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from: Kaohsiung
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| 2024-01-19 12:45:42 | onclick： | New mechanism of autophagy regulation of human granulocyte progenitor cells |
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Recently, Pan Guangjin, a researcher at the Guangzhou Institute of Biomedicine and Health of the Chinese Academy of Sciences, revealed the key mechanism of rapid manufacturing amplification of human leukocytes under emergency conditions.The results were published in the Stem Cell Report.
In emergency situations such as infection, a large number of white blood cells are produced to fight infection, called leukocyte emergency manufacturing (EM).Some patients have leukemia emergency manufacturing and lead to a decrease in white blood cells, which is easy to induce various serious infections.At present, the mechanism of human leukocyte emergency manufacturing is not very clear. Based on the pre-developed human pluripotent stem cells in vitro hematopoietic differentiation system, the researchers established human leukemia emergency manufacturing (EM).In the process of human mobilization of hematopoietic stem/progenitor cells (HSPCs) and human pluripotent stem cell-derived HSPCs, they discovered that cells can rapidly proliferate and amplify white blood cells by eating p53.
The results showed that the autophagy-deficient granulocyte could recover the amplification ability of autophagy-deficient granulocyte by overexpression of full-length ATG7 instead of mutant ATG7.These results demonstrate that ATG7 maintains the amplification ability of granulocyte progenitors during EM through autophagy-dependent functions.The researchers found that autophagy-deficient granulocyte progenitors accumulated large amounts of p53 protein, which has a strong ability to inhibit cell proliferation, suggesting that autophagy may promote stable value-added granulocytes by degrading p53 protein.Furthermore, after knocking down p53 in autophagy-deficient granulocyte progenitor cells, the amplification ability of granulocyte progenitor cells in EM process can be significantly restored.
The study showed that ATG7-dependent autophagy released the proliferation ability of granulocyte progenitor cells by degrading p53 protein, thus guaranteeing the amplification of granulocyte progenitor cells during EM.This study provides new insights into the differentiation and amplification regulation of human granulocytes and potential targets for clinical development of leukemia caused by granulocyte heterozygosity and granulocytosis caused by amplification disorders.
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