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Article: Decreasing ELK3 expression improves Bone Morphogenetic Protein Receptor 2 signaling and pulmonary vascular cell function in PAH.

Ali, Md Khadem / Zhao, Lan / de Jesus Perez, Vinicio / Nicolls, Mark R / Spiekerkoetter, Edda F

bioRxiv : the preprint server for biology

2023

Abstract: ELK3 is upregulated in blood and pulmonary vascular cells of PAH patients and may play a significant role in PAH potentially through modulating BMPR2 signaling. ...

Abstract	ELK3 is upregulated in blood and pulmonary vascular cells of PAH patients and may play a significant role in PAH potentially through modulating BMPR2 signaling.
Language	English
Publishing date	2023-01-16
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.01.14.524023
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Article: Colorectal Cancer-Associated Microbiome Patterns and Signatures.

Zhao, Lan / Cho, William C / Nicolls, Mark R

Frontiers in genetics

2021 Volume 12, Page(s) 787176

Abstract: The gut microbiome is dynamic and shaped by diet, age, geography, and environment. The disruption of normal gut microbiota (dysbiosis) is closely related to colorectal cancer (CRC) risk and progression. To better identify and characterize CRC-associated ... ...

Abstract	The gut microbiome is dynamic and shaped by diet, age, geography, and environment. The disruption of normal gut microbiota (dysbiosis) is closely related to colorectal cancer (CRC) risk and progression. To better identify and characterize CRC-associated dysbiosis, we collected six independent cohorts with matched normal pairs (when available) for comparison and exploration of the microbiota and their interactions with the host. Comparing the microbial community compositions between cancerous and adjacent noncancerous tissues, we found that more microbes were depleted than enriched in tumors. Despite taxonomic variations among cohorts, consistent depletion of normal microbiota (members of
Language	English
Publishing date	2021-12-22
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606823-0
ISSN	1664-8021
ISSN	1664-8021
DOI	10.3389/fgene.2021.787176
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Article ; Online: B-cells in pulmonary arterial hypertension: friend, foe or bystander?

Sanges, Sébastien / Tian, Wen / Dubucquoi, Sylvain / Chang, Jason L / Collet, Aurore / Launay, David / Nicolls, Mark R

The European respiratory journal

2024 Volume 63, Issue 4

Abstract: There is an unmet need for new therapeutic strategies that target alternative pathways to improve the prognosis of patients with pulmonary arterial hypertension (PAH). As immunity has been involved in the development and progression of vascular lesions ... ...

Abstract	There is an unmet need for new therapeutic strategies that target alternative pathways to improve the prognosis of patients with pulmonary arterial hypertension (PAH). As immunity has been involved in the development and progression of vascular lesions in PAH, we review the potential contribution of B-cells in its pathogenesis and evaluate the relevance of B-cell-targeted therapies. Circulating B-cell homeostasis is altered in PAH patients, with total B-cell lymphopenia, abnormal subset distribution (expansion of naïve and antibody-secreting cells, reduction of memory B-cells) and chronic activation. B-cells are recruited to the lungs through local chemokine secretion, and activated by several mechanisms: 1) interaction with lung vascular autoantigens through cognate B-cell receptors; 2) costimulatory signals provided by T follicular helper cells (interleukin (IL)-21), type 2 T helper cells and mast cells (IL-4, IL-6 and IL-13); and 3) increased survival signals provided by B-cell activating factor pathways. This activity results in the formation of germinal centres within perivascular tertiary lymphoid organs and in the local production of pathogenic autoantibodies that target the pulmonary vasculature and vascular stabilisation factors (including angiotensin-II/endothelin-1 receptors and bone morphogenetic protein receptors). B-cells also mediate their effects through enhanced production of pro-inflammatory cytokines, reduced anti-inflammatory properties by regulatory B-cells, immunoglobulin (Ig)G-induced complement activation, and IgE-induced mast cell activation. Precision-medicine approaches targeting B-cell immunity are a promising direction for select PAH conditions, as suggested by the efficacy of anti-CD20 therapy in experimental models and a trial of rituximab in systemic sclerosis-associated PAH.
MeSH term(s)	Humans ; B-Lymphocytes/immunology ; Pulmonary Arterial Hypertension/immunology ; Animals ; Lung/immunology ; Autoantibodies/immunology ; Hypertension, Pulmonary/immunology
Chemical Substances	Autoantibodies
Language	English
Publishing date	2024-04-25
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	639359-7
ISSN	1399-3003 ; 0903-1936
ISSN (online)	1399-3003
ISSN	0903-1936
DOI	10.1183/13993003.01949-2023
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Zs.A 2322: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Airway hypoxia in lung transplantation.

Pasnupneti, Shravani / Nicolls, Mark R

Current opinion in physiology

2018 Volume 7, Page(s) 21–26

Abstract: Lung transplantation is a life-saving operation for patients with advanced lung disease. Pulmonary allografts eventually fail because of infection, thromboembolism, malignancy, airway complications, and chronic rejection, otherwise known as chronic lung ... ...

Abstract	Lung transplantation is a life-saving operation for patients with advanced lung disease. Pulmonary allografts eventually fail because of infection, thromboembolism, malignancy, airway complications, and chronic rejection, otherwise known as chronic lung allograft dysfunction (CLAD). Emerging evidence suggests that a highly-compromised airway circulation contributes to the evolution of airway complications and CLAD. There are two significant causes of poor perfusion and airway hypoxia in lung transplantation: an abnormal bronchial circulation which causes airway complications and microvascular rejection which induces CLAD. At the time of transplantation, the bronchial artery circulation, a natural component of the airway circulatory anatomy, is not surgically connected, and bronchi distal to the anastomosis become hypoxic. Subsequently, the bronchial anastomosis is left to heal under ischemic conditions. Still later, the extant microvessels in transplant bronchi are subjected to alloimmune insults that can further negatively impact pulmonary function. This review describes how airway tissue hypoxia evolves in lung transplantation, why depriving oxygenation in the bronchi and more distal bronchioles contributes to disease pathology and what therapeutic interventions are currently emerging to address these vascular injuries. Improving anastomotic vascular healing at the time of transplantation and preventing microvascular loss during acute rejection episodes are two steps that could limit airway hypoxia and improve patient outcomes.
Language	English
Publishing date	2018-12-13
Publishing country	England
Document type	Journal Article
ZDB-ID	2918626-2
ISSN	2468-8673 ; 2468-8681
ISSN (online)	2468-8673
ISSN	2468-8681
DOI	10.1016/j.cophys.2018.12.002
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Article ; Online: The Human Respiratory Microbiome: Current Understandings and Future Directions.

Zhao, Lan / Luo, Jun-Li / Ali, Mohammed Khadem / Spiekerkoetter, Edda / Nicolls, Mark R

American journal of respiratory cell and molecular biology

2022 Volume 68, Issue 3, Page(s) 245–255

Abstract: Microorganisms colonize the human body. The lungs and respiratory tract, previously believed to be sterile, harbor diverse microbial communities and the genomes of bacteria (bacteriome), viruses (virome), and fungi (mycobiome). Recent advances in ... ...

Abstract	Microorganisms colonize the human body. The lungs and respiratory tract, previously believed to be sterile, harbor diverse microbial communities and the genomes of bacteria (bacteriome), viruses (virome), and fungi (mycobiome). Recent advances in amplicon and shotgun metagenomic sequencing technologies and data-analyzing methods have greatly aided the identification and characterization of microbial populations from airways. The respiratory microbiome has been shown to play roles in human health and disease and is an area of rapidly emerging interest in pulmonary medicine. In this review, we provide updated information in the field by focusing on four lung conditions, including asthma, chronic obstructive pulmonary disease, cystic fibrosis, and idiopathic pulmonary fibrosis. We evaluate gut, oral, and upper airway microbiomes and how they contribute to lower airway flora. The discussion is followed by a systematic review of the lower airway microbiome in health and disease. We conclude with promising research avenues and implications for evolving therapeutics.
MeSH term(s)	Humans ; Lung/microbiology ; Asthma ; Pulmonary Disease, Chronic Obstructive/microbiology ; Microbiota ; Cystic Fibrosis/microbiology
Language	English
Publishing date	2022-12-07
Publishing country	United States
Document type	Systematic Review ; 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.2022-0208TR
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Zs.A 2851: Show issues

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Article ; Online: PTPN1 Deficiency Modulates BMPR2 Signaling and Induces Endothelial Dysfunction in Pulmonary Arterial Hypertension.

Ali, Md Khadem / Tian, Xuefei / Zhao, Lan / Schimmel, Katharina / Rhodes, Christopher J / Wilkins, Martin R / Nicolls, Mark R / Spiekerkoetter, Edda F

Cells

2023 Volume 12, Issue 2

Abstract: Bone morphogenic protein receptor 2 (BMPR2) expression and signaling are impaired in pulmonary arterial hypertension (PAH). How BMPR2 signaling is decreased in PAH is poorly understood. Protein tyrosine phosphatases (PTPs) play important roles in ... ...

Abstract	Bone morphogenic protein receptor 2 (BMPR2) expression and signaling are impaired in pulmonary arterial hypertension (PAH). How BMPR2 signaling is decreased in PAH is poorly understood. Protein tyrosine phosphatases (PTPs) play important roles in vascular remodeling in PAH. To identify whether PTPs modify BMPR2 signaling, we used a siRNA-mediated high-throughput screening of 22,124 murine genes in mouse myoblastoma reporter cells using ID1 expression as readout for BMPR2 signaling. We further experimentally validated the top hit, PTPN1 (PTP1B), in healthy human pulmonary arterial endothelial cells (PAECs) either silenced by siRNA or exposed to hypoxia and confirmed its relevance to PAH by measuring PTPN1 levels in blood and PAECs collected from PAH patients. We identified PTPN1 as a novel regulator of BMPR2 signaling in PAECs, which is downregulated in the blood of PAH patients, and documented that downregulation of PTPN1 is linked to endothelial dysfunction in PAECs. These findings point to a potential involvement for PTPN1 in PAH and will aid in our understanding of the molecular mechanisms involved in the disease.
MeSH term(s)	Animals ; Humans ; Mice ; Bone Morphogenetic Protein Receptors, Type II/genetics ; Bone Morphogenetic Protein Receptors, Type II/metabolism ; Endothelial Cells/metabolism ; Hypertension, Pulmonary/metabolism ; Protein Tyrosine Phosphatase, Non-Receptor Type 1/genetics ; Protein Tyrosine Phosphatase, Non-Receptor Type 1/metabolism ; Pulmonary Arterial Hypertension/metabolism ; Pulmonary Artery/metabolism ; RNA, Small Interfering/metabolism ; Vascular Diseases/metabolism
Chemical Substances	BMPR2 protein, human (EC 2.7.11.30) ; Bone Morphogenetic Protein Receptors, Type II (EC 2.7.11.30) ; Protein Tyrosine Phosphatase, Non-Receptor Type 1 (EC 3.1.3.48) ; PTPN1 protein, human (EC 3.1.3.48) ; RNA, Small Interfering ; Ptpn1 protein, mouse (EC 3.1.3.48) ; Bmpr2 protein, mouse (EC 2.7.11.30)
Language	English
Publishing date	2023-01-14
Publishing country	Switzerland
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; 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/cells12020316
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Article ; Online: Endotyping COPD: hypoxia-inducible factor-2 as a molecular "switch" between the vascular and airway phenotypes?

Myronenko, Oleh / Foris, Vasile / Crnkovic, Slaven / Olschewski, Andrea / Rocha, Sonia / Nicolls, Mark R / Olschewski, Horst

European respiratory review : an official journal of the European Respiratory Society

2023 Volume 32, Issue 167

Abstract: COPD is a heterogeneous disease with multiple clinical phenotypes. COPD endotypes can be determined by different expressions of hypoxia-inducible factors (HIFs), which, in combination with individual susceptibility and environmental factors, may cause ... ...

Abstract	COPD is a heterogeneous disease with multiple clinical phenotypes. COPD endotypes can be determined by different expressions of hypoxia-inducible factors (HIFs), which, in combination with individual susceptibility and environmental factors, may cause predominant airway or vascular changes in the lung. The pulmonary vascular phenotype is relatively rare among COPD patients and characterised by out-of-proportion pulmonary hypertension (PH) and low diffusing capacity of the lung for carbon monoxide, but only mild-to-moderate airway obstruction. Its histologic feature, severe remodelling of the small pulmonary arteries, can be mediated by HIF-2 overexpression in experimental PH models. HIF-2 is not only involved in the vascular remodelling but also in the parenchyma destruction. Endothelial cells from human emphysema lungs express reduced HIF-2α levels, and the deletion of pulmonary endothelial
MeSH term(s)	Animals ; Humans ; Mice ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Emphysema/metabolism ; Emphysema/pathology ; Endothelial Cells/pathology ; Hypertension, Pulmonary/genetics ; Hypertension, Pulmonary/metabolism ; Hypoxia ; Pulmonary Disease, Chronic Obstructive/genetics ; Pulmonary Disease, Chronic Obstructive/metabolism ; Pulmonary Disease, Chronic Obstructive/pathology ; Pulmonary Emphysema/genetics ; Pulmonary Emphysema/metabolism
Chemical Substances	Basic Helix-Loop-Helix Transcription Factors ; endothelial PAS domain-containing protein 1 (1B37H0967P)
Language	English
Publishing date	2023-01-11
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1077620-5
ISSN	1600-0617 ; 0905-9180
ISSN (online)	1600-0617
ISSN	0905-9180
DOI	10.1183/16000617.0173-2022
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Zs.A 3265: Show issues

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Article ; Online: Rat microbial biogeography and age-dependent lactic acid bacteria in healthy lungs.

Zhao, Lan / Cunningham, Christine M / Andruska, Adam M / Schimmel, Katharina / Ali, Md Khadem / Kim, Dongeon / Gu, Shenbiao / Chang, Jason L / Spiekerkoetter, Edda / Nicolls, Mark R

Lab animal

2024 Volume 53, Issue 2, Page(s) 43–55

Abstract: The laboratory rat emerges as a useful tool for studying the interaction between the host and its microbiome. To advance principles relevant to the human microbiome, we systematically investigated and defined the multitissue microbial biogeography of ... ...

Abstract	The laboratory rat emerges as a useful tool for studying the interaction between the host and its microbiome. To advance principles relevant to the human microbiome, we systematically investigated and defined the multitissue microbial biogeography of healthy Fischer 344 rats across their lifespan. Microbial community profiling data were extracted and integrated with host transcriptomic data from the Sequencing Quality Control consortium. Unsupervised machine learning, correlation, taxonomic diversity and abundance analyses were performed to determine and characterize the rat microbial biogeography and identify four intertissue microbial heterogeneity patterns (P1-P4). We found that the 11 body habitats harbored a greater diversity of microbes than previously suspected. Lactic acid bacteria (LAB) abundance progressively declined in lungs from breastfed newborn to adolescence/adult, and was below detectable levels in elderly rats. Bioinformatics analyses indicate that the abundance of LAB may be modulated by the lung-immune axis. The presence and levels of LAB in lungs were further evaluated by PCR in two validation datasets. The lung, testes, thymus, kidney, adrenal and muscle niches were found to have age-dependent alterations in microbial abundance. The 357 microbial signatures were positively correlated with host genes in cell proliferation (P1), DNA damage repair (P2) and DNA transcription (P3). Our study established a link between the metabolic properties of LAB with lung microbiota maturation and development. Breastfeeding and environmental exposure influence microbiome composition and host health and longevity. The inferred rat microbial biogeography and pattern-specific microbial signatures could be useful for microbiome therapeutic approaches to human health and life quality enhancement.
MeSH term(s)	Humans ; Rats ; Animals ; Bacteria ; Lactobacillales ; Lung/microbiology ; Microbiota/genetics
Language	English
Publishing date	2024-01-31
Publishing country	United States
Document type	Journal Article
ISSN	1548-4475
ISSN (online)	1548-4475
DOI	10.1038/s41684-023-01322-x
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Article ; Online: VIEWING PULMONARY HYPERTENSION THROUGH A PEDIATRIC LENS.

Agarwal, Stuti / Fineman, Jeffrey / Cornfield, David N / Alvira, Cristina M / Zamanian, Roham T / Goss, Kara / Yuan, Ke / Bonnet, Sebastien / Boucherat, Olivier / Pullamsetti, Soni / Alcázar, Miguel A / Goncharova, Elena / Kudryashova, Tatiana V / Nicolls, Mark R / de Jesús Pérez, Vinicio

The European respiratory journal

2024

Language	English
Publishing date	2024-04-04
Publishing country	England
Document type	Journal Article
ZDB-ID	639359-7
ISSN	1399-3003 ; 0903-1936
ISSN (online)	1399-3003
ISSN	0903-1936
DOI	10.1183/13993003.01518-2023
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Zs.A 2322: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 292: Show issues

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Article ; Online: The Roles of Immunity in the Prevention and Evolution of Pulmonary Arterial Hypertension.

Nicolls, Mark R / Voelkel, Norbert F

American journal of respiratory and critical care medicine

2016 Volume 195, Issue 10, Page(s) 1292–1299

MeSH term(s)	Animals ; Autoimmunity/immunology ; Disease Progression ; Humans ; Hypertension, Pulmonary/drug therapy ; Hypertension, Pulmonary/immunology ; Immunity/immunology ; Immunotherapy ; Inflammation/immunology ; Translational Research, Biomedical
Language	English
Publishing date	2016-10-26
Publishing country	United States
Document type	Journal Article ; 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.201608-1630PP
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