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A grainyhead transcription factor Tfcp2l1 controls the timing for lung alveolar regeneration (scRNA-Seq)

ABSTRACT: A grainyhead transcription factor Tfcp2l1 controls the timing for lung alveolar regeneration (scRNA-Seq)

PROVIDER: PRJNA842346 | ENA |

REPOSITORIES: ENA

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A grainyhead transcription factor Tfcp2l1 controls the timing for lung alveolar regeneration

Project description:A grainyhead transcription factor Tfcp2l1 controls the timing for lung alveolar regeneration

| PRJNA842341 | ENA

A grainyhead transcription factor Tfcp2l1 controls the timing for lung alveolar regeneration (RNA-Seq)

Project description:Alveolar epithelial type 2 (AT2) cells are facultative progenitor cells that drive adult alveolar regeneration after acute lung injury. Using transcriptomic analyses from in vivo mouse injury models, we define the role of Tfcp2l1 in regulating AT2 cell behavior during lung regeneration.

2023-09-12 | GSE204784 | GEO

A grainyhead transcription factor Tfcp2l1 controls the timing for lung alveolar regeneration (scRNA-Seq)

2023-09-12 | GSE204786 | GEO

A grainyhead transcription factor Tfcp2l1 controls the timing for lung alveolar regeneration (RNA-Seq)

Project description:A grainyhead transcription factor Tfcp2l1 controls the timing for lung alveolar regeneration (RNA-Seq)

| PRJNA842347 | ENA

A grainyhead transcription factor Tfcp2l1 controls the timing for lung alveolar regeneration

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-09-12 | GSE204787 | GEO

Interleukin-11 causes alveolar type 2 cell dysfunction and prevents alveolar regeneration [RNA-seq]

Project description:Following lung injury, alveolar regeneration is characterized by the transformation of alveolar type 2 (AT2) cells, via a transitional KRT8+ state, into alveolar type 1 (AT1) cells. In lung disease, dysfunctional intermediate cells accumulate, AT1 cells are diminished and fibrosis occurs. Using single cell RNA sequencing datasets of human interstitial lung disease, we found that interleukin-11 (IL11) is specifically expressed in aberrant KRT8 expressing KRT5-/KRT17+ and basaloid cells. Stimulation of AT2 cells with IL11 or TGFβ1 caused EMT, induced KRT8+ and stalled AT1 differentiation, with TGFβ1 effects being IL11 dependent. In bleomycin injured mouse lung, IL11 was increased in AT2-derived KRT8+ cells and deletion of Il11ra1 in lineage labeled AT2 cells reduced KRT8+ expression, enhanced AT1 differentiation and promoted alveolar regeneration, which was replicated in therapeutic studies using anti-IL11. These data show that IL11 maintains AT2 cells in a dysfunctional transitional state, impairs AT1 differentiation and blocks alveolar regeneration across species.

2024-08-12 | GSE218386 | GEO

Aging disrupts gene expression timing during muscle regeneration

Project description:Aging disrupts gene expression timing during muscle regeneration

| PRJNA747053 | ENA

Stat3-Bdnf-TrkB axis promotes alveolar regeneration

Project description:Stat3-Bdnf-TrkB axis promotes alveolar regeneration

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Targeted alveolar regeneration with Frizzled-specific agonists

Project description:Targeted alveolar regeneration with Frizzled-specific agonists

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Alveolar Injury and Regeneration Following Deletion of ABCA3

Project description:Surfactant deficiency, diffuse alveolar damage and respiratory failure caused by loss of Abca3 in AT2 cells was followed by remarkable proliferation of alveolar cells and selective survival of ABCA3 sufficient cells resulting in regeneration of alveolar structure and function, providing the conceptual framework for the development of therapies to ameliorate lung diseases caused by mutations in ABCA3 and other genes critical for AT2 cell function or surfactant homeostasis.

2018-02-15 | GSE103506 | GEO

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