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Aneurysm Is Restricted by CD34 + Cell-Formed Fibrous Collars Through the PDGFRb-PI3K Axis.

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  • معلومة اضافية
    • المصدر:
      Publisher: WILEY-VCH Country of Publication: Germany NLM ID: 101664569 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2198-3844 (Electronic) Linking ISSN: 21983844 NLM ISO Abbreviation: Adv Sci (Weinh) Subsets: MEDLINE
    • بيانات النشر:
      Original Publication: Weinheim : WILEY-VCH, [2014]-
    • الموضوع:
      Antigens, CD34*/metabolism ; Antigens, CD34*/genetics ; Aortic Aneurysm, Abdominal*/metabolism ; Aortic Aneurysm, Abdominal*/pathology ; Aortic Aneurysm, Abdominal*/genetics ; Receptor, Platelet-Derived Growth Factor beta*/metabolism ; Receptor, Platelet-Derived Growth Factor beta*/genetics ; Phosphatidylinositol 3-Kinases*/metabolism ; Phosphatidylinositol 3-Kinases*/genetics; Animals ; Mice ; Humans ; Myofibroblasts/metabolism ; Disease Models, Animal ; Male ; Signal Transduction ; Mice, Inbred C57BL
    • نبذة مختصرة :
      Aortic aneurysm is a life-threatening disease caused by progressive dilation of the aorta and weakened aortic walls. Its pathogenesis involves an imbalance between connective tissue repair and degradation. CD34 + cells comprise a heterogeneous population that exhibits stem cell and progenitor cell properties. However, the role of CD34 + cells in abdominal aortic aneurysm (AAA) remains unclear. In this study, downregulated CD34 expression is observed in aneurysmal aortas from both patients and mouse models compared to that in non-dilated aortas. Furthermore, by combining Cd34-CreER T2 ;Rosa26-tdTomato;(Apoe -/- ) lineage tracing, bone marrow transplantation, and single-cell sequencing, it is found that during AAA development, non-bone marrow CD34 + cells are activated to transdifferentiate into Periostin + myofibroblasts, thereby contributing to the formation of fibrotic collars. Dual recombinase-based lineage tracing confirms the presence and involvement of CD34 + /Periostin + myofibroblasts in fibrotic collar formation during AAA development. Functionally, selective depletion of systemic or non-bone marrow CD34 + cells, as well as CD34 + /Periostin + myofibroblasts, by diphtheria toxin significantly exacerbates AAA progression and increases disease mortality. Mechanistically, it is identified that the PDGF-PDGFRb-PI3K axis is indispensable for Periostin + myofibroblast generation from non-bone marrow CD34 + cells in AAA, offering a new therapeutic target for patients with AAA at a high risk of rupture.
      (© 2024 The Author(s). Advanced Science published by Wiley‐VCH GmbH.)
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    • Grant Information:
      82030008 National Natural Science Foundation of China; 82400550 National Natural Science Foundation of China; 82170489 National Natural Science Foundation of China; 82470428 National Natural Science Foundation of China; 81700420 National Natural Science Foundation of China; 32300945 National Natural Science Foundation of China; 31830039 National Natural Science Foundation of China; LR22H020001 Natural Science Foundation of Zhejiang Province; LQ23H020006 Natural Science Foundation of Zhejiang Province; LHDMZ24H02000 Natural Science Foundation of Zhejiang Province; 2024Z232 Ningbo Key Research and Development Program; 2024Z210 Ningbo Key Research and Development Program; 2024KY281 Medical and Health Science and Technology Projects of Zhejiang Province; PG/15/11/31279 United Kingdom BHF_ British Heart Foundation; PG/15/86/31723 United Kingdom BHF_ British Heart Foundation; PG/20/10458 United Kingdom BHF_ British Heart Foundation; PG/23/11371 United Kingdom BHF_ British Heart Foundation
    • Contributed Indexing:
      Keywords: CD34+ cells; PDGFRb; aneurysms; fibroblasts; genetic cell lineage tracings
    • الرقم المعرف:
      0 (Antigens, CD34)
      EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor beta)
      EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
    • الموضوع:
      Date Created: 20241228 Date Completed: 20250429 Latest Revision: 20250429
    • الموضوع:
      20250429
    • الرقم المعرف:
      PMC11831520
    • الرقم المعرف:
      10.1002/advs.202408996
    • الرقم المعرف:
      39731355