The effect of high fat diet on the transcriptome of murine dermal fibroblasts
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PROVIDER: PRJNA435492 | ENA |
REPOSITORIES: ENA
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Project description:During aging, stromal functions are thought to be impaired, yet little is known whether this stems from molecular and cellular changes of fibroblasts, a major component of stroma. Using population- and single-cell whole transcriptomics, and long-term lineage tracing, we studied alterations in murine dermal fibroblasts during physiological aging under different dietary regimes known to affect longevity. We show that the identity of aged fibroblasts becomes undefined, with the distinct fibroblast states present in young skin no longer clearly demarcated. In addition, old fibroblasts not only reduce the expression of genes involved in the formation of the extracellular matrix, but intriguingly, also gain adipogenic traits, paradoxically becoming similar to neonatal pro-adipogenic fibroblasts. These age-related alterations are sensitive to systemic changes in metabolism: long-term caloric restriction prevents them in old fibroblasts in a reversible manner, whereas a high-fat diet potentiates them in young fibroblasts. Finally, inhibition of the master regulator of adipogenesis, PPARgamma, attenuates fibroblast aging in vivo, providing potential anti-aging therapeutic alternatives to caloric restriction.
2018-11-14 | GSE110981 | GEO
Project description:The transcriptome of murine dermal fibroblasts
| PRJNA435488 | ENA
Project description:During aging, stromal functions are thought to be impaired, yet little is known whether this stems from molecular and cellular changes of fibroblasts, a major component of stroma. Using population- and single-cell whole transcriptomics, and long-term lineage tracing, we studied alterations in murine dermal fibroblasts during physiological aging under different dietary regimes known to affect longevity. We show that the identity of aged fibroblasts becomes undefined, with the distinct fibroblast states present in young skin no longer clearly demarcated. In addition, old fibroblasts not only reduce the expression of genes involved in the formation of the extracellular matrix, but intriguingly, also gain adipogenic traits, paradoxically becoming similar to neonatal pro-adipogenic fibroblasts. These age-related alterations are sensitive to systemic changes in metabolism: long-term caloric restriction prevents them in old fibroblasts in a reversible manner, whereas a high-fat diet potentiates them in young fibroblasts. Finally, inhibition of the master regulator of adipogenesis, PPARgamma, attenuates fibroblast aging in vivo, providing potential anti-aging therapeutic alternatives to caloric restriction.
2018-11-14 | GSE110978 | GEO
Project description:During aging, stromal functions are thought to be impaired, yet little is known whether this stems from molecular and cellular changes of fibroblasts, a major component of stroma. Using population- and single-cell whole transcriptomics, and long-term lineage tracing, we studied alterations in murine dermal fibroblasts during physiological aging under different dietary regimes known to affect longevity. We show that the identity of aged fibroblasts becomes undefined, with the distinct fibroblast states present in young skin no longer clearly demarcated. In addition, old fibroblasts not only reduce the expression of genes involved in the formation of the extracellular matrix, but intriguingly, also gain adipogenic traits, paradoxically becoming similar to neonatal pro-adipogenic fibroblasts. These age-related alterations are sensitive to systemic changes in metabolism: long-term caloric restriction prevents them in old fibroblasts in a reversible manner, whereas a high-fat diet potentiates them in young fibroblasts. Finally, inhibition of the master regulator of adipogenesis, PPARgamma, attenuates fibroblast aging in vivo, providing potential anti-aging therapeutic alternatives to caloric restriction.
2018-11-14 | GSE117762 | GEO
Project description:Transcriptomic analysis of murine aging dermal fibroblasts at single cell level.
2018-11-14 | GSE111136 | GEO
Project description:Younger age and obesity increase the incidence and rates of metastasis of triple-negative breast cancer (TNBC), an aggressive subtype of breast cancer. The tissue microenvironment, specifically the extracellular matrix (ECM), is known to promote tumor invasion and metastasis. We sought to characterize the effect of both age and obesity on the ECM of mammary fat pads. We used a diet-induced obesity (DIO) model where 10-week-old female mice were fed a high-fat diet (HFD) for 16 weeks or a control chow diet (CD) where time points were every 4 weeks to monitor age and obesity HFD progression. We isolated the mammary fat pads to characterize the ECM at each time point. Utilizing proteomics, we found that the early stages of obesity were sufficient to induce distinct differences in the ECM composition of mammary fat pads that promote TNBC cell invasion. ECM proteins previously implicated in driving TNBC invasion Collagen IV and Collagen VI, were enriched with weight gain. Together these data implicate ECM changes in the primary tumor microenvironment as mechanisms by which age and obesity contribute to breast cancer progression.
2024-06-06 | PXD050250 | Pride
Project description:We were interested in identifying proteins that are regulated in response to the extracellular matrix molecule, fibronectin, in dermal fibroblasts. To determine proteins regulated by exposure to fibronectin, primary murine dermal fibroblasts were cultured on tissue culture plastic or on tissue culture plates coated with a thin layer of fibronectin (2 μg/cm2). Fibroblasts were seeded at 35,000 cells/10 cm2 and were harvested 48 hours later. Cell pellets from these fibroblasts were shipped to Kinexus Bioinformatics Corp. (Vancouver, B.C.) where they were lysed and analyzed using the Kinex TM Antibody Microarray (KAM 1.2), which contains 800 (500 pan-specific and 300 phosphorylation site-specific) antibodies. This enabled us to identify candidate proteins regulated by exposure to fibronectin.
2011-06-22 | GSE30135 | GEO
Project description:During aging, stromal functions are thought to be impaired, yet little is known whether this stems from molecular and cellular changes of fibroblasts, a major component of stroma. Using population- and single-cell whole transcriptomics, and long-term lineage tracing, we studied alterations in murine dermal fibroblasts during physiological aging under different dietary regimes known to affect longevity. We show that the identity of aged fibroblasts becomes undefined, with the distinct fibroblast states present in young skin no longer clearly demarcated. In addition, old fibroblasts not only reduce the expression of genes involved in the formation of the extracellular matrix, but intriguingly, also gain adipogenic traits, paradoxically becoming similar to neonatal pro-adipogenic fibroblasts. These age-related alterations are sensitive to systemic changes in metabolism: long-term caloric restriction prevents them in old fibroblasts in a reversible manner, whereas a high-fat diet potentiates them in young fibroblasts. Finally, inhibition of the master regulator of adipogenesis, PPARgamma, attenuates fibroblast aging in vivo, providing potential anti-aging therapeutic alternatives to caloric restriction.
2018-11-14 | GSE110982 | GEO
Project description:During aging, stromal functions are thought to be impaired, yet little is known whether this stems from molecular and cellular changes of fibroblasts, a major component of stroma. Using population- and single-cell whole transcriptomics, and long-term lineage tracing, we studied alterations in murine dermal fibroblasts during physiological aging under different dietary regimes known to affect longevity. We show that the identity of aged fibroblasts becomes undefined, with the distinct fibroblast states present in young skin no longer clearly demarcated. In addition, old fibroblasts not only reduce the expression of genes involved in the formation of the extracellular matrix, but intriguingly, also gain adipogenic traits, paradoxically becoming similar to neonatal pro-adipogenic fibroblasts. These age-related alterations are sensitive to systemic changes in metabolism: long-term caloric restriction prevents them in old fibroblasts in a reversible manner, whereas a high-fat diet potentiates them in young fibroblasts. Finally, inhibition of the master regulator of adipogenesis, PPARgamma, attenuates fibroblast aging in vivo, providing potential anti-aging therapeutic alternatives to caloric restriction.
2018-11-14 | GSE117763 | GEO
Project description:During aging, stromal functions are thought to be impaired, yet little is known whether this stems from molecular and cellular changes of fibroblasts, a major component of stroma. Using population- and single-cell whole transcriptomics, and long-term lineage tracing, we studied alterations in murine dermal fibroblasts during physiological aging under different dietary regimes known to affect longevity. We show that the identity of aged fibroblasts becomes undefined, with the distinct fibroblast states present in young skin no longer clearly demarcated. In addition, old fibroblasts not only reduce the expression of genes involved in the formation of the extracellular matrix, but intriguingly, also gain adipogenic traits, paradoxically becoming similar to neonatal pro-adipogenic fibroblasts. These age-related alterations are sensitive to systemic changes in metabolism: long-term caloric restriction prevents them in old fibroblasts in a reversible manner, whereas a high-fat diet potentiates them in young fibroblasts. Finally, inhibition of the master regulator of adipogenesis, PPARgamma, attenuates fibroblast aging in vivo, providing potential anti-aging therapeutic alternatives to caloric restriction.
2018-11-14 | GSE110980 | GEO