• Medientyp: E-Artikel
  • Titel: Substance P stimulates the recovery of bone marrow after the irradiation
  • Beteiligte: An, You Sun; Lee, EunAh; Kang, Mi‐Hyun; Hong, Hyun Sook; Kim, Mi‐Ra; Jang, Won Seok; Son, Youngsook; Yi, Jae Youn
  • Erschienen: Wiley, 2011
  • Erschienen in: Journal of Cellular Physiology
  • Sprache: Englisch
  • DOI: 10.1002/jcp.22447
  • ISSN: 0021-9541; 1097-4652
  • Schlagwörter: Cell Biology ; Clinical Biochemistry ; Physiology
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  • Beschreibung: <jats:title>Abstract</jats:title><jats:p>The therapeutic use of ionizing radiation (e.g., X‐rays and γ‐rays) needs to inflict minimal damage on non‐target tissue. Recent studies have shown that substance P (SP) mediates multiple activities in various cell types, including cell proliferation, anti‐apoptotic responses, and inflammatory processes. The present study investigated the effects of SP on γ‐irradiated bone marrow stem cells (BMSCs). In mouse bone marrow extracts, SP prolonged activation of Erk1/2 and enhanced Bcl‐2 expression, but attenuated the activation of apoptotic molecules (e.g., p38 and cleaved caspase‐3) and down‐regulated Bax. We also observed that SP‐decreased apoptotic cell death and stimulated cell proliferation in γ‐irradiated mouse bone marrow tissues through TUNEL assay and PCNA analysis. To determine how SP affects bone marrow stem cell populations, mouse bone marrow cells were isolated and colony‐forming unit (CFU) of mesenchymal stem cells (MSCs) and hematopoietic stem cells (HSCs) was estimated. SP‐pretreated ones showed higher CFUs of MSC and HSC than untreated ones. Furthermore, when SP was pretreated in cultured human MSC, it significantly decreased apoptotic cells at 48 and 72 h after γ‐irradiation. Compared with untreated cells, SP‐treated human MSCs showed reduced cleavage of apoptotic molecules such as caspase‐8, ‐9, ‐3, and poly ADP‐ribose polymerase (PARP). Thus, our results suggest that SP alleviates γ‐radiation‐induced damage to mouse BMSCs and human MSCs via regulation of the apoptotic pathway. J. Cell. Physiol. 226: 1204–1213, 2011. © 2010 Wiley‐Liss, Inc.</jats:p>