect on fibroblast differentiation or metabolic reprogramming. While hypoxia- together with TGFβ1- increased mRNA levels of differentiation and glycolysis genes, such as ACTA2, LDHA, and HK2, protein levels of α-SMA and collagen 1 were significantly reduced. Hypoxia induced cytoplasmic translocation of HuR. Knockdown of HuR reduced features of fibroblast differentiation in response to TGF-β1 with and without hypoxia, including α-SMA and the ECM marker collagen I, but had no effect on lactate secretion. Conclusions: Hypoxia reduced myofibroblasts differentiation and lactate secretion in conjunction with TGF-β. HuR is an important protein in the regulation of myofibroblast differentiation but does not control glycolysis in HLFs in response to hypoxia. More research is needed to understand the functional implications of HuR in IPF pathogenesis.
MeSH term(s)	Cell Differentiation/drug effects ; Cell Differentiation/physiology ; Cell Hypoxia/drug effects ; Cell Hypoxia/physiology ; Cells, Cultured ; Cellular Reprogramming/drug effects ; Cellular Reprogramming/physiology ; Dose-Response Relationship, Drug ; ELAV-Like Protein 1/genetics ; ELAV-Like Protein 1/metabolism ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; Humans ; Lung/cytology ; Lung/drug effects ; Lung/metabolism ; Transforming Growth Factor beta/pharmacology
Chemical Substances	ELAV-Like Protein 1 ; ELAVL1 protein, human ; Transforming Growth Factor beta
Language	English
Publishing date	2021-12-28
Publishing country	England
Document type	Journal Article
ZDB-ID	2041675-1
ISSN	1465-993X ; 1465-993X
ISSN (online)	1465-993X
ISSN	1465-993X
DOI	10.1186/s12931-021-01916-4
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Article ; Online: Endogenous regulation of the Akt pathway by the aryl hydrocarbon receptor (AhR) in lung fibroblasts

Fangyi Shi / Noof Aloufi / Hussein Traboulsi / Jean-François Trempe / David H. Eidelman / Carolyn J. Baglole

Scientific Reports, Vol 11, Iss 1, Pp 1-

2021 Volume 16

Abstract: Abstract The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor known to mediate toxic responses to dioxin. However, the role of the AhR in the regulation of cellular physiology has only recently been appreciated, including its ... ...

Abstract	Abstract The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor known to mediate toxic responses to dioxin. However, the role of the AhR in the regulation of cellular physiology has only recently been appreciated, including its ability to control cell cycle progression and apoptosis by unknown mechanisms. We hypothesized that the AhR enhances the activation of the AKT serine/threonine kinase (Akt) pathway to promote cell survival. Utilizing AhR knock-out (Ahr −/−) and wild-type (Ahr +/+) mouse lung fibroblasts (MLFs), we found that Ahr −/− MLFs have significantly higher basal Akt phosphorylation but that AhR did not affect Akt phosphorylation in MLFs exposed to growth factors or AhR ligands. Basal Akt phosphorylation was dependent on PI3K but was unaffected by changes in intracellular glutathione (GSH) or p85α. There was no significant decrease in cell viability in Ahr −/− MLFs treated with LY294002—a PI3K inhibitor—although LY294002 did attenuate MTT reduction, indicating an affect on mitochondrial function. Using a mass spectrometry (MS)-based approach, we identified several proteins that were differentially phosphorylated in the Ahr −/− MLFs compared to control cells, including proteins involved in the regulation of extracellular matrix (ECM), focal adhesion, cytoskeleton remodeling and mitochondrial function. In conclusion, Ahr ablation increased basal Akt phosphorylation in MLFs. Our results indicate that AhR may modulate the phosphorylation of a variety of novel proteins not previously identified as AhR targets, findings that help advance our understanding of the endogenous functions of AhR.
Keywords	Medicine ; R ; Science ; Q
Subject code	500
Language	English
Publishing date	2021-11-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Role of Human Antigen R (HuR) in the Regulation of Pulmonary ACE2 Expression

Noof Aloufi / Zahraa Haidar / Jun Ding / Parameswaran Nair / Andrea Benedetti / David H. Eidelman / Imed-Eddine Gallouzi / Sergio Di Marco / Sabah N. Hussain / Carolyn J. Baglole

Cells, Vol 11, Iss 22, p

2022 Volume 22

Abstract: Patients with COPD may be at an increased risk for severe illness from COVID-19 because of ACE2 upregulation, the entry receptor for SARS-CoV-2. Chronic exposure to cigarette smoke, the main risk factor for COPD, increases pulmonary ACE2. How ACE2 ... ...

Abstract	Patients with COPD may be at an increased risk for severe illness from COVID-19 because of ACE2 upregulation, the entry receptor for SARS-CoV-2. Chronic exposure to cigarette smoke, the main risk factor for COPD, increases pulmonary ACE2. How ACE2 expression is controlled is not known but may involve HuR, an RNA binding protein that increases protein expression by stabilizing mRNA. We hypothesized that HuR would increase ACE2 protein expression. We analyzed scRNA-seq data to profile ELAVL1 expression in distinct respiratory cell populations in COVID-19 and COPD patients. HuR expression and cellular localization was evaluated in COPD lung tissue by multiplex immunohistochemistry and in human lung cells by imaging flow cytometry. The regulation of ACE2 expression was evaluated using siRNA-mediated knockdown of HuR. There is a significant positive correlation between ELAVL1 and ACE2 in COPD cells. HuR cytoplasmic localization is higher in smoker and COPD lung tissue; there were also higher levels of cleaved HuR (CP-1). HuR binds to ACE2 mRNA but knockdown of HuR does not change ACE2 protein levels in primary human lung fibroblasts (HLFs). Our work is the first to investigate the association between ACE2 and HuR. Further investigation is needed to understand the mechanistic underpinning behind the regulation of ACE2 expression.
Keywords	HuR ; ACE2 ; fibroblast ; COVID-19 ; chronic obstructive pulmonary disease ; ELAVL1 ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2022-12-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Role of Human Antigen R (HuR) in the Regulation of Pulmonary ACE2 Expression.

Aloufi, Noof / Haidar, Zahraa / Ding, Jun / Nair, Parameswaran / Benedetti, Andrea / Eidelman, David H / Gallouzi, Imed-Eddine / Di Marco, Sergio / Hussain, Sabah N / Baglole, Carolyn J

Cells

2021 Volume 11, Issue 1

Abstract	Patients with COPD may be at an increased risk for severe illness from COVID-19 because of ACE2 upregulation, the entry receptor for SARS-CoV-2. Chronic exposure to cigarette smoke, the main risk factor for COPD, increases pulmonary ACE2. How ACE2 expression is controlled is not known but may involve HuR, an RNA binding protein that increases protein expression by stabilizing mRNA. We hypothesized that HuR would increase ACE2 protein expression. We analyzed scRNA-seq data to profile
MeSH term(s)	Aged ; Angiotensin-Converting Enzyme 2/genetics ; Angiotensin-Converting Enzyme 2/metabolism ; COVID-19/genetics ; COVID-19/metabolism ; COVID-19/virology ; Cells, Cultured ; ELAV-Like Protein 1/genetics ; ELAV-Like Protein 1/metabolism ; Female ; Fibroblasts/metabolism ; Gene Expression Profiling/methods ; Gene Expression Regulation ; Humans ; Lung/metabolism ; Lung/pathology ; Lung/virology ; Male ; Middle Aged ; Pulmonary Disease, Chronic Obstructive/genetics ; Pulmonary Disease, Chronic Obstructive/metabolism ; Pulmonary Disease, Chronic Obstructive/virology ; RNA Interference ; RNA-Seq/methods ; SARS-CoV-2/physiology ; Single-Cell Analysis/methods
Chemical Substances	ELAV-Like Protein 1 ; ELAVL1 protein, human ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
Language	English
Publishing date	2021-12-22
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11010022
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Article ; Online: Human antigen R promotes lung fibroblast differentiation to myofibroblasts and increases extracellular matrix production.

Al-Habeeb, Fatmah / Aloufi, Noof / Traboulsi, Hussein / Liu, Xingxing / Nair, Parameswaran / Haston, Christina / Azuelos, Ilan / Huang, Steven K / White, Eric S / Gallouzi, Imed E / Di Marco, Sergio / Eidelman, David H / Baglole, Carolyn J

Journal of cellular physiology

2021 Volume 236, Issue 10, Page(s) 6836–6851

Abstract: Idiopathic pulmonary fibrosis (IPF) is a disease of progressive scarring caused by excessive extracellular matrix (ECM) deposition and activation of α-SMA-expressing myofibroblasts. Human antigen R (HuR) is an RNA binding protein that promotes protein ... ...

Abstract	Idiopathic pulmonary fibrosis (IPF) is a disease of progressive scarring caused by excessive extracellular matrix (ECM) deposition and activation of α-SMA-expressing myofibroblasts. Human antigen R (HuR) is an RNA binding protein that promotes protein translation. Upon translocation from the nucleus to the cytoplasm, HuR functions to stabilize messenger RNA (mRNA) to increase protein levels. However, the role of HuR in promoting ECM production, myofibroblast differentiation, and lung fibrosis is unknown. Human lung fibroblasts (HLFs) treated with transforming growth factor β1 (TGF-β1) showed a significant increase in translocation of HuR from the nucleus to the cytoplasm. TGF-β-treated HLFs that were transfected with HuR small interfering RNA had a significant reduction in α-SMA protein as well as the ECM proteins COL1A1, COL3A, and FN1. HuR was also bound to mRNA for ACTA2, COL1A1, COL3A1, and FN. HuR knockdown affected the mRNA stability of ACTA2 but not that of the ECM genes COL1A1, COL3A1, or FN. In mouse models of pulmonary fibrosis, there was higher cytoplasmic HuR in lung structural cells compared to control mice. In human IPF lungs, there was also more cytoplasmic HuR. This study is the first to show that HuR in lung fibroblasts controls their differentiation to myofibroblasts and consequent ECM production. Further research on HuR could assist in establishing the basis for the development of new target therapy for fibrotic diseases, such as IPF.
MeSH term(s)	Actins/genetics ; Actins/metabolism ; Animals ; Cell Transdifferentiation/drug effects ; Cells, Cultured ; Disease Models, Animal ; ELAV-Like Protein 1/genetics ; ELAV-Like Protein 1/metabolism ; Extracellular Matrix/drug effects ; Extracellular Matrix/metabolism ; Extracellular Matrix/pathology ; Extracellular Matrix Proteins/genetics ; Extracellular Matrix Proteins/metabolism ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Gene Expression Regulation ; Humans ; Idiopathic Pulmonary Fibrosis/genetics ; Idiopathic Pulmonary Fibrosis/metabolism ; Idiopathic Pulmonary Fibrosis/pathology ; Lung/drug effects ; Lung/metabolism ; Lung/pathology ; Mice ; Myofibroblasts/metabolism ; Myofibroblasts/pathology ; Transforming Growth Factor beta1/pharmacology
Chemical Substances	ACTA2 protein, human ; Acta2 protein, mouse ; Actins ; ELAV-Like Protein 1 ; ELAVL1 protein, human ; Elavl1 protein, mouse ; Extracellular Matrix Proteins ; Transforming Growth Factor beta1
Language	English
Publishing date	2021-04-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3116-1
ISSN	1097-4652 ; 0021-9541
ISSN (online)	1097-4652
ISSN	0021-9541
DOI	10.1002/jcp.30380
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