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Enalapril mitigates senescence and aging-related phenotypes by targeting antioxidative genes via phosphorylated Smad1/5/9 [CUT&Tag]

ABSTRACT: Enalapril mitigates senescence and aging-related phenotypes by targeting antioxidative genes via phosphorylated Smad1/5/9 [CUT&Tag]

PROVIDER: PRJNA1164659 | ENA |

REPOSITORIES: ENA

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Enalapril mitigates senescence and aging-related phenotypes by targeting antioxidative genes via phosphorylated Smad1/5/9 [CUT&Tag]

Project description:Aging increases the risk of a myriad of chronic diseases, which are expensive and difficult to treat owing to their various risk factors. Repurposing existing medications has accelerated the development of therapies aimed at slowing aging. In this study, we revealed that enalapril, a drug widely prescribed for hypertension, can improve both cellular senescence and individual health. Mechanistically, phosphorylated Smad1/5/9 act as pivotal mediators of the anti-senescence properties of enalapril. It stimulates downstream genes involved in cell cycle regulation and antioxidative defense, facilitating cell proliferation and diminishing the production of reactive oxygen species (ROS), thus increasing the antioxidative ability of enalapril. At the organismal level, enalapril has been shown to bolster the physiological performance of various organs; it notably enhances memory capacity and renal function and relieves lipid accumulation. Our work highlights the potential of enalapril to augment antioxidant defenses and combat the effects of aging, thereby indicating its promise as a treatment strategy for aging-associated diseases and its use for healthy aging.

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Enalapril mitigates senescence and aging-related phenotypes by targeting antioxidative genes via phosphorylated Smad1/5/9 [RNA-seq]

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Enalapril mitigates senescence and aging-related phenotypes by targeting antioxidative genes via phosphorylated Smad1/5/9 [RNA-seq]

Project description:Enalapril mitigates senescence and aging-related phenotypes by targeting antioxidative genes via phosphorylated Smad1/5/9 [RNA-seq]

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ZSWIM4 regulates early embryonic patterning and BMP signaling pathway by promoting nuclear Smad1 degradation

Project description:The dorsoventral gradient of BMP signaling plays an essential role in embryonic patterning, with high BMP signal activating ventral-lateral mesoderm markers directly, and low BMP signal inducing neural tissues. The Zinc finger SWIM domain-containing protein 4 (zswim4) is expressed in the dorsal blastopore lip at the onset of Xenopus gastrula and then enriched at the forming neuroectoderm at mid-gastrula stages. Overexpression of zswim4 in Xenopus embryos causes inhibition of the anterior axis and shortened, curved body, and knockdown or knockout of zswim4 disturbed embryonic body axis formation and head development. The expression of ventral-lateral mesoderm marker genes was reduced after zswim4 overexpression and increased in embryos with zswim4 knockdown. Neural marker genes were repressed in zswim4 morphant. Mechanistically Zswim4 attenuates BMP signal through reducing protein stability of Smad1 in both Xenopus embryos and HEK293T cells. Zswim4 interacts with Smad1 and promotes ubiquitination of Smad1 in HEK293T cells. To identify the interaction partner of Zswim4 in regulating Smad1 stability, we performed SILAC based IP in HEK293T cells, and the precipitates were analyzed by Mass Spectrometry.

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Gene expression profiling of Smad1/5 cKO and Acvr2a cKO mice

Project description:We generated mice with single or double conditional inactivation of SMAD1 and SMAD5 using progesterone receptor (PR) cre (Smad1flox/flox;Smad5flox/flox;Pgr-cre+/-, or “Smad1/5 cKO”). Female mice with single SMAD1 or SMAD5 deletion were subfertile, whereas Smad1/5 cKO were infertile and had no visible implantation sites at 4.5 days post-coitum (dpc), indicating functional redundancy of SMAD1 and SMAD5. Histological and molecular analyses of the Smad1/5 cKO uteri during pregnancy determined that the infertility was the result of impaired uterine receptivity. During the window of implantation, uteri of Smad1/5 cKO mice responded abnormally to estradiol (E2) and to progesterone (P4), retained luminal PR expression, and displayed cytoplasmic FOXO1 mis-localization. Furthermore, uteri of Smad1/5 cKO mice did not respond to an artificial decidual stimulus and the stroma failed to differentiate. To determine the cell surface receptor complex that controls BMP signaling during implantation, we generated mice with conditional deletion of Acvr2a and Acvr2b using Pgr-cre+/-. We determined that Acvr2b cKO females were subfertile, while Acvr2a cKOs were infertile and displayed a range of ovarian and uterine abnormalities, including endometrial and implantation defects that phenocopied those of Smad1/5 cKO mice. Transcriptomic profiling of the Smad1/5 cKO and Acvr2a cKO uterus showed that genes involved in epithelial cell remodeling and microvilli/ciliated cell function were overrepresented in both genotypes. These results demonstrate that BMP signals mediated via ACVR2A and SMAD1/5 control endometrial receptivity and embryo implantation by remodeling the apicobasal polarity of the epithelium during the window of implantation.

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TGF-beta signalling through SMAD1/5 is required for epithelial-to-mesenchymal transition

Project description:TGF-beta treatment leads to SMAD1/5 phosphorylation. However, the ability of SMAD1/5 to bind chromatin downstream of TGF-beta signalling is unknown. We performed ChIP-sequencing for pSMAD1/5 and SMAD3 to identify binding sites for pSMAD1/5 upon TGF-beta stimulation and identified preferential pSMAD1/5 binding at SMAD1/5:SMAD4 consensus sites.

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SMAD1/5 binding regions of human umbilical vein endothelial cells (HUVECs) treated with BMP.

Project description:Smad1/5 binding regions were identified by ChIP-seq. HUVECs were treated with BMP for 1.5 h and anti-SMAD1/5 ChIP-seq analyses were performed using Illumina genome analyzer.

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SMAD1/5 binding regions of human pulmonary arterial smooth muscle cells (PASMCs) treated with BMP

Project description:Smad1/5 are transcription factors that engage in BMP-induced transcription. We determined and analyzed Smad1/5 binding sites by ChIP-sequencing. We used expression microarrays to compare the Smad1/5 binding sites identified by ChIP-seq to BMP-induced gene expressions.

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