Blood: Transplanted hematopoietic cells transfer mitochondrials to recipient interstate-charged stem cells to promote bone marrow reconstruction.

The fate of hematocytes/subgeneration cells (HSPC) is strictly regulated by their bone marrow (BM) micro-environment (ME).
bone marrow transplantation (BMT) often requires radiation pre-treatment to remove endologic hematologic cells.
so far, it is not clear whether the mesotherapic ME is damaged after radiotherapy and how it will recover.
24h and 48h after radiotherapy, the mitochondrial volume of bone marrow substation premediotic cells decreased significantly, and the study found that BM interstate-charged stem cells (MSCs) suffered severe damage to their mitochondrial function after radiotherapy.
healthy HSPC transfers functional mitochondrials to the substiter ME, thereby improving the mitochondrial activity of the subject MSC.
the transfer of mitochondrials from healthy HSPC to MSC depends on cell contact and is mediated by the HSPC-connected protein 43 (Cx43). the mitochondrial transfer of
Cx43 defective supply HSPC to BM MSC reduced the amount of mitochondrial transfer in chisel mice with hematocyte Cx43 defects, and the reduction in mitochondrial transfer was achieved by re-expression of Cx43 in HSPC or by adding to the medium mitochondrial isolated from Cx43 defective HSPC.
AMPK inhibits the transfer of ATP levels within the transferred HSPC cells of the mitochondrial, which activates the pyrethromemum receptor P2RX7, resulting in a decrease in AMPK activity, which significantly increases the transport of mitochondrials to BM MSC.
mitochondrial metastasis promotes the proliferation of the substrate cells and hematosis restores mitochondrial metastasis, the host substrate ME is restored and the supply HSPC implantation increases.
Cx43 delays the regeneration of interstate and osteoblasts, while AMPK inhibition in the body promotes interstate recovery.
, the reconstruction of the hemast chambers has also been improved as a result of the recovery of the supportive substitin ME.
, the results show that the HSPC of a healthy provider not only reconstructs the transplanted hema production system, but also supports and induces metabolic recovery of ME from radiation damage in the recipient through mitochondrial metastasis.
understanding the regulatory mechanism of substation recovery after myelin stress is of great clinical significance for optimizing bone marrow transplantation procedures and emphasizing the importance of auxiliary, non-HSC in promoting hema production implantation.
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