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Impact of BMP and WNT signaling modulation on mesendoderm progenitor cells specification from hPSCs in 3D culture conditions

ABSTRACT: We report a bulk RNA sequencing analysis of a population containing different mesendoderm progenitor cells derived from hiPSCs in 3D environment. Specifically, 3D aggregates of hPSCs were differentiated into cardiac progenitor cells through WNT signaling activation from day 0 to day 1 and WNT signaling inhibition from day 3 to day 5 of differentiation, which allowed further efficient and reproducible specification into hiPSC-derived CMs. This represents the control protocol from which samples from D3 (D3N) and D5 (D5N) were collected. Additionally, adaptation of this control protocol by performing WNT and BMP signalling pathways activation from day 3 to day 5 of differentiation, allowed the modulation of the progenitor cells population to a more posterior splanchnic mesoderm which favours further specification of those progenitors into hiPSC-derived pro-epicardium/septum transversum cells. This represents the CB protocol from where samples from D3 (D3CB) and D5 (D5CB) were collected.

ORGANISM(S): Homo sapiens

PROVIDER: GSE184302 | GEO | 2022/08/01

REPOSITORIES: GEO

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Project description:Longevity mechanisms increase lifespan by counteracting the effects of aging. However, whether longevity mechanisms counteract the effects of aging continually throughout life, or whether they act during specific periods of life, preventing changes that precede mortality is unclear. Here, we uncover transcriptional drift, a phenomenon that describes how aging causes genes within functional groups to change expression in opposing directions. These changes cause a transcriptome-wide loss in mRNA stoichiometry and loss of co-expression patterns in aging animals, as compared to young adults. Using Caenorhabditis elegans as a model, we show that extending lifespan by inhibiting serotonergic signals by the antidepressant mianserin attenuates transcriptional drift, allowing the preservation of a younger transcriptome into an older age. Our data are consistent with a model in which inhibition of serotonergic signals slows age-dependent physiological decline and the associated rise in mortality levels exclusively in young adults, thereby postponing the onset of major mortality. In this study set out to measure aging in the transcriptome by determining drift-variance changes with age in C.elegans. We set up three different cohorts of water or mianserin treated animals. The title of each cohort indicates the treatment (e.g. h2o or mia), the concentration (mia2, mia10, mia50), the day when the treatment was started (e.g. d1= day 1 of adulthood) and the day when the sample was collected (e.g. d10= day 10 of adulthood). cohort #1: Celegans was treated with water or mianserin (50uM) on day 1 and RNA was harvested on day1 (water only), d3, d5 and day 10 (file titles: h2o d1/d1, h2o d1/d3, h2o d1/d5, h2o d1/d10, mia50 d1/d3, mia50 d1/d5, mia50 d1/d10) cohort #2: Celegans was treated with mianserin (50uM) starting on day 3, and day 5, RNA was harvested on day 5 or 10 (file titles: mia50 d3/d10, mia50 d5/d10, mia50 d3/d5) cohort #3: Celegans was treated with mianserin 2 uM and 10 uM Mianserin on day 1 and Rna harvested on day 5 (file titles: mia2 d1/d5, mia10 d1/d5)

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Impact of BMP and WNT signaling modulation on mesendoderm progenitor cells specification from hPSCs in 3D culture conditions

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