Pericytes in Chronic Lung Disease

Shammout, Bushra; Johnson, Jill

doi:10.1007/978-3-030-16908-4_14

Cited by 12 publications

(14 citation statements)

References 57 publications

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“…On the other hand, pericytes also interact with AT2 cells to promote secondary septa formation through the Hippo pathway components Yap and Taz [ 71 ]. In addition, pericytes can also function as pulmonary stem cells, upon stimulation, transdifferentiating into VSMCs and myofibroblasts [ 72 , 73 ].…”

Section: Development Of Normal Pulmonary Vasculature and Bpd-ph Frmentioning

confidence: 99%

Targeting Bronchopulmonary Dysplasia-Associated Pulmonary Hypertension (BPD-PH): Potential Role of the FGF Signaling Pathway in the Development of the Pulmonary Vascular System

Chao

Lei

Chu

et al. 2020

Cells

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More than 50 years after the first description of Bronchopulmonary dysplasia (BPD) by Northway, this chronic lung disease affecting many preterm infants is still poorly understood. Additonally, approximately 40% of preterm infants suffering from severe BPD also suffer from Bronchopulmonary dysplasia-associated pulmonary hypertension (BPD-PH), leading to a significant increase in total morbidity and mortality. Until today, there is no curative therapy for both BPD and BPD-PH available. It has become increasingly evident that growth factors are playing a central role in normal and pathologic development of the pulmonary vasculature. Thus, this review aims to summarize the recent evidence in our understanding of BPD-PH from a basic scientific point of view, focusing on the potential role of Fibroblast Growth Factor (FGF)/FGF10 signaling pathway contributing to disease development, progression and resolution.

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Section: Development Of Normal Pulmonary Vasculature and Bpd-ph Frmentioning

confidence: 99%

Targeting Bronchopulmonary Dysplasia-Associated Pulmonary Hypertension (BPD-PH): Potential Role of the FGF Signaling Pathway in the Development of the Pulmonary Vascular System

Chao

Lei

Chu

et al. 2020

Cells

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“…Mouse models with knockout of TGF-b show protection from fibrosis and EMT (153)(154)(155). Growth factors such as VEGF and TGF-b also mediate interactions between the lung endothelium and pericytes and have been independently studied as drivers of fibrosis (156,157). Myofibroblasts can also differentiate from donor-derived resident mesenchymal stem cells in response to Th2 lymphocytic inflammation (158).…”

Section: Airway Inflammation In the Pathogenesis Of Cladmentioning

confidence: 99%

Lymphocytic Airway Inflammation in Lung Allografts

2022

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Lung transplant remains a key therapeutic option for patients with end stage lung disease but short- and long-term survival lag other solid organ transplants. Early ischemia-reperfusion injury in the form of primary graft dysfunction (PGD) and acute cellular rejection are risk factors for chronic lung allograft dysfunction (CLAD), a syndrome of airway and parenchymal fibrosis that is the major barrier to long term survival. An increasing body of research suggests lymphocytic airway inflammation plays a significant role in these important clinical syndromes. Cytotoxic T cells are observed in airway rejection, and transcriptional analysis of airways reveal common cytotoxic gene patterns across solid organ transplant rejection. Natural killer (NK) cells have also been implicated in the early allograft damage response to PGD, acute rejection, cytomegalovirus, and CLAD. This review will examine the roles of lymphocytic airway inflammation across the lifespan of the allograft, including: 1) The contribution of innate lymphocytes to PGD and the impact of PGD on the adaptive immune response. 2) Acute cellular rejection pathologies and the limitations in identifying airway inflammation by transbronchial biopsy. 3) Potentiators of airway inflammation and heterologous immunity, such as respiratory infections, aspiration, and the airway microbiome. 4) Airway contributions to CLAD pathogenesis, including epithelial to mesenchymal transition (EMT), club cell loss, and the evolution from constrictive bronchiolitis to parenchymal fibrosis. 5) Protective mechanisms of fibrosis involving regulatory T cells. In summary, this review will examine our current understanding of the complex interplay between the transplanted airway epithelium, lymphocytic airway infiltration, and rejection pathologies.

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“…All tissue was obtained from patients treated at Shriners Hospitals for Children-Cincinnati or the University of Cincinnati Medical Center, Cincinnati, OH. The University of Cincinnati Institutional Review Board determined that this does not constitute human subjects research and is exempt from requirements for informed consent according to 45CFR46.101 (b) (4). Patient information was anonymized, and samples were de-identified prior to analysis.…”

Section: Discarded Human Skin Tissuesmentioning

confidence: 99%

“…Several cell populations, including inflammatory cells, fibroblasts, and keratinocytes, play a crucial role in coordinating the wound healing outcome [1,2]. Recently, pericytes (PCs), a mesenchymal stem cell-like population, have been reported to contribute to liver [3], lung [4], kidney [5], and skin fibrosis [6]. However, PCs role in burn wound healing is still yet to be deciphered.…”

Section: Introductionmentioning

confidence: 99%

Characterization of Burn Eschar Pericytes

Evdokiou

Kanisicak

Gierek

et al. 2020

JCM

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Pericytes are cells that reside adjacent to microvasculature and regulate vascular function. Pericytes gained great interest in the field of wound healing and regenerative medicine due to their multipotential fate and ability to enhance angiogenesis. In burn wounds, scarring and scar contractures are the major pathologic feature and cause loss of mobility. The present study investigated the influence of burn wound environment on pericytes during wound healing. Pericytes isolated from normal skin and tangentially excised burn eschar tissues were analyzed for differences in gene and protein expression using RNA-seq., immunocytochemistry, and ELISA analyses. RNA-seq identified 443 differentially expressed genes between normal- and burn eschar-derived pericytes. Whereas, comparing normal skin pericytes to normal skin fibroblasts identified 1021 distinct genes and comparing burn eschar pericytes to normal skin fibroblasts identified 2449 differential genes. Altogether, forkhead box E1 (FOXE1), a transcription factor, was identified as a unique marker for skin pericytes. Interestingly, FOXE1 levels were significantly elevated in burn eschar pericytes compared to normal. Additionally, burn wound pericytes showed increased expression of profibrotic genes periostin, fibronectin, and endosialin and a gain in contractile function, suggesting a contribution to scarring and fibrosis. Our findings suggest that the burn wound environment promotes pericytes to differentiate into a myofibroblast-like phenotype promoting scar formation and fibrosis.

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Pericytes in Chronic Lung Disease

Cited by 12 publications

References 57 publications

Targeting Bronchopulmonary Dysplasia-Associated Pulmonary Hypertension (BPD-PH): Potential Role of the FGF Signaling Pathway in the Development of the Pulmonary Vascular System

Targeting Bronchopulmonary Dysplasia-Associated Pulmonary Hypertension (BPD-PH): Potential Role of the FGF Signaling Pathway in the Development of the Pulmonary Vascular System

Lymphocytic Airway Inflammation in Lung Allografts

Characterization of Burn Eschar Pericytes

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