ArticleProceedings of the National Academy of Sciences of the United States of America2019
TP53INP1 deficiency maintains murine B lymphopoiesis in aged bone marrow through redox-controlled IL-7R/STAT5 signaling.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 20 citations in OpenAlex.
- Thioredoxin is a metabolic rheostat controlling regulatory B cells.Nature immunology · 2024Article
- Advances in IL-7 Research on Tumour Therapy.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Myc-Interacting Zinc Finger Protein 1 (Miz-1) Is Essential to Maintain Homeostasis and Immunocompetence of the B Cell Lineage.Biology · 2022Article
- Autophagy Contributes to Metabolic Reprogramming and Therapeutic Resistance in Pancreatic Tumors.Cells · 2022Review
- TP53INP1 exerts neuroprotection under ageing and Parkinson's disease-related stress condition.Cell death & disease · 2021Article
- Distinct profile of CD34Journal of experimental & clinical cancer research : CR · 2021Article
- Single-cell RNA-seq reveals a concomitant delay in differentiation and cell cycle of aged hematopoietic stem cells.BMC biology · 2021Article
- MicroRNA-155-5p Contributes to 5-Fluorouracil Resistance Through Down-Regulating TP53INP1 in Oral Squamous Cell Carcinoma.Frontiers in oncology · 2021Article
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Authors and funding
11 authors at 1 institution in 1 country.
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Abstract
Bone marrow (BM) produces all blood and immune cells deriving from hematopoietic stem cells (HSCs). The decrease of immune cell production during aging is one of the features of immunosenescence. The impact of redox dysregulation in BM aging is still poorly understood. Here we use TP53INP1-deficient (KO) mice endowed with chronic oxidative stress to assess the influence of aging-associated redox alterations in BM homeostasis. We show that TP53INP1 deletion has no impact on aging-related accumulation of HSCs. In contrast, the aging-related contraction of the lymphoid compartment is mitigated in TP53INP1 KO mice. B cells that accumulate in old KO BM are differentiating cells that can mature into functional B cells. Importantly, this phenotype results from B cell-intrinsic events associated with defective redox control. Finally, we show that oxidative stress in aged TP53INP1-deficient mice maintains STAT5 expression and activation in early B cells, driving high
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