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Senotherapeutic peptide treatment reduces biological age and senescence burden in human skin models

ABSTRACT: this work shows the safe reduction of the biological age of ex vivo human skins by a senomorphic peptide.

ORGANISM(S): Homo sapiens

PROVIDER: GSE230026 | GEO | 2023/04/20

REPOSITORIES: GEO

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Senotherapeutic peptide treatment reduces biological age and senescence burden in human skin models.

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Senotherapeutic peptide treatment reduces biological age and senescence burden in human skin models

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Project description:Cellular senescence contributes to aging and age-related dysfunction across multiple tissues, including the brain. Here, we identify tomatidine, an aglycone of tomatine naturally found in tomatoes, as a senotherapeutic agent. In vitro, tomatidine selectively suppressed SASP expression without affecting p16Ink4a or p21Cip1 levels in senescent human brain microvascular endothelial cells. In aged mice, dietary tomatidine reduced frailty and improved motor coordination and cognitive performance. These functional benefits were accompanied by a reduction in senescence markers (e.g., p16, p21, and telomere-associated DNA damage foci) in liver, skin, and hippocampal neurons, as well as decreased neuroinflammation and microglial activation. Tomatidine also reduced senescence in brain endothelial cells and increased the expression of tight junction–associated proteins. Together, these findings suggest that tomatidine is as a promising senotherapeutic with the potential to preserve cognitive and vascular function during aging. As a naturally occurring compound with oral bioavailability and a favorable safety profile, tomatidine holds strong translational promise for future therapeutic development.

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Correction to: Old plasma dilution reduces human biological age: a clinical study.

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Endothelial AGO1 Deficiency Reduces Breast Cancer Burden in Mice

Project description:Endothelial cells are crucial in cancer development and progression, in part through tumor angiogenesis and immune modulation. As a key component of RNA-induced silencing complex, Argonaute 1 (AGO1) protein has been shown to regulate tumor biology. However, its role in ECs within the tumor microenvironment remains undefined. In this study, we investigated the effects of EC-conditional AGO1 knockout (EC-AGO1-KO) on tumor vascularization and immune regulation in a mouse xenograft breast cancer model. EC-AGO1-KO developed significantly reduced tumor burden when compared to their wild-type littermates. The tumor suppression was accompanied by lower tumor vascularization and stronger immune infiltration. Histological and single cell RNA sequencing analysis revealed that tumors in the EC-AGO1-KO mice exhibited increased CD8⁺ T cells and macrophages, reflecting a pro-immunostimulatory microenvironment. In vitro experiments show that EC-AGO1-knockdown (AGO1-KD) conditioned media suppresses breast cancer cell migration, attendant with the downregulation of C-X-C chemokine receptor type 4 (CXCR4) and upregulation of RUNX1 Partner Transcriptional Co-Repressor 1 (RUNX1T1). These findings suggest that EC-AGO1 plays a crucial role in regulating tumor angiogenesis and immune cell infiltration, thereby influencing tumor progression. Targeting EC AGO1 may offer a novel therapeutic strategy for disrupting tumor vascularization while enhancing anti-tumor immunity.

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