Anxa4 mediated airway progenitor cell migration promotes distal epithelial cell fate specification

Jiang, Kewu; Tang, Zan; Li, Juan; Wang, Fengchao; Tang, Nan

doi:10.1038/s41598-018-32494-z

Cited by 11 publications

(10 citation statements)

References 52 publications

(62 reference statements)

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“…While the latter may implicate a role in repair mechanisms, administration of pharmacological AnxA4 concentrations caused bleeding in skin wound repair [ 80 ]. AnxA4a-deficient urothelium did not reveal alterations in bladder function [ 217 ], but airway epithelial cell migration was impaired upon AnxA4 depletion, with consequences for airway branching morphogenesis during lung development [ 218 ].…”

Section: Anxa4mentioning

confidence: 99%

Annexin Animal Models—From Fundamental Principles to Translational Research

Grewal

Rentero

Enrich

et al. 2021

IJMS

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Routine manipulation of the mouse genome has become a landmark in biomedical research. Traits that are only associated with advanced developmental stages can now be investigated within a living organism, and the in vivo analysis of corresponding phenotypes and functions advances the translation into the clinical setting. The annexins, a family of closely related calcium (Ca2+)- and lipid-binding proteins, are found at various intra- and extracellular locations, and interact with a broad range of membrane lipids and proteins. Their impacts on cellular functions has been extensively assessed in vitro, yet annexin-deficient mouse models generally develop normally and do not display obvious phenotypes. Only in recent years, studies examining genetically modified annexin mouse models which were exposed to stress conditions mimicking human disease often revealed striking phenotypes. This review is the first comprehensive overview of annexin-related research using animal models and their exciting future use for relevant issues in biology and experimental medicine.

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Section: Anxa4mentioning

confidence: 99%

Annexin Animal Models—From Fundamental Principles to Translational Research

Grewal

Rentero

Enrich

et al. 2021

IJMS

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“…The genetic inactivation of either Mek1/2 or Erk1/2 specifically in the airway epithelium results in lung agenesis 19 , implying that ERK and its activation were essential for lung development 20 . Previously, immunofluorescence staining results suggested that the phosphorylation of ERK was most likely to occur in the distal tips of the lung epithelium, and may thus be involved in the budding process during lung development [21][22][23] . FGFR2-mediated ERK activation reportedly upregulates the expression of Anxa4, whose products are able to bind with F-actin bundles, and promote cell migration within epithelial tissues 22 .…”

Section: Introductionmentioning

confidence: 98%

ERK-mediated Curvature Feedback Regulates Branching Morphogenesis in Lung Epithelial Tissue

Hirashima

2021

Preprint

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Intricate branching patterns emerge in internal organs because of the repetitive presence of simple deformations in epithelial tissues. During murine lung development, epithelial cells in distal tips of a single tube require fibroblast growth factor (FGF) signals generated by their surrounding mesenchyme to form repetitive tip bifurcations. However, it remains unknown how the cells employ FGF signaling to convert their behaviors to achieve the recursive branching processes. Here we show a self-sustained epithelial regulatory system during the murine lung branching morphogenesis, mediated by extracellular signal-regulated kinase (ERK), which acts as a downstream driver of FGF signaling. We found that tissue-scale curvature regulates ERK activity in the lung epithelium using two-photon live cell imaging and mechanical perturbations. ERK is activated specifically in epithelial tissues with a positive curvature, regardless of whether the change in curvature was attributable to morphogenesis or artificial perturbations. Moreover, we found that ERK activation accelerates actin polymerization specifically at the apical side of cells, and mechanically contributes to the extension of the apical membrane, leading to a decrease in epithelial tissue curvature. These results indicate the existence of a negative feedback loop between tissue curvature and ERK activity beyond scale. We confirmed that this regulation was sufficient to generate the recursive branching processes by a mathematical model. Taken together, we propose that ERK mediates the curvature feedback loop underlying the process of branching morphogenesis in developing lungs.

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“…This smooth muscle wraps around the cleft and the neck as the daughter branches elongate, likely providing support and directional cues to the growing epithelium. Also during this stage, progenitor cells marked by Annexin A4 (Anxa4) expression actively migrate to the daughter bud tips, and help maintain those cells in an undifferentiated progenitor status (Jiang et al, 2018 ). This process is regulated by Fgfr2b ERK1/2 signaling (these ideas are summarized in Figure 5 ).…”

Section: Regulation Of Cell and Tissue Geometry In The Developing Lunmentioning

confidence: 99%

Fgf10/Fgfr2b Signaling Orchestrates the Symphony of Molecular, Cellular, and Physical Processes Required for Harmonious Airway Branching Morphogenesis

Jones

Lei

Bellusci

2021

Front. Cell Dev. Biol.

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Airway branching morphogenesis depends on the intricate orchestration of numerous biological and physical factors connected across different spatial scales. One of the key regulatory pathways controlling airway branching is fibroblast growth factor 10 (Fgf10) signaling via its epithelial fibroblast growth factor receptor 2b (Fgfr2b). Fine reviews have been published on the molecular mechanisms, in general, involved in branching morphogenesis, including those mechanisms, in particular, connected to Fgf10/Fgfr2b signaling. However, a comprehensive review looking at all the major biological and physical factors involved in branching, at the different scales at which branching operates, and the known role of Fgf10/Fgfr2b therein, is missing. In the current review, we attempt to summarize the existing literature on airway branching morphogenesis by taking a broad approach. We focus on the biophysical and mechanical forces directly shaping epithelial bud initiation, branch elongation, and branch tip bifurcation. We then shift focus to more passive means by which branching proceeds, via extracellular matrix remodeling and the influence of the other pulmonary arborized networks: the vasculature and nerves. We end the review by briefly discussing work in computational modeling of airway branching. Throughout, we emphasize the known or speculative effects of Fgfr2b signaling at each point of discussion. It is our aim to promote an understanding of branching morphogenesis that captures the multi-scalar biological and physical nature of the phenomenon, and the interdisciplinary approach to its study.

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Anxa4 mediated airway progenitor cell migration promotes distal epithelial cell fate specification

Cited by 11 publications

References 52 publications

Annexin Animal Models—From Fundamental Principles to Translational Research

Annexin Animal Models—From Fundamental Principles to Translational Research

ERK-mediated Curvature Feedback Regulates Branching Morphogenesis in Lung Epithelial Tissue

Fgf10/Fgfr2b Signaling Orchestrates the Symphony of Molecular, Cellular, and Physical Processes Required for Harmonious Airway Branching Morphogenesis

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