ArticleCell death & disease2016
β-Arrestin1 inhibits chemotherapy-induced intestinal stem cell apoptosis and mucositis.
Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 42 citations in OpenAlex.
- Article
- GPCR Biased Signaling in Cancer.Handbook of experimental pharmacology · 2026Review
- The secreted protein Amuc_1409 from Akkermansia muciniphila improves gut health through intestinal stem cell regulation.Nature communications · 2024Article
- Modulation of stem cell fate in intestinal homeostasis, injury and repair.World journal of stem cells · 2023Review
- Reg3α concentrations at day of allogeneic stem cell transplantation predict outcome and correlate with early antibiotic use.Blood advances · 2023Article
- From birth to death: The hardworking life of Paneth cell in the small intestine.Frontiers in immunology · 2023Review
- Experimental Chemotherapy-Induced Mucositis: A Scoping Review Guiding the Design of Suitable Preclinical Models.International journal of molecular sciences · 2022Article
- Structural basis and molecular mechanism of biased GPBAR signaling in regulating NSCLC cell growth via YAP activity.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Mechanisms modulating the activities of intestinal stem cells upon radiation or chemical agent exposure.Journal of radiation research · 2022Article
- Role of ARRB1 in prognosis and immunotherapy: A Pan-Cancer analysis.Frontiers in molecular biosciences · 2022Article
- Activation of G protein coupled estrogen receptor prevents chemotherapy-induced intestinal mucositis by inhibiting the DNA damage in crypt cell in an extracellular signal-regulated kinase 1- and 2- dependent manner.Cell death & disease · 2021Article
- Adult stem cells in endometrial regeneration: Molecular insights and clinical applications.Molecular reproduction and development · 2021Review
- Chemotherapeutics-Induced Intestinal Mucositis: Pathophysiology and Potential Treatment Strategies.Frontiers in pharmacology · 2021Review
- miR‑379‑5p inhibits cell proliferation and promotes cell apoptosis in non‑small cell lung cancer by targeting β‑arrestin‑1.Molecular medicine reports · 2020Article
- Exogenous L-arginine increases intestinal stem cell function through CD90+ stromal cells producing mTORC1-induced Wnt2b.Communications biology · 2020Article
- Regulation of HMGB1 release protects chemoradiotherapy-associated mucositis.Mucosal immunology · 2019Article
- Mechanisms of apoptosis modulation by curcumin: Implications for cancer therapy.Journal of cellular physiology · 2019Review
- β-Arrestins Regulate Stem Cell-Like Phenotype and Response to Chemotherapy in Bladder Cancer.Molecular cancer therapeutics · 2019Article
- Cleavage of arrestin-3 by caspases attenuates cell death by precluding arrestin-dependent JNK activation.Cellular signalling · 2019Article
- Blocking endothelin-1-receptor/β-catenin circuit sensitizes to chemotherapy in colorectal cancer.Cell death and differentiation · 2017Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanism of chemotherapy-induced gastrointestinal (GI) syndrome (CIGIS) is still controversial, and it is unclear whether chemotherapy induces intestinal stem cell (ISC) apoptosis. β-Arrestins are regulators and mediators of G protein-coupled receptor signaling in cell apoptosis, division and growth. In this study, we aimed to investigate whether chemotherapy induces ISC apoptosis to contribute to mucositis in CIGIS and whether β-arrestin1 (β-arr1) is involved in this apoptosis. Different chemotherapeutic agents were used to generate a CIGIS model. Lgr5-EGFP-IRES-creERT2(+/-) knock-in mice were used as a CIGIS model to investigate ISC apoptosis. β-arr1 knockout mice were used to determine whether β-arr1 is involved in the apoptosis in CIGIS. Intestinal histology was performed, the ISC apoptosis was analyzed and the mucosal barrier was examined. The effects of β-arr1 in apoptosis were investigated in the samples from humans and mice as well as in cell lines. Here, we demonstrate that chemotherapy induced intestinal mucositis by promoting crypt cell apoptosis, especially in Lgr5+ stem cells and Paneth cells but not in goblet cells, epithelial cells or vascular endothelial cells. Furthermore, β-arr1 deficiency exacerbated the Lgr5+ stem cell apoptosis, but not Paneth cell apoptosis, in CIGIS. In addition, the data showed that β-arr1 reduced the chemotherapy-induced Lgr5+ stem cell apoptosis by inhibiting endoplasmic reticulum stress-mediated mitochondrial apoptotic signaling. Our study indicates that β-arr1 inhibits chemotherapy-induced ISC apoptosis to alleviate intestinal mucositis in CIGIS.
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