Forkhead Box m1 transcription factor is required for perinatal lung function

Kalin, Tanya V.; Wang, I‐Ching; Meliton, Lucille N.; Zhang, Yufang; Wert, Susan E.; Ren, Xiaomeng; Snyder, Jonathan; Bell, Sheila M.; Graf, Liselotte; Whitsett, Jeffrey A.; Kalinichenko, Vladimir V.

doi:10.1073/pnas.0806748105

Cited by 70 publications

(123 citation statements)

References 24 publications

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“…CMV-Renilla was used as an internal control to normalize transfection efficiency. A dual luciferase assay (Promega) was performed 24 h after transfection as described previously (38).…”

Section: Cloning Of the Mouse 11␤-hsd2 Promoter Region And Luciferasementioning

confidence: 99%

Foxm1 Expression in Prostate Epithelial Cells Is Essential for Prostate Carcinogenesis

Cai

Balli

Ustiyan

et al. 2013

Journal of Biological Chemistry

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Background: Foxm1 is up-regulated in prostate adenocarcinomas and its expression correlates with the poor prognosis. Results: Conditional depletion of Foxm1 in prostate epithelial cells inhibits tumor cell proliferation, angiogenesis, and metastasis. Conclusion: Foxm1 expression in prostate epithelial cells is essential for prostate carcinogenesis in mouse models. Significance: Foxm1 may play a key role in the pathogenesis of prostate cancer in human patients.

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“…CMV-Renilla was used as an internal control to normalize transfection efficiency. A dual luciferase assay (Promega) was performed 24 h after transfection as described previously (38).…”

Section: Cloning Of the Mouse 11␤-hsd2 Promoter Region And Luciferasementioning

confidence: 99%

Foxm1 Expression in Prostate Epithelial Cells Is Essential for Prostate Carcinogenesis

Cai

Balli

Ustiyan

et al. 2013

Journal of Biological Chemistry

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“…The test data for this purpose consisted of 21 developing mouse whole lung transcriptome profiles at six discrete time points: embryonic Days 14 (34), 17 (33), and 19 (34) and postnatal Days 7 (33), 14 (33), and 28 (34) (16,18). When projected in human lung development transcriptomic PC space, the mouse samples, especially the embryonic time points (14,17, and 19 dpc), were correlated with their true developmental age ( Figures 4B, E6, and E7).…”

Section: Estimating the Age/developmental Maturity Of The Human/ Mousmentioning

confidence: 99%

Transcriptomic Analysis of Human Lung Development

Kho

Bhattacharya

Tantisira

et al. 2010

Am J Respir Crit Care Med

110

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Rationale: Current understanding of the molecular regulation of lung development is limited and derives mostly from animal studies. Objectives: To define global patterns of gene expression during human lung development. Methods: Genome-wide expression profiling was used to measure the developing lung transcriptome in RNA samples derived from 38 normal human lung tissues at 53 to 154 days post conception. Principal component analysis was used to characterize global expression variation and to identify genes and bioontologic attributes contributing to these variations. Individual gene expression patterns were verified by quantitative reverse transcriptase-polymerase chain reaction analysis. Measurements and Main Results: Gene expression analysis identified attributes not previously associated with lung development, such as chemokine-immunologic processes. Lung characteristics attributes (e.g., surfactant function) were observed at an earlier-than-anticipated age. We defined a 3,223 gene developing lung characteristic subtranscriptome capable of describing a majority of the process. In gene expression space, the samples formed a time-contiguous trajectory with transition points correlating with histological stages and suggesting the existence of novel molecular substages. Induction of surfactant gene expression characterized a pseudoglandular ''molecular phase'' transition. Individual gene expression patterns were independently validated. We predicted the age of independent human lung transcriptome profiles with a median absolute error of 5 days, supporting the validity of the data and modeling approach. Conclusions: This study extends our knowledge of key gene expression patterns and bioontologic attributes underlying early human lung developmental processes. The data also suggest the existence of molecular phases of lung development.

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“…Depending on cell/tissue specificity, FOXM1 induces surfactant production by type II alveolar epithelial cells (31), increases differentiation of type I epithelial cells (32), regulates expression of tight junction proteins in endothelial cells (33,34), and increases macrophage recruitment after liver injury (35). Deletion of Foxm1 from embryonic lung epithelium causes respiratory failure after birth (31), whereas deletion of Foxm1 from alveolar type II cells of adult mice impairs alveolar barrier repair after acute lung injury (32). Although these studies demonstrated that FOXM1 is a critical transcriptional regulator of alveolar epithelial cells, the role of FOXM1 in the airway epithelium remains unknown.…”

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confidence: 99%

FOXM1 Promotes Allergen-Induced Goblet Cell Metaplasia and Pulmonary Inflammation

Ren

Shah

Ustiyan

et al. 2013

Molecular and Cellular Biology

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Chronic airway disorders, including chronic obstructive pulmonary disease (COPD), cystic fibrosis, and asthma, are associated with persistent pulmonary inflammation and goblet cell metaplasia and contribute to significant morbidity and mortality worldwide. While the molecular pathogenesis of these disorders is actively studied, little is known regarding the transcriptional control of goblet cell differentiation and mucus hyperproduction. Herein, we demonstrated that pulmonary allergen sensitization induces expression of FOXM1 transcription factor in airway epithelial and inflammatory cells. Conditional deletion of the Foxm1 gene from either airway epithelium or myeloid inflammatory cells decreased goblet cell metaplasia, reduced lung inflammation, and decreased airway resistance in response to house dust mite allergen (HDM). FOXM1 induced goblet cell metaplasia and Muc5AC expression through the transcriptional activation of Spdef. FOXM1 deletion reduced expression of CCL11, CCL24, and the chemokine receptors CCR2 and CX3CR1, resulting in decreased recruitment of eosinophils and macrophages to the lung. Deletion of FOXM1 from dendritic cells impaired the uptake of HDM antigens and decreased cell surface expression of major histocompatibility complex II (MHC II) and costimulatory molecule CD86, decreasing production of Th2 cytokines by activated T cells. Finally, pharmacological inhibition of FOXM1 by ARF peptide prevented HDM-mediated pulmonary responses. FOXM1 regulates genes critical for allergen-induced lung inflammation and goblet cell metaplasia.

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Forkhead Box m1 transcription factor is required for perinatal lung function

Cited by 70 publications

References 24 publications

Foxm1 Expression in Prostate Epithelial Cells Is Essential for Prostate Carcinogenesis

Foxm1 Expression in Prostate Epithelial Cells Is Essential for Prostate Carcinogenesis

Transcriptomic Analysis of Human Lung Development

FOXM1 Promotes Allergen-Induced Goblet Cell Metaplasia and Pulmonary Inflammation

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