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  1. Article ; Online: Aging Delays Lung Repair: Insights from Omics Analysis in Mice with Pulmonary Fibrosis.

    Liang, Jiurong / Ligresti, Giovanni

    American journal of respiratory cell and molecular biology

    2023  Volume 69, Issue 4, Page(s) 376–377

    MeSH term(s) Animals ; Mice ; Pulmonary Fibrosis/genetics ; Pulmonary Fibrosis/pathology ; Proteomics ; Aging/genetics ; Lung/pathology ; Gene Expression Profiling
    Language English
    Publishing date 2023-07-11
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2023-0171ED
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2851: Show issues Location:
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  2. Article ; Online: Vascular Contribution to Lung Repair and Fibrosis.

    Caporarello, Nunzia / Ligresti, Giovanni

    American journal of respiratory cell and molecular biology

    2023  Volume 69, Issue 2, Page(s) 135–146

    Abstract: Lungs are constantly exposed to environmental perturbations and therefore have remarkable capacity to regenerate in response to injury. Sustained lung injuries, aging, and increased genomic instability, however, make lungs particularly susceptible to ... ...

    Abstract Lungs are constantly exposed to environmental perturbations and therefore have remarkable capacity to regenerate in response to injury. Sustained lung injuries, aging, and increased genomic instability, however, make lungs particularly susceptible to disrepair and fibrosis. Pulmonary fibrosis constitutes a major cause of morbidity and is often relentlessly progressive, leading to death from respiratory failure. The pulmonary vasculature, which is critical for gas exchanges and plays a key role during lung development, repair, and regeneration, becomes aberrantly remodeled in patients with progressive pulmonary fibrosis. Although capillary rarefaction and increased vascular permeability are recognized as distinctive features of fibrotic lungs, the role of vasculature dysfunction in the pathogenesis of pulmonary fibrosis has only recently emerged as an important contributor to the progression of this disease. This review summarizes current findings related to lung vascular repair and regeneration and provides recent insights into the vascular abnormalities associated with the development of persistent lung fibrosis.
    MeSH term(s) Humans ; Pulmonary Fibrosis/pathology ; Lung/pathology ; Fibrosis ; Lung Injury/pathology ; Respiratory Insufficiency ; Idiopathic Pulmonary Fibrosis/pathology
    Language English
    Publishing date 2023-05-01
    Publishing country United States
    Document type Review ; Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2022-0431TR
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2851: Show issues Location:
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  3. Article ; Online: Kidney endothelial cell heterogeneity, angiocrine activity and paracrine regulatory mechanisms.

    Ribatti, Domenico / Ligresti, Giovanni / Nicosia, Roberto F

    Vascular pharmacology

    2022  Volume 148, Page(s) 107139

    Abstract: The blood microvascular endothelium consists of a heterogeneous population of cells with regionally distinct morphologies and transcriptional signatures in different tissues and organs. In addition to providing an anti-thrombogenic surface for blood flow, ...

    Abstract The blood microvascular endothelium consists of a heterogeneous population of cells with regionally distinct morphologies and transcriptional signatures in different tissues and organs. In addition to providing an anti-thrombogenic surface for blood flow, endothelial cells perform a multitude of additional regulatory tasks involving organogenesis, metabolism, angiogenesis, inflammation, repair and organ homeostasis. To communicate with surrounding cells and accomplish their many functions, endothelial cells secrete angiocrine factors including growth factors, chemokines, cytokines, extracellular matrix components, and proteolytic enzymes. Nonendothelial parenchymal and stromal cells in turn regulate endothelial growth, differentiation and survival during embryonal development and in the adult by paracrine mechanisms. Driven by advances in molecular biology, animal genetics, single cell transcriptomics and microscopic imaging, knowledge of organotypic vasculatures has expanded rapidly in recent years. The kidney vasculature, in particular, has been the focus of intensive investigation and represents a primary example of how endothelial heterogeneity and crosstalk with nonendothelial cells contribute to the development and function of a vital organ. In this paper, we review the morphology, function, and development of the kidney vasculature, with an emphasis on blood microvascular endothelial heterogeneity, and provide examples of endothelial and nonendothelial-derived factors that are critically involved in kidney development, growth, response to injury, and homeostasis.
    MeSH term(s) Animals ; Endothelial Cells/metabolism ; Endothelium ; Cell Differentiation ; Kidney
    Language English
    Publishing date 2022-12-17
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 2082846-9
    ISSN 1879-3649 ; 1537-1891 ; 1879-3649
    ISSN (online) 1879-3649 ; 1537-1891
    ISSN 1879-3649
    DOI 10.1016/j.vph.2022.107139
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    Zs.A 591: Show issues Location:
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  4. Article ; Online: Circular RNA Methylation: A New Twist in Lung Fibrosis.

    Ligresti, Giovanni / Pham, Tho X / Sanders, Yan Y

    American journal of respiratory cell and molecular biology

    2022  Volume 66, Issue 5, Page(s) 471–472

    MeSH term(s) Fibrosis ; Humans ; Methylation ; Pulmonary Fibrosis/genetics ; RNA, Circular/genetics ; Transforming Growth Factor beta1/metabolism
    Chemical Substances RNA, Circular ; Transforming Growth Factor beta1
    Language English
    Publishing date 2022-03-03
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2022-0044ED
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2851: Show issues Location:
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  5. Article ; Online: Mesenchymal cells in the Lung: Evolving concepts and their role in fibrosis

    Ligresti, Giovanni / Raslan, Ahmed A. / Hong, Jeongmin / Caporarello, Nunzia / Confalonieri, Marco / Huang, Steven K.

    Gene. 2023 Apr., v. 859 p.147142-

    2023  

    Abstract: Mesenchymal cells in the lung are crucial during development, but also contribute to the pathogenesis of fibrotic disorders, including idiopathic pulmonary fibrosis (IPF), the most common and deadly form of fibrotic interstitial lung diseases. Originally ...

    Abstract Mesenchymal cells in the lung are crucial during development, but also contribute to the pathogenesis of fibrotic disorders, including idiopathic pulmonary fibrosis (IPF), the most common and deadly form of fibrotic interstitial lung diseases. Originally thought to behave as supporting cells for the lung epithelium and endothelium with a singular function of producing basement membrane, mesenchymal cells encompass a variety of cell types, including resident fibroblasts, lipofibroblasts, myofibroblasts, smooth muscle cells, and pericytes, which all occupy different anatomic locations and exhibit diverse homeostatic functions in the lung. During injury, each of these subtypes demonstrate remarkable plasticity and undergo varying capacity to proliferate and differentiate into activated myofibroblasts. Therefore, these cells secrete high levels of extracellular matrix (ECM) proteins and inflammatory cytokines, which contribute to tissue repair, or in pathologic situations, scarring and fibrosis. Whereas epithelial damage is considered the initial trigger that leads to lung injury, lung mesenchymal cells are recognized as the ultimate effector of fibrosis and attempts to better understand the different functions and actions of each mesenchymal cell subtype will lead to a better understanding of why fibrosis develops and how to better target it for future therapy. This review summarizes current findings related to various lung mesenchymal cells as well as signaling pathways, and their contribution to the pathogenesis of pulmonary fibrosis.
    Keywords basement membrane ; cytokines ; endothelium ; extracellular matrix ; fibroblasts ; fibrosis ; genes ; lungs ; pathogenesis ; plasticity ; pulmonary fibrosis ; smooth muscle ; therapeutics ; tissue repair ; Mesenchymal cells ; Myofibroblast ; Differentiation ; Fibrosis resolution
    Language English
    Dates of publication 2023-04
    Publishing place Elsevier B.V.
    Document type Article ; Online
    ZDB-ID 391792-7
    ISSN 1879-0038 ; 0378-1119
    ISSN (online) 1879-0038
    ISSN 0378-1119
    DOI 10.1016/j.gene.2022.147142
    Database NAL-Catalogue (AGRICOLA)

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  6. Article: Endothelial

    Chakraborty, Adri / Kim, Alex / AlAbdullatif, Salam / Campbell, Joshua D / Alekseyev, Yuriy O / Kaplan, Ulas / Dambal, Vrinda / Ligresti, Giovanni / Trojanowska, Maria

    Research square

    2024  

    Abstract: The ETS transcription factor ERG is a master regulator of endothelial gene specificity and highly enriched in the capillary, vein, and arterial endothelial cells. ERG expression is critical for endothelial barrier function, permeability, and vascular ... ...

    Abstract The ETS transcription factor ERG is a master regulator of endothelial gene specificity and highly enriched in the capillary, vein, and arterial endothelial cells. ERG expression is critical for endothelial barrier function, permeability, and vascular inflammation. A dysfunctional vascular endothelial ERG has been shown to impair lung capillary homeostasis, contributing to pulmonary fibrosis as previously observed in IPF lungs. Our preliminary observations indicate that lymphatic endothelial cells (LEC) in the human IPF lung also lack ERG. To understand the role of ERG in pulmonary LECs, we developed LEC-specific inducible
    Language English
    Publishing date 2024-01-24
    Publishing country United States
    Document type Preprint
    DOI 10.21203/rs.3.rs-3808970/v1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Mesenchymal cells in the Lung: Evolving concepts and their role in fibrosis.

    Ligresti, Giovanni / Raslan, Ahmed A / Hong, Jeongmin / Caporarello, Nunzia / Confalonieri, Marco / Huang, Steven K

    Gene

    2023  Volume 859, Page(s) 147142

    Abstract: Mesenchymal cells in the lung are crucial during development, but also contribute to the pathogenesis of fibrotic disorders, including idiopathic pulmonary fibrosis (IPF), the most common and deadly form of fibrotic interstitial lung diseases. Originally ...

    Abstract Mesenchymal cells in the lung are crucial during development, but also contribute to the pathogenesis of fibrotic disorders, including idiopathic pulmonary fibrosis (IPF), the most common and deadly form of fibrotic interstitial lung diseases. Originally thought to behave as supporting cells for the lung epithelium and endothelium with a singular function of producing basement membrane, mesenchymal cells encompass a variety of cell types, including resident fibroblasts, lipofibroblasts, myofibroblasts, smooth muscle cells, and pericytes, which all occupy different anatomic locations and exhibit diverse homeostatic functions in the lung. During injury, each of these subtypes demonstrate remarkable plasticity and undergo varying capacity to proliferate and differentiate into activated myofibroblasts. Therefore, these cells secrete high levels of extracellular matrix (ECM) proteins and inflammatory cytokines, which contribute to tissue repair, or in pathologic situations, scarring and fibrosis. Whereas epithelial damage is considered the initial trigger that leads to lung injury, lung mesenchymal cells are recognized as the ultimate effector of fibrosis and attempts to better understand the different functions and actions of each mesenchymal cell subtype will lead to a better understanding of why fibrosis develops and how to better target it for future therapy. This review summarizes current findings related to various lung mesenchymal cells as well as signaling pathways, and their contribution to the pathogenesis of pulmonary fibrosis.
    MeSH term(s) Humans ; Lung/metabolism ; Fibrosis ; Pulmonary Fibrosis/metabolism ; Mesenchymal Stem Cells/metabolism ; Myofibroblasts/metabolism ; Myofibroblasts/pathology ; Fibroblasts/metabolism ; Extracellular Matrix Proteins/metabolism ; Idiopathic Pulmonary Fibrosis/metabolism ; Idiopathic Pulmonary Fibrosis/pathology
    Chemical Substances Extracellular Matrix Proteins
    Language English
    Publishing date 2023-01-02
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 391792-7
    ISSN 1879-0038 ; 0378-1119
    ISSN (online) 1879-0038
    ISSN 0378-1119
    DOI 10.1016/j.gene.2022.147142
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1357: Show issues Location:
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  8. Article ; Online: Survivin IPF: Targeting Cellular Metabolism to Promote Apoptosis in IPF Fibroblasts.

    Jones, Dakota L / Ligresti, Giovanni

    American journal of respiratory cell and molecular biology

    2018  Volume 60, Issue 1, Page(s) 5–6

    MeSH term(s) Apoptosis ; Fibroblasts ; Gene Expression ; Humans ; Idiopathic Pulmonary Fibrosis ; Survivin
    Chemical Substances Survivin
    Language English
    Publishing date 2018-09-13
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2018-0270ED
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: The matricellular protein CCN3 supports lung endothelial homeostasis and function.

    Betageri, Kalpana R / Link, Patrick A / Haak, Andrew J / Ligresti, Giovanni / Tschumperlin, Daniel J / Caporarello, Nunzia

    American journal of physiology. Lung cellular and molecular physiology

    2022  Volume 324, Issue 2, Page(s) L154–L168

    Abstract: Aberrant vascular remodeling contributes to the progression of many aging-associated diseases, including idiopathic pulmonary fibrosis (IPF), where heterogeneous capillary density, endothelial transcriptional alterations, and increased vascular ... ...

    Abstract Aberrant vascular remodeling contributes to the progression of many aging-associated diseases, including idiopathic pulmonary fibrosis (IPF), where heterogeneous capillary density, endothelial transcriptional alterations, and increased vascular permeability correlate with poor disease outcomes. Thus, identifying disease-driving mechanisms in the pulmonary vasculature may be a promising strategy to limit IPF progression. Here, we identified
    MeSH term(s) Mice ; Humans ; Animals ; Pulmonary Fibrosis ; Endothelial Cells/metabolism ; Nephroblastoma Overexpressed Protein/metabolism ; Cells, Cultured ; Lung/metabolism
    Chemical Substances Nephroblastoma Overexpressed Protein
    Language English
    Publishing date 2022-12-27
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1013184-x
    ISSN 1522-1504 ; 1040-0605
    ISSN (online) 1522-1504
    ISSN 1040-0605
    DOI 10.1152/ajplung.00248.2022
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  10. Article ; Online: Rapid Generation of hPSC-Derived High Endothelial Venule Organoids with In Vivo Ectopic Lymphoid Tissue Capabilities.

    Wang, Xichi / Li, Xiaofei / Zhao, Jing / Li, Yi / Shin, Su Ryon / Ligresti, Giovanni / Ng, Alex H M / Bromberg, Jonathan S / Church, George / Lemos, Dario R / Abdi, Reza

    Advanced materials (Deerfield Beach, Fla.)

    2024  Volume 36, Issue 15, Page(s) e2308760

    Abstract: Bioengineering strategies for the fabrication of implantable lymphoid structures mimicking lymph nodes (LNs) and tertiary lymphoid structures (TLS) could amplify the adaptive immune response for therapeutic applications such as cancer immunotherapy. No ... ...

    Abstract Bioengineering strategies for the fabrication of implantable lymphoid structures mimicking lymph nodes (LNs) and tertiary lymphoid structures (TLS) could amplify the adaptive immune response for therapeutic applications such as cancer immunotherapy. No method to date has resulted in the consistent formation of high endothelial venules (HEVs), which is the specialized vasculature responsible for naïve T cell recruitment and education in both LNs and TLS. Here orthogonal induced differentiation of human pluripotent stem cells carrying a regulatable ETV2 allele is used to rapidly and efficiently induce endothelial differentiation. Assembly of embryoid bodies combining primitive inducible endothelial cells and primary human LN fibroblastic reticular cells results in the formation of HEV-like structures that can aggregate into 3D organoids (HEVOs). Upon transplantation into immunodeficient mice, HEVOs successfully engraft and form lymphatic structures that recruit both antigen-presenting cells and adoptively-transferred lymphocytes, therefore displaying basic TLS capabilities. The results further show that functionally, HEVOs can organize an immune response and promote anti-tumor activity by adoptively-transferred T lymphocytes. Collectively, the experimental approaches represent an innovative and scalable proof-of-concept strategy for the fabrication of bioengineered TLS that can be deployed in vivo to enhance adaptive immune responses.
    MeSH term(s) Mice ; Humans ; Animals ; Tertiary Lymphoid Structures/pathology ; Venules ; Endothelial Cells ; Lymph Nodes ; Organoids ; Transcription Factors
    Chemical Substances ETV2 protein, human ; Transcription Factors
    Language English
    Publishing date 2024-02-11
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 1474949-X
    ISSN 1521-4095 ; 0935-9648
    ISSN (online) 1521-4095
    ISSN 0935-9648
    DOI 10.1002/adma.202308760
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