G protein-coupled receptor 68 increases the number of B lymphocytes
AJBR Copyright © 2020..
G protein-coupled receptor 68 (GPR68) is a proton sensor that is activated upon binding to extracellular protons. We have previously found that GPR68 induces a proapoptotic pathway in bone marrow (BM) cells from the patients with myelodysplastic syndromes (MDS) after treated with lenalidomide. However, the function of GPR68 in normal hematopoietic cells remains unclear. With genetic loss of function approach, we found reduced frequency and number of B lymphocytes in the peripheral blood (PB) of whole body Gpr68-/- mice compared to control littermates upon aging. During hematopoietic regeneration, such as in response to fluorouracil (5-FU), we also found reduced frequency and number of B lymphocytes in Gpr68-/- mice compared to wild type mice. Mechanism studies revealed that Gpr68 expression was upregulated in B lymphocytes of BM during aging and in hematopoietic progenitor cells after treatment with 5-FU. In addition, activation of Gpr68 by its activators increased the frequency and number of B lymphocytes. Our studies indicate that Gpr68 expression is upregulated in hematopoietic cells upon aging and during hematopoietic regeneration that ends up with increased number of B lymphocytes.
Medienart: |
Artikel |
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Erscheinungsjahr: |
2020 |
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Erschienen: |
2020 |
Enthalten in: |
Zur Gesamtaufnahme - volume:10 |
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Enthalten in: |
American journal of blood research - 10(2020), 2 vom: 08., Seite 15-21 |
Sprache: |
Englisch |
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Beteiligte Personen: |
He, Xiaofei [VerfasserIn] |
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Themen: |
G protein-coupled receptors |
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Anmerkungen: |
Date Revised 28.09.2020 published: Electronic-eCollection Citation Status PubMed-not-MEDLINE |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM309942225 |
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520 | |a G protein-coupled receptor 68 (GPR68) is a proton sensor that is activated upon binding to extracellular protons. We have previously found that GPR68 induces a proapoptotic pathway in bone marrow (BM) cells from the patients with myelodysplastic syndromes (MDS) after treated with lenalidomide. However, the function of GPR68 in normal hematopoietic cells remains unclear. With genetic loss of function approach, we found reduced frequency and number of B lymphocytes in the peripheral blood (PB) of whole body Gpr68-/- mice compared to control littermates upon aging. During hematopoietic regeneration, such as in response to fluorouracil (5-FU), we also found reduced frequency and number of B lymphocytes in Gpr68-/- mice compared to wild type mice. Mechanism studies revealed that Gpr68 expression was upregulated in B lymphocytes of BM during aging and in hematopoietic progenitor cells after treatment with 5-FU. In addition, activation of Gpr68 by its activators increased the frequency and number of B lymphocytes. Our studies indicate that Gpr68 expression is upregulated in hematopoietic cells upon aging and during hematopoietic regeneration that ends up with increased number of B lymphocytes | ||
650 | 4 | |a Journal Article | |
650 | 4 | |a G protein-coupled receptors | |
650 | 4 | |a GPR68 agonist | |
650 | 4 | |a GPR68 allosteric modulator | |
650 | 4 | |a hematologic regeneration | |
650 | 4 | |a hematopoiesis | |
650 | 4 | |a stress hematopoiesis | |
700 | 1 | |a Feng, Saran |e verfasserin |4 aut | |
700 | 1 | |a Hawkins, Caleb |e verfasserin |4 aut | |
700 | 1 | |a Lawley, Lauren |e verfasserin |4 aut | |
700 | 1 | |a Fan, Wenxin |e verfasserin |4 aut | |
700 | 1 | |a Xu, Yan |e verfasserin |4 aut | |
700 | 1 | |a Zha, Xiang-Ming |e verfasserin |4 aut | |
700 | 1 | |a Fang, Jing |e verfasserin |4 aut | |
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