Senotherapeutic peptide treatment reduces biological age and senescence burden in human skin models
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ABSTRACT:
PROVIDER: PRJNA956991 | ENA |
REPOSITORIES: ENA
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Project description:this work shows the safe reduction of the biological age of ex vivo human skins by a senomorphic peptide.
2023-04-20 | GSE230026 | GEO
Project description:Cellular senescence is known to play a role in age-related skin function deterioration which potentially influences longevity. Here, a two-step phenotypic screening was performed to identify senotherapeutic peptides, leading to the identification of Peptide (Pep) 14. Pep 14 effectively decreased human dermal fibroblast senescence burden induced by Hutchinson-Gilford Progeria Syndrome (HGPS), chronological aging, ultraviolet-B radiation (UVB), and etoposide treatment, without inducing significant toxicity. Pep 14 functions via modulation of PP2A, an understudied holoenzyme that promotes genomic stability and is involved in DNA repair and senescence pathways. At the single-cell level, Pep 14 modulates genes that prevent senescence progression by arresting the cell cycle and enhancing DNA repair, which consequently reduce the number of cells progressing to late senescence. When applied on aged ex vivo skin, Pep 14 promoted a healthy skin phenotype with structural and molecular resemblance to young ex vivo skin, decreased the expression of senescence markers, including SASP, and reduced the DNA methylation age. In summary, this work shows the safe reduction of the biological age of ex vivo human skins by a senomorphic peptide.
| S-EPMC10203313 | biostudies-literature
Project description:PRDM16 reduces cellular senescence by upregulating GSTM1
| PRJNA1314125 | ENA
Project description:The widespread use of chemical inputs in agriculture has raised concern over their long-term environmental and health impacts, driving demand for sustainable, natural product-based alternatives. Peptide-hormone signaling interactions, particularly those regulating senescence, are promising targets for developing such alternatives to advance postharvest technologies. However, most current insights stem from model species, limiting their translation to crops and ornamental plants. This study identifies the CLAVATA3/EMBRYO-SURROUNDING REGION-related (CLE) family CLE12 peptide (CLE12p) in Lactuca sativa as a peptide that shows potential for postharvest management of crops and ornamental flowers. CLE12p interacts with salt (NaCl), abscisic acid (ABA) and ethylene pathways, influencing lettuce development and morphology. Notably, CLE12p induced stomatal closure in a similar manner to that of ABA, suggesting overlapping signalling pathways. Transcriptomic analyses revealed how CLE12p modulates immune and defence responses, fluid transport, and leaf senescence, indicating a broader role in leaf senescence regulation similar to that of ethylene. Functionally, CLE12p delayed senescence in lettuce by preserving leaf greenness and water content following dark treatment and harvest. Additionally, CLE12p extended the longevity of cut roses by maintaining fresh weight and water content. These findings demonstrate the practical potential of CLE peptides in non-model species and support their application as natural tools for extending postharvest shelf life in crops and ornamental plants, paving the way for further exploration of their role in agricultural biotechnology.
2025-11-18 | GSE299676 | GEO
Project description:To understand the mechanism underlying the role of MOTS-c in protecting pancreatic islets from senescence, we performed gene microarray analyses in pancreatic islet cells treated with either MOTS-c or a scrambled peptide
2025-09-11 | GSE305383 | GEO
Project description:FXR Agonism with Bile Acid Mimetic Reduces Pre-Clinical Triple-Negative Breast Cancer Burden
| PRJNA1096356 | ENA
Project description:LsCLE12 peptide delays senescence in lettuce and prolongs postharvest life of roses
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Project description:Aberrant protein aggregation jeopardize cellular functionality and underlies the development of a myriad of late-onset maladies including Alzheimer’s disease (AD) and Huntington’s disease (HD). Accordingly, molecules that mitigate the toxicity of hazardous protein aggregates are of great interest as potential future therapeutics. Here we asked whether a small peptide, composed of five amino acids (5MER peptide) that was derived from the human pro-inflammatory CD44, could protect model nematodes from the toxicity of aggregative proteins that underlie the development of neurodegenerative disorders in humans. We found that the 5MER peptide mitigates the toxicity that stems from both, the AD-causing Aβ peptide and a stretch of poly-glutamine that is accountable to the development of several disorders including HD, without affecting lifespan. This protection was dependent on the activity of the aging-regulating transcription factors and associated with enhanced Aβ and polyQ35-YFP aggregation. A transcriptomic analysis unveiled that the peptide modulates the expression of various genes including these which are known as protein homeostasis (proteostasis) regulators such as txt-13, and modifiers of proteasome activity. The knockdown of txt-13 protects worms from proteotoxicity to the same extent as the 5MER peptide, suggesting that the peptide activates the transcellular chaperone signaling to promote proteostasis. Together, our results propose that the 5MER peptide should be considered as a component of future therapeutic cocktails for the treatment of neurodegenerative maladies.
2023-12-27 | GSE230640 | GEO
Project description:Cellular senescence is a hallmark of aging and the accumulation of senescent cells (SnCs) accelerates the aging process, contributing to aging-related organ disorders. The PRDF1 and RIZ1 homology domain (PRDM) protein exhibits robust transcriptional regulatory activities and governs a wide range of biological processes. However, its roles in cellular senescence remain unclear. Here, we demonstrated that PRDM16, a member of the PRDM protein family, decreased significantly in multiple organs of aged mice compared to young mice. Global Prdm16 deletion contributed to cellular senescence in various organs, including the kidneys, heart, lungs, hippocampus, stomach, and gut, leading to accelerated aging-related organ injury. Furthermore, tubular-specific Prdm16 deletion aggravated irradiation-induced kidney aging and aging-related kidney diseases in irradiated mice subjected to ischemia-reperfusion surgery. Exogenous PRDM16 gene delivery by lentivirus effectively attenuated cellular senescence in vitro and in vivo. Mechanistically, PRDM16 improved glutathione metabolism and inhibited oxidative DNA damage, which is a driving force of senescence. Specifically, PRDM16 upregulated the transcription of glutathione S-transferase mu 1 (GSTM1) by binding to its promoter region. Transfection with GSTM1 reversed PRDM16 deficiency-induced cellular senescence and kidney aging. Collectively, our results provide a potential target for the investigation of anti-aging therapies.
2025-09-02 | GSE307024 | GEO
Project description:Mitochondrial-encoded peptide MOTS-c prevents pancreatic islet cell senescence to delay diabetes
| PRJNA1305433 | ENA