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[Relation of notch pathway to senescence of murine bone marrow stromal cells]

Ke-Jie Zhang1, Li-Fang Huang, Han-Ying Sun

  • 1Department of Hematology, Zhongshan Hospital, Xiamen University, Fujian Medical University Clinic Teaching Hospital, Xiamen 361004, Fujian Province, China.

Zhongguo Shi Yan Xue Ye Xue Za Zhi
|April 27, 2010
PubMed

Insights

Activating the Notch signaling pathway triggers premature senescence in bone marrow stromal cells. This process involves the p53-p21Cip1/Waf1 pathway, inhibiting cell proliferation and increasing senescence markers.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Aging Research

Background:

  • The Notch signaling pathway plays a crucial role in cellular processes, including cell differentiation and proliferation.
  • Cellular senescence is a state of irreversible growth arrest associated with aging and disease.

Purpose of the Study:

  • To investigate the relationship between Notch signaling and senescence in murine bone marrow stromal cells.
  • To elucidate the molecular mechanisms by which Notch signaling influences stromal cell senescence.

Main Methods:

  • Transfection of intracellular domain of Notch 1 (ICN) into cultured murine bone marrow stromal cells.
  • Assessment of cell proliferation (MTT assay), cell cycle distribution (flow cytometry), and senescence-associated beta-galactosidase (SA-beta-Gal) activity.
  • Analysis of p53 and p21Cip1/Waf1 expression at both mRNA (RT-PCR) and protein (Western blot) levels.

Main Results:

  • Activation of Notch signaling inhibited stromal cell proliferation and induced G1 arrest.
  • Increased percentage of SA-beta-Gal positive cells indicated induced senescence.
  • Upregulation of p53 and p21Cip1/Waf1 at both gene and protein levels was observed.

Conclusions:

  • Activated Notch signaling can induce premature senescence in bone marrow stromal cells.
  • The p53-p21Cip1/Waf1 pathway is implicated in Notch-induced senescence of these cells.

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