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Timing and cell specificity of senescence drives postnatal lung development and injury

ABSTRACT: Senescence causes age-related diseases and stress-related injury. Paradoxically, it is also essential for organismal development. Whether senescence contributes to lung development or injury in early life remains unclear. This work defines the ontogeny of lung senescence and provides an optimal therapeutic window for mitigating neonatal hyperoxic lung injury by clearing senescence.

ORGANISM(S): Mus musculus

PROVIDER: GSE207866 | GEO | 2022/12/05

REPOSITORIES: GEO

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Mus musculus

Project description:Hyperoxic lung injury

| PRJNA85199 | ENA

Role of Gdf15 in neonatal hyperoxic lung injury

Project description:Growth Differentiation Factor 15 (GDF15) is a divergent member of the TGF-β superfamily, and its expression increases under various stress conditions, including inflammation, hyperoxia, and senescence. GDF15 expression is increased in neonatal murine BPD models, and GDF15 loss exacerbates oxidative stress and decreases viability in vitro in pulmonary epithelial and endothelial cells. Our overall hypothesis is that the loss of GDF15 will exacerbate hyperoxic lung injury in the neonatal lung in vivo. We exposed neonatal Gdf15-/- mice and wild-type (WT) controls on a similar background to room air or hyperoxia (95% O2) for 5 days after birth. The mice were euthanized on PND 21. Gdf15 -/- mice had higher mortality and lower body weight than WT mice after exposure to hyperoxia. Upon exposure to hyperoxia, female mice had higher alveolar simplification in the Gdf15-/- group than the female WT group. Gdf15-/- and WT mice showed no difference in the degree of the arrest in angiogenesis upon exposure to hyperoxia. Gdf15-/- mice showed lower macrophage count in the lungs compared to WT mice. Our results suggest that Gdf15 deficiency decreases the tolerance to hyperoxic lung injury with evidence of sex-specific differences.

2023-07-20 | GSE211744 | GEO

Impact of Diet Induced Obesity on Hyperoxic Lung Injury

Project description:Impact of Diet Induced Obesity on Hyperoxic Lung Injury

| PRJNA510361 | ENA

Impact of Sphingosine Kinase-1 knock out in neonatal mice lungs

Project description:Sphingosine Kinase-1 knock out protects against hyperoxic lung injury One day old Wild type (WT) control and Sphingosine Kinase-1 knock out (SphK-1 KO)pups exposed to room air (RA) or hyperoxia (HO). Microarray based profiling of lung tissue after 7 days of hyperoxia of 75%

2016-10-30 | GSE87350 | GEO

Transcription profiling of wild type and Nrf2 knock out treated with 100% oxygen to induce lung injury mice to provide insight to the downstream effector genes regulated by Nrf2

Project description:Nrf2 is a transcription factor that binds to antioxidant response elements of the regulatory region of a number of antioxidant genes. A mutation in the Nrf2 gene increases susceptibility to hyperoxic lung injury. This project examines expression differences between wild type and Nrf2 knock out mice with the hope of providing insight to the downstream effector genes regulated by Nrf2.

2007-12-14 | E-GEOD-495 | biostudies-arrayexpress

Sex chromosomes versus gonadal hormones in neonatal hyperoxic lung injury

Project description:Sex chromosomes versus gonadal hormones in neonatal hyperoxic lung injury

| PRJNA683593 | ENA

Fgf10 knock-down effects in normoxia

Project description:Our previous data obtained by using immunohistochemistry showed, that Fgf10+/- (50% Fgf10 expression compared to WT) in hyperoxic condition at postnatal day 3 (P3) compared to WT has less vessel count in the lung and less muscularization of small capillaries in the lung. Furthermore, Fgf10+/- showed a drastic increase in mortality upon hyperoxic lung injury. Main question to be answer by this experiment is as followed: Does Fgf10+/- mice in normoxia from P0-P3 show different expression profiles at P3 compared to WT? To adress this question we harvest lungs at P3 from WT and Fgf10+/- . For this the mice were sacrificed by Ketamin/ Dormitor ip, lungs were perfused transcardiac with PBS and directly frozen in liquid nitrogen.

2019-05-01 | GSE113103 | GEO

Fgf10 knock-down effects in hyperoxia

Project description:Our previous data obtained by using immunohistochemistry showed, that Fgf10+/- (50% Fgf10 expression compared to WT) in hyperoxic condition at postnatal day 3 (P3) compared to WT has less vessel count in the lung and less muscularization of small capillaries in the lung. Furthermore, Fgf10+/- showed a drastic increase in mortality upon hyperoxic lung injury. Main question to be answer by this experiment is as followed: Does Fgf10+/- mice after hyperoxia from P0-P3 show different expression profiles at P3 compared to WT? To adress this question we harvest lungs at P3 from WT and Fgf10+/- after hyperoxia treatment from P0-P3. For this the mice were sacrificed by Ketamin/ Dormitor ip, lungs were perfused transcardiac with PBS and directly frozen in liquid nitrogen.

2019-05-01 | GSE113102 | GEO

Hyperoxia in FGF10 knock-down mice [Lung]

Project description:Our previous data obtained by using immunohistochemistry showed, that Fgf10+/- (50% Fgf10 expression compared to WT) in hyperoxic condition at postnatal day 3 (P3) compared to WT has less vessel count in the lung and less muscularization of small capillaries in the lung. Furthermore, Fgf10+/- showed a drastic increase in mortality upon hyperoxic lung injury. Main question to be answer by this experiment is as followed: Does Fgf10+/- mice after hyperoxia from P0-P3 show different expression profiles at P3 compared to WT? To adress this question we harvest lungs at P3 from WT and Fgf10+/- after hyperoxia treatment from P0-P3. For this the mice were sacrificed by Ketamin/ Dormitor ip, lungs were perfused transcardiac with PBS and directly frozen in liquid nitrogen.

2016-12-31 | GSE76301 | GEO

Hyperoxia in FGF10 knock-down mice [AEC II cells]

Project description:Our previous data obtained by using immunohistochemistry showed, that Fgf10+/- (50% Fgf10 expression compared to WT) in hyperoxic condition at postnatal day 3 (P3) compared to WT has less vessel count in the lung and less muscularization of small capillaries in the lung. Furthermore, Fgf10+/- showed a drastic increase in mortality upon hyperoxic lung injury. Main question to be answer by this experiment is as followed: Does AEC II from Fgf10+/- mice in normoxia show different expression profiles at P3 compared to AEC II from WT? To adress this question we harvest lungs at P3 from WT and Fgf10+/- . For this the mice were sacrificed by Ketamin/ Dormitor ip, lungs were perfused transcardiac with PBS and directly frozen in liquid nitrogen.

2016-12-31 | GSE76300 | GEO

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