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In vivo partial reprogramming alters manifestation of age-associated molecular changes in aging mice (1 months; sort-term treatment)

ABSTRACT: Various length of in vivo 4F (four Yamanaka factors) partial reprogramming protocols were performed to evaluate effects of longer-term partial reprogramming in physiologically aging wild-type mice. Here, short-term (1 months) partial reprogramming was induced and transcriptional changes in various tissues were compared to age-matched, untreated mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE190984 | GEO | 2022/01/11

REPOSITORIES: GEO

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In vivo partial reprogramming alters manifestation of age-associated molecular changes in aging mice (7 months; long-term treatment)

Project description:Various length of in vivo 4F (four Yamanaka factors) partial reprogramming protocols were performed to evaluate effects of longer-term partial reprogramming in physiologically aging wild-type mice. Here, long-term (7 months) partial reprogramming was induced and transcriptional changes in various tissues were compared to age-matched, untreated mice.

2022-01-11 | GSE190983 | GEO

In vivo partial reprogramming alters manifestation of age-associated molecular changes in aging mice (10 months; long-term treatment)

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2022-01-11 | GSE190985 | GEO

In vivo partial reprogramming in 4F mice

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In vivo partial reprogramming in 4F mice

Project description:In vivo partial reprogramming in 4F mice

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In vivo partial reprogramming alters manifestation of age-associated molecular changes in aging mice (1 months sort-term treatment)

Project description:In vivo partial reprogramming alters manifestation of age-associated molecular changes in aging mice (1 months sort-term treatment)

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In vivo reprogramming drives dedifferentiation and enhances liver regeneration

Project description:Mammalian tissues have a limited regenerative capacity. Previous studies showed that dedifferentiation contributes to tissue regeneration in non-mammalian vertebrate species such as zebrafish and newt. However, dedifferentiation is rarely observed in mammalian tissues even in the neonatal stage and therefore artificial induction of dedifferentiation might enhance regeneration in mammalian tissues. Here we demonstrate that short-term expression of Yamanaka 4 factors (4F) induces dedifferentiation and proliferation in the liver by using lineage-traceable, hepatocyte-specific 4F inducible mouse model. Global transcriptome analysis shows that 4F expression transiently reduces the expression of hepatic-lineage markers and induces the expression of a large set of proliferative markers and epigenetic modifiers along with global epigenetic changes as assessed by DNA-accessibility analysis. More importantly, lineage-tracing experiments showed that 4F-expressing hepatocytes acquire liver stem/progenitor cell markers, suggesting that 4F induces partial reprogramming. Moreover, 4F enhances MyoD-mediated transdifferentiation in the liver, suggesting that 4F endows hepatocytes with plasticity. Lastly, 4F expression attenuated liver injury associated with more proliferative capacity and better survival rate, indicating that 4F enhances liver regeneration. Taken together, these results demonstrate that liver-specific 4F expression induces dedifferentiation and promotes liver regeneration.

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Partial pluripotent reprogramming in C2C12 myoblasts

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Multi-omics characterization of partial chemical reprogramming reveals evidence of cell rejuvenation [RNA-seq]

Project description:Partial reprogramming by cyclic short-term expression of Yamanaka factors holds promise for shifting cells to younger states and consequently delaying the onset of many diseases of aging. However, the delivery of transgenes and potential risk of teratoma formation present challenges forin vivoapplications. Recent advances include the use of cocktails of compounds to reprogram somatic cells, but the characteristics and mechanisms of partial cellular reprogramming by chemicals remain unclear. Here, we report a multi-omics characterization of partial chemical reprogramming in fibroblasts from young and aged mice. We measured the effects of partial chemical reprogramming on the epigenome, transcriptome, proteome, phosphoproteome, and metabolome. At the transcriptome, proteome, and phosphoproteome levels, we saw widescale changes induced by this treatment, with the most notable signature being an upregulation of mitochondrial oxidative phosphorylation. Furthermore, at the metabolome level, we observed a reduction in the accumulation of aging-related metabolites. Using both transcriptomic and epigenetic clock-based analyses, we show that partial chemical reprogramming reduces the biological age of mouse fibroblasts. We demonstrate that these changes have functional impacts, as evidenced by changes in cellular respiration and mitochondrial membrane potential. Taken together, these results illuminate the potential for chemical reprogramming reagents to rejuvenate aged biological systems, and warrant further investigation into adapting these approaches forin vivoage reversal.

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Multi-omics characterization of partial chemical reprogramming reveals evidence of cell rejuvenation [Array]

Project description:Partial reprogramming by cyclic short-term expression of Yamanaka factors holds promise for shifting cells to younger states and consequently delaying the onset of many diseases of aging. However, the delivery of transgenes and potential risk of teratoma formation present challenges for in vivo applications. Recent advances include the use of cocktails of compounds to reprogram somatic cells, but the characteristics and mechanisms of partial cellular reprogramming by chemicals remain unclear. Here, we report a multi-omics characterization of partial chemical reprogramming in fibroblasts from young and aged mice. We measured the effects of partial chemical reprogramming on the epigenome, transcriptome, proteome, phosphoproteome, and metabolome. At the transcriptome, proteome, and phosphoproteome levels, we saw widescale changes induced by this treatment, with the most notable signature being an upregulation of mitochondrial oxidative phosphorylation. Furthermore, at the metabolome level, we observed a reduction in the accumulation of aging-related metabolites. Using both transcriptomic and epigenetic clock-based analyses, we show that partial chemical reprogramming reduces the biological age of mouse fibroblasts. We demonstrate that these changes have functional impacts, as evidenced by changes in cellular respiration and mitochondrial membrane potential. Taken together, these results illuminate the potential for chemical reprogramming reagents to rejuvenate aged biological systems, and warrant further investigation into adapting these approaches for in vivo age reversal.

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In vivo partial reprogramming alters manifestation of age-associated molecular changes in aging mice (7 months long-term treatment)

Project description:In vivo partial reprogramming alters manifestation of age-associated molecular changes in aging mice (7 months long-term treatment)

| PRJNA789253 | ENA

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