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Article ; Online: Functions of RNA-Binding Proteins in Cardiovascular Disease.

Ruffenach, Grégoire / Medzikovic, Lejla / Sun, Wasila / Hong, Jason / Eghbali, Mansoureh

2023 Volume 12, Issue 24

Abstract: Gene expression is under tight regulation from the chromatin structure that regulates gene accessibility by the transcription machinery to protein degradation. At the transcript level, this regulation falls on RNA-binding proteins (RBPs). RBPs are a ... ...

Abstract	Gene expression is under tight regulation from the chromatin structure that regulates gene accessibility by the transcription machinery to protein degradation. At the transcript level, this regulation falls on RNA-binding proteins (RBPs). RBPs are a large and diverse class of proteins involved in all aspects of a transcript's lifecycle: splicing and maturation, localization, stability, and translation. In the past few years, our understanding of the role of RBPs in cardiovascular diseases has expanded. Here, we discuss the general structure and function of RBPs and the latest discoveries of their role in pulmonary and systemic cardiovascular diseases.
MeSH term(s)	Humans ; Cardiovascular Diseases/genetics ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism ; RNA Splicing
Chemical Substances	RNA-Binding Proteins
Language	English
Publishing date	2023-12-08
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; 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/cells12242794
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Article ; Online: Role of miRNA-1 and miRNA-21 in Acute Myocardial Ischemia-Reperfusion Injury and Their Potential as Therapeutic Strategy.

Jayawardena, Eranthi / Medzikovic, Lejla / Ruffenach, Gregoire / Eghbali, Mansoureh

International journal of molecular sciences

2022 Volume 23, Issue 3

Abstract: Coronary artery disease remains the leading cause of death. Acute myocardial infarction (MI) is characterized by decreased blood flow to the coronary arteries, resulting in cardiomyocytes death. The most effective strategy for treating an MI is early and ...

Abstract	Coronary artery disease remains the leading cause of death. Acute myocardial infarction (MI) is characterized by decreased blood flow to the coronary arteries, resulting in cardiomyocytes death. The most effective strategy for treating an MI is early and rapid myocardial reperfusion, but restoring blood flow to the ischemic myocardium can induce further damage, known as ischemia-reperfusion (IR) injury. Novel therapeutic strategies are critical to limit myocardial IR injury and improve patient outcomes following reperfusion intervention. miRNAs are small non-coding RNA molecules that have been implicated in attenuating IR injury pathology in pre-clinical rodent models. In this review, we discuss the role of miR-1 and miR-21 in regulating myocardial apoptosis in ischemia-reperfusion injury in the whole heart as well as in different cardiac cell types with special emphasis on cardiomyocytes, fibroblasts, and immune cells. We also examine therapeutic potential of miR-1 and miR-21 in preclinical studies. More research is necessary to understand the cell-specific molecular principles of miRNAs in cardioprotection and application to acute myocardial IR injury.
MeSH term(s)	Animals ; Gene Expression Regulation ; Genetic Therapy ; Humans ; MicroRNAs/genetics ; Myocardial Reperfusion Injury/genetics ; Myocardial Reperfusion Injury/therapy ; Translational Science, Biomedical
Chemical Substances	MIRN1 microRNA, human ; MIRN21 microRNA, human ; MicroRNAs
Language	English
Publishing date	2022-01-28
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/ijms23031512
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Article ; Online: HNRNPA2B1: RNA-Binding Protein That Orchestrates Smooth Muscle Cell Phenotype in Pulmonary Arterial Hypertension.

Ruffenach, Grégoire / Medzikovic, Lejla / Aryan, Laila / Li, Min / Eghbali, Mansoureh

Circulation

2022 Volume 146, Issue 16, Page(s) 1243–1258

Abstract: Background: RNA-binding proteins are master orchestrators of gene expression regulation. They regulate hundreds of transcripts at once by recognizing specific motifs. Thus, characterizing RNA-binding proteins targets is critical to harvest their full ... ...

Abstract	Background: RNA-binding proteins are master orchestrators of gene expression regulation. They regulate hundreds of transcripts at once by recognizing specific motifs. Thus, characterizing RNA-binding proteins targets is critical to harvest their full therapeutic potential. However, such investigation has often been restricted to a few RNA-binding protein targets, limiting our understanding of their function. In cancer, the RNA-binding protein HNRNPA2B1 (heterogeneous nuclear ribonucleoprotein A2B1; A2B1) promotes the pro-proliferative/anti-apoptotic phenotype. The same phenotype in pulmonary arterial smooth muscle cells (PASMCs) is responsible for the development of pulmonary arterial hypertension (PAH). However, A2B1 function has never been investigated in PAH. Method: Through the integration of computational and experimental biology, the authors investigated the role of A2B1 in human PAH-PASMC. Bioinformatics and RNA sequencing allowed them to investigate the transcriptome-wide function of A2B1, and RNA immunoprecipitation and A2B1 silencing experiments allowed them to decipher the intricate molecular mechanism at play. In addition, they performed a preclinical trial in the monocrotaline-induced pulmonary hypertension rat model to investigate the relevance of A2B1 inhibition in mitigating pulmonary hypertension severity. Results: They found that A2B1 expression and its nuclear localization are increased in human PAH-PASMC. Using bioinformatics, they identified 3 known motifs of A2B1 and all mRNAs carrying them. In PAH-PASMC, they demonstrated the complementary nonredundant function of A2B1 motifs because all motifs are implicated in different aspects of the cell cycle. In addition, they showed that in PAH-PASMC, A2B1 promotes the expression of its targets. A2B1 silencing in PAH-PASMC led to a decrease of all tested mRNAs carrying an A2B1 motif and a concomitant decrease in proliferation and resistance to apoptosis. Last, in vivo A2B1 inhibition in the lungs rescued pulmonary hypertension in rats. Conclusions: Through the integration of computational and experimental biology, the study revealed the role of A2B1 as a master orchestrator of the PAH-PASMC phenotype and its relevance as a therapeutic target in PAH.
MeSH term(s)	Animals ; Humans ; Rats ; Cell Proliferation ; Familial Primary Pulmonary Hypertension/metabolism ; Heterogeneous-Nuclear Ribonucleoproteins/genetics ; Hypertension, Pulmonary/metabolism ; Monocrotaline/metabolism ; Monocrotaline/toxicity ; Muscle, Smooth, Vascular/metabolism ; Myocytes, Smooth Muscle/metabolism ; Phenotype ; Pulmonary Arterial Hypertension ; Pulmonary Artery ; RNA/metabolism ; RNA-Binding Proteins/genetics
Chemical Substances	Heterogeneous-Nuclear Ribonucleoproteins ; Monocrotaline (73077K8HYV) ; RNA (63231-63-0) ; RNA-Binding Proteins
Language	English
Publishing date	2022-08-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80099-5
ISSN	1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
ISSN (online)	1524-4539
ISSN	0009-7322 ; 0069-4193 ; 0065-8499
DOI	10.1161/CIRCULATIONAHA.122.059591
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Article ; Online: Pulmonary hypertension secondary to pulmonary fibrosis: clinical data, histopathology and molecular insights.

Ruffenach, Grégoire / Hong, Jason / Vaillancourt, Mylène / Medzikovic, Lejla / Eghbali, Mansoureh

Respiratory research

2020 Volume 21, Issue 1, Page(s) 303

Abstract: Pulmonary hypertension (PH) developing secondarily in pulmonary fibrosis (PF) patients (PF-PH) is a frequent co-morbidity. The high prevalence of PH in PF patients is very concerning since the presence of PH is a strong predictor of mortality in PF ... ...

Abstract	Pulmonary hypertension (PH) developing secondarily in pulmonary fibrosis (PF) patients (PF-PH) is a frequent co-morbidity. The high prevalence of PH in PF patients is very concerning since the presence of PH is a strong predictor of mortality in PF patients. Until recently, PH was thought to arise solely from fibrotic destruction of the lung parenchyma, leading to hypoxic vasoconstriction and loss of vascular bed density. Thus, potential cellular and molecular dysregulation of vascular remodeling as a driver of PF-PH has been under-investigated. The recent demonstrations that there is no correlation between the severity of the fibrosis and development of PH, along with the finding that significant vascular histological and molecular differences exist between patients with and without PH have shifted the etiological paradigm of PF-PH. This review aims to provide a comprehensive translational overview of PH in PF patients from clinical diagnosis and outcome to the latest understanding of the histology and molecular pathophysiology of PF-PH.
MeSH term(s)	Animals ; Echocardiography/methods ; Humans ; Hypertension, Pulmonary/etiology ; Hypertension, Pulmonary/metabolism ; Hypertension, Pulmonary/pathology ; Inflammation Mediators/metabolism ; Lung/metabolism ; Lung/pathology ; Pulmonary Fibrosis/complications ; Pulmonary Fibrosis/metabolism ; Pulmonary Fibrosis/pathology ; Respiratory Function Tests/methods ; Vascular Remodeling/physiology
Chemical Substances	Inflammation Mediators
Language	English
Publishing date	2020-11-18
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2041675-1
ISSN	1465-993X ; 1465-9921
ISSN (online)	1465-993X
ISSN	1465-9921
DOI	10.1186/s12931-020-01570-2
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Article ; Online: Tm4sf1

Hong, Jason / Wong, Brenda / Huynh, Caroline / Tang, Brian / Ruffenach, Gregoire / Li, Min / Umar, Soban / Yang, Xia / Eghbali, Mansoureh

American journal of respiratory cell and molecular biology

2022 Volume 68, Issue 4, Page(s) 381–394

Abstract: The identification and role of endothelial progenitor cells in pulmonary arterial hypertension (PAH) remain controversial. Single-cell omics analysis can shed light on endothelial progenitor cells and their potential contribution to PAH pathobiology. We ... ...

Abstract	The identification and role of endothelial progenitor cells in pulmonary arterial hypertension (PAH) remain controversial. Single-cell omics analysis can shed light on endothelial progenitor cells and their potential contribution to PAH pathobiology. We aim to identify endothelial cells that may have stem/progenitor potential in rat lungs and assess their relevance to PAH. Differential expression, gene set enrichment, cell-cell communication, and trajectory reconstruction analyses were performed on lung endothelial cells from single-cell RNA sequencing of Sugen-hypoxia, monocrotaline, and control rats. Relevance to human PAH was assessed in multiple independent blood and lung transcriptomic data sets. Rat lung endothelial cells were visualized by immunofluorescence
MeSH term(s)	Animals ; Humans ; Rats ; Antigens, Surface/metabolism ; Disease Models, Animal ; Endothelial Progenitor Cells ; Endothelium ; Familial Primary Pulmonary Hypertension/metabolism ; Monocrotaline ; Neoplasm Proteins/metabolism ; Pulmonary Arterial Hypertension/metabolism ; Pulmonary Artery/metabolism
Chemical Substances	Antigens, Surface ; Monocrotaline (73077K8HYV) ; Neoplasm Proteins ; TM4SF1 protein, human (147016-68-0) ; Tm4sf1 protein, rat
Language	English
Publishing date	2022-10-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1025960-0
ISSN	1535-4989 ; 1044-1549
ISSN (online)	1535-4989
ISSN	1044-1549
DOI	10.1165/rcmb.2022-0020OC
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Article ; Online: Myocardial fibrosis and calcification are attenuated by microRNA-129-5p targeting Asporin and Sox9 in cardiac fibroblasts.

Medzikovic, Lejla / Aryan, Laila / Ruffenach, Grégoire / Li, Min / Savalli, Nicoletta / Sun, Wasila / Sarji, Shervin / Hong, Jason / Sharma, Salil / Olcese, Riccardo / Fishbein, Gregory / Eghbali, Mansoureh

JCI insight

2023 Volume 8, Issue 9

Abstract: Myocardial fibrosis and calcification associate with adverse outcomes in nonischemic heart failure. Cardiac fibroblasts (CF) transition into myofibroblasts (MF) and osteogenic fibroblasts (OF) to promote myocardial fibrosis and calcification. However, ... ...

Abstract	Myocardial fibrosis and calcification associate with adverse outcomes in nonischemic heart failure. Cardiac fibroblasts (CF) transition into myofibroblasts (MF) and osteogenic fibroblasts (OF) to promote myocardial fibrosis and calcification. However, common upstream mechanisms regulating both CF-to-MF transition and CF-to-OF transition remain unknown. microRNAs are promising targets to modulate CF plasticity. Our bioinformatics revealed downregulation of miR-129-5p and upregulation of its targets small leucine-rich proteoglycan Asporin (ASPN) and transcription factor SOX9 as common in mouse and human heart failure (HF). We experimentally confirmed decreased miR-129-5p and enhanced SOX9 and ASPN expression in CF in human hearts with myocardial fibrosis and calcification. miR-129-5p repressed both CF-to-MF and CF-to-OF transition in primary CF, as did knockdown of SOX9 and ASPN. Sox9 and Aspn are direct targets of miR-129-5p that inhibit downstream β-catenin expression. Chronic Angiotensin II infusion downregulated miR-129-5p in CF in WT and TCF21-lineage CF reporter mice, and it was restored by miR-129-5p mimic. Importantly, miR-129-5p mimic not only attenuated progression of myocardial fibrosis, calcification marker expression, and SOX9 and ASPN expression in CF but also restored diastolic and systolic function. Together, we demonstrate miR-129-5p/ASPN and miR-129-5p/SOX9 as potentially novel dysregulated axes in CF-to-MF and CF-to-OF transition in myocardial fibrosis and calcification and the therapeutic relevance of miR-129-5p.
MeSH term(s)	Humans ; Mice ; Animals ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Cardiomyopathies/metabolism ; Fibroblasts/metabolism ; Heart Failure/metabolism ; Fibrosis ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; SOX9 Transcription Factor/genetics ; SOX9 Transcription Factor/metabolism
Chemical Substances	MicroRNAs ; TCF21 protein, human ; Basic Helix-Loop-Helix Transcription Factors ; SOX9 protein, human ; SOX9 Transcription Factor ; Mirn129 microRNA, human ; MIRN129 microRNA, mouse
Language	English
Publishing date	2023-05-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.168655
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Article: Experimental Pulmonary Hypertension Is Associated With Neuroinflammation in the Spinal Cord.

Vaillancourt, Mylene / Chia, Pamela / Medzikovic, Lejla / Cao, Nancy / Ruffenach, Gregoire / Younessi, David / Umar, Soban

Frontiers in physiology

2019 Volume 10, Page(s) 1186

Abstract: Rationale: Pulmonary hypertension (PH) is a rare but fatal disease characterized by elevated pulmonary pressures and vascular remodeling, leading to right ventricular failure and death. Recently, neuroinflammation has been suggested to be involved in ... ...

Abstract	Rationale: Pulmonary hypertension (PH) is a rare but fatal disease characterized by elevated pulmonary pressures and vascular remodeling, leading to right ventricular failure and death. Recently, neuroinflammation has been suggested to be involved in the sympathetic activation in experimental PH. Whether PH is associated with neuroinflammation in the spinal cord has never been investigated. Methods/results: PH was well-established in adult male Wistar rats 3-week after pulmonary endothelial toxin Monocrotaline (MCT) injection. Using the thoracic segments of the spinal cord, we found a 5-fold increase for the glial fibrillary acidic protein (GFAP) in PH rats compared to controls ( Conclusion: We report for the first time evidence for neuroinflammation in the thoracic spinal cord of pulmonary hypertensive rats. The impact of spinal cord inflammation on cardiopulmonary function in PH remains elusive.
Language	English
Publishing date	2019-09-20
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2019.01186
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Article ; Online: Y-Chromosome Gene,

Cunningham, Christine M / Li, Min / Ruffenach, Gregoire / Doshi, Mitali / Aryan, Laila / Hong, Jason / Park, John / Hrncir, Haley / Medzikovic, Lejla / Umar, Soban / Arnold, Arthur P / Eghbali, Mansoureh

American journal of respiratory and critical care medicine

2022 Volume 206, Issue 2, Page(s) 186–196

Abstract: Rationale: ...

Abstract	Rationale:
MeSH term(s)	Animals ; Chemokines/metabolism ; Disease Models, Animal ; Endothelial Cells/metabolism ; Familial Primary Pulmonary Hypertension/genetics ; Female ; Genes, Y-Linked ; Humans ; Hypertension, Pulmonary/genetics ; Hypoxia ; Male ; Mice ; Minor Histocompatibility Antigens/genetics ; Nuclear Proteins/genetics ; Pulmonary Artery ; Rats
Chemical Substances	Chemokines ; Minor Histocompatibility Antigens ; Nuclear Proteins ; UTY protein, human
Language	English
Publishing date	2022-04-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	1180953-x
ISSN	1535-4970 ; 0003-0805 ; 1073-449X
ISSN (online)	1535-4970
ISSN	0003-0805 ; 1073-449X
DOI	10.1164/rccm.202110-2309OC
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Article ; Online: Adaptation and remodelling of the pulmonary circulation in pulmonary hypertension.

Vaillancourt, Mylène / Ruffenach, Grégoire / Meloche, Jolyane / Bonnet, Sébastien

The Canadian journal of cardiology

2015 Volume 31, Issue 4, Page(s) 407–415

Abstract: Pulmonary arterial hypertension (PAH) is characterized by remodelling of pulmonary arteries caused by a proliferation/apoptosis imbalance within the vascular wall. This pathological phenotype seems to be triggered by different environmental stress and ... ...

Abstract	Pulmonary arterial hypertension (PAH) is characterized by remodelling of pulmonary arteries caused by a proliferation/apoptosis imbalance within the vascular wall. This pathological phenotype seems to be triggered by different environmental stress and injury events such as increased inflammation, DNA damage, and epigenetic deregulation. It appears that one of the first hit to occur is endothelial cells (ECs) injury and apoptosis, which leads to paracrine signalling to other ECs, pulmonary artery smooth muscle cells (PASMCs), and fibroblasts. These signals promote a phenotypic change of surviving ECs by disturbing different signalling pathways leading to sustained vasoconstriction, proproliferative and antiapoptotic phenotype, deregulated angiogenesis, and formation of plexiform lesions. EC signalling also recruits proinflammatory cells, leading to pulmonary infiltration of lymphocytes, macrophages, and dendritic cells, sustaining the inflammatory environment and autoimmune response. Finally, EC signalling promotes proliferative and antiapoptotic PAH-PASMC phenotypes, which acquire migratory capacities, resulting in increased vascular wall thickness and muscularization of small pulmonary arterioles. Adaptation and remodelling of pulmonary circulation also involves epigenetic components, such as microRNA deregulation, DNA methylation, and histone modification. This review will focus on the different cellular and epigenetic aspects including EC stress response, molecular mechanisms contributing to PAH-PASMC and PAEC proliferation and resistance to apoptosis, as well as epigenetic control involved in adaptation and remodelling of the pulmonary circulation in PAH.
MeSH term(s)	Adaptation, Physiological/physiology ; Humans ; Hypertension, Pulmonary/physiopathology ; Pulmonary Artery/physiopathology ; Pulmonary Circulation/physiology ; Pulmonary Wedge Pressure ; Vascular Remodeling/physiology
Language	English
Publishing date	2015-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	632813-1
ISSN	1916-7075 ; 0828-282X
ISSN (online)	1916-7075
ISSN	0828-282X
DOI	10.1016/j.cjca.2014.10.023
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Article ; Online: The Role of Estrogen Receptors in Cardiovascular Disease.

Aryan, Laila / Younessi, David / Zargari, Michael / Banerjee, Somanshu / Agopian, Jacqueline / Rahman, Shadie / Borna, Reza / Ruffenach, Gregoire / Umar, Soban / Eghbali, Mansoureh

International journal of molecular sciences

2020 Volume 21, Issue 12

Abstract: Cardiovascular Diseases (CVDs) are the leading cause of death globally. More than 17 million people die worldwide from CVD per year. There is considerable evidence suggesting that estrogen modulates cardiovascular physiology and function in both health ... ...

Abstract	Cardiovascular Diseases (CVDs) are the leading cause of death globally. More than 17 million people die worldwide from CVD per year. There is considerable evidence suggesting that estrogen modulates cardiovascular physiology and function in both health and disease, and that it could potentially serve as a cardioprotective agent. The effects of estrogen on cardiovascular function are mediated by nuclear and membrane estrogen receptors (ERs), including estrogen receptor alpha (ERα), estrogen receptor beta (ERβ), and G-protein-coupled ER (GPR30 or GPER). Receptor binding in turn confers pleiotropic effects through both genomic and non-genomic signaling to maintain cardiovascular homeostasis. Each ER has been implicated in multiple pre-clinical cardiovascular disease models. This review will discuss current reports on the underlying molecular mechanisms of the ERs in regulating vascular pathology, with a special emphasis on hypertension, pulmonary hypertension, and atherosclerosis, as well as in regulating cardiac pathology, with a particular emphasis on ischemia/reperfusion injury, heart failure with reduced ejection fraction, and heart failure with preserved ejection fraction.
MeSH term(s)	Animals ; Cardiovascular Diseases/diagnosis ; Cardiovascular Diseases/etiology ; Cardiovascular Diseases/metabolism ; Cardiovascular System/metabolism ; Cardiovascular System/pathology ; Cardiovascular System/physiopathology ; Disease Susceptibility ; Gene Expression Regulation ; Humans ; Receptors, Estrogen/genetics ; Receptors, Estrogen/metabolism ; Signal Transduction
Chemical Substances	Receptors, Estrogen
Language	English
Publishing date	2020-06-17
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/ijms21124314
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