We have located links that may give you full text access.
[The mechanism of bone marrow-derived mesenchymal stem cells excessive senescence in severe aplastic anemia mouse model].
Zhonghua Xue Ye Xue za Zhi = Zhonghua Xueyexue Zazhi 2017 April 15
Objective: To explore the mechanism of excessive senescence in bone marrow-derived mesenchymal stem cells (BM-MSC) of mouse model with severe aplastic anemia (SAA) . Methods: 40 BALB/c mice were randomly assigned to two groups of control ( n =20) and AA ( n =20) . SAA mouse model was induced by intraperitoneal injection with IFN-γ and intragastric infusion with busulfan. BM-MSC were isolated and cultured from bone marrow of SAA and healthy mice. The cell morphology was observed by inverted microscope and cell cytoskeleton was stained by Rhodamine-Phalloidin; The level of proliferation was analyzed by CCK-8 method, and cell cycle was tested by flow cytometry. Senescence-associated β-galactosidase (SA-β-gal) assay was used to detect senescent BM-MSC; The expression of mTOR protein was detected by Western blot method. Results: BM-MSC from normal mice presented spindle-shaped, clear boundaries and stress fibers were arranged in parallel, neat. while BM-MSCs from SAA mice presented cell volume increases, tiled, ill-shaped and the stress fiber appeared to be disordered. The decreased activity of proliferation [more cells restricted in G(0)/G(1) phase [ (77.461±1.567) % vs (46.045±2.055) %, t =-34.384, P <0.001], increased percentage of SA-β-gal positive cells [ (75±11) % vs (28±8) %, t =15.454, P <0.001] and notably enhanced expression of mTOR of BM-MSC from SAA mice were observed when compared with those from normal mice. Conclusion: This study clarified senescent BM-MSCs from SAA model mice, which could be caused by the excessive activation of mTOR pathway.
Full text links
Related Resources
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app