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Acetylated proteomic identification of stored platelets

ABSTRACT: In this project, the protein acetylation levels in human platelets and in WT and SIRT3-/- mouse platelets during storage were examined.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human) Mus Musculus (mouse)

TISSUE(S): Blood Platelet, Blood Cell

SUBMITTER: Xuemei Fan

LAB HEAD: Junling Liu

PROVIDER: PXD026341 | Pride | 2022-06-09

REPOSITORIES: pride

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			Action	DRS
	7684TPAC.zip	Other
	7684TPAc_1.raw	Raw
	7684TPAc_2.raw	Raw
	7684TPAc_3.raw	Raw
	7684TPAc_4.raw	Raw

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Publications

CPT2 K79 acetylation regulates platelet life span.

Fan Xuemei X Wang Yang Y Cai Xiaohong X Shen Yingzhi Y Xu Tongran T Xu Yanyan Y Cheng Jinke J Wang Xuefeng X Zhang Lin L Dai Jing J Lin Shuhai S Liu Junling J

Blood advances 20220901 17

The short life span of platelets is a major challenge to platelet transfusion services because of the lack of effective intervention. Here, we found that the accumulation of long-chain acylcarnitines (LCACs) is responsible for mitochondrial damage and platelet storage lesion. Further studies showed that the blockade of fatty acid oxidation and the activation of AMP-activated protein kinase (AMPK)/acetyl-CoA carboxylase/carnitine palmitoyltransferase 1 (CPT1) pathways that promote fatty acid meta ...[more]

PMID: 35728063

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Project description:Sirtuin 3 (SIRT3) is an NAD+-dependent deacetylase involved in various physiological and pathological processes. However, the role of SIRT3 in regulating human stem cell senescence remains largely unknown. Here, we observed the downregulated expression of SIRT3 in senescent human mesenchymal stem cells (hMSCs). SIRT3 deficiency accelerated cellular senescence in hMSCs, along with compromised nuclear integrity, loss of heterochromatin and increased DNA damage. These aging-associated nuclear defects were attenuated by the reintroduction of SIRT3. Mechanistic studies demonstrated the interaction of SIRT3 with nuclear envelope proteins and heterochromatin-associated proteins. Further findings revealed that SIRT3 deficiency led to the loss of lamina-associated domains (LADs) from the nuclear lamina, increased chromatin accessibility and aberrant transcription of repetitive sequences. Meanwhile, the overexpression of nuclear-localized SIRT3 rescued the senescence phenotypes. Taken together, our study reveals a novel role of nuclear SIRT3 in stabilizing heterochromatin and counteracting hMSC senescence, which may provide new clinical therapeutic targets to ameliorate aging-related diseases.

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SIRT3 interactions and mitochondrial proteome during HCMV infection

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Remodelling of the acetylproteome by SIRT3 manipulation fails to affect insulin secretion or beta-cell metabolism in the absence of over nutrition

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