scholarly journals Apocynin suppression of NADPH oxidase reverses the aging process in mesenchymal stem cells to promote osteogenesis and increase bone mass

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Jinlong Sun ◽  
Leiguo Ming ◽  
Fengqing Shang ◽  
Lijuan Shen ◽  
Jihua Chen ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Bone Mass ◽  
Nadph Oxidase ◽  
Aging Process ◽  
Increase Bone Mass

scholarly journals Directing mesenchymal stem cells to bone to augment bone formation and increase bone mass

2012 ◽  
Vol 18 (3) ◽  
pp. 456-462 ◽  
Author(s):  
Min Guan ◽  
Wei Yao ◽  
Ruiwu Liu ◽  
Kit S Lam ◽  
Jan Nolta ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Bone Formation ◽  
Bone Mass ◽  
Increase Bone Mass

scholarly journals Licochalcone A up-regulates of FasL in mesenchymal stem cells to strengthen bone formation and increase bone mass

2014 ◽  
Vol 4 (1) ◽  
Author(s):  
Leiguo Ming ◽  
Fang Jin ◽  
Ping Huang ◽  
Hailang Luo ◽  
Wenjia Liu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Bone Formation ◽  
Bone Mass ◽  
Licochalcone A ◽  
Increase Bone Mass

scholarly journals Restoration of Bone Mass and Strength in Glucocorticoid-Treated Mice by Systemic Transplantation of CXCR4 and Cbfa-1 Co-Expressing Mesenchymal Stem Cells

2009 ◽  
Vol 24 (5) ◽  
pp. 837-848 ◽  
Author(s):  
Chun-Yang Lien ◽  
Kevin Chih-Yuan Ho ◽  
Oscar K Lee ◽  
Gordon W Blunn ◽  
Yeu Su
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Bone Mass

Application of Cell Therapy for Anti-Aging Facial Skin

2019 ◽  
Vol 14 (3) ◽  
pp. 244-248 ◽  
Author(s):  
Farshad Zarei ◽  
Abolfazl Abbaszadeh
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Stem Cell ◽  
Aging Process ◽  
Skin Aging ◽  
Facial Skin ◽  
Complex Process ◽  
Aged Skin ◽  
Adipose Derived Stem Cell

The human skin undergoes the complex process of aging which is prompted by the interplay of intrinsic mechanisms and extrinsic influences. Aging is unavoidable but can be somewhat delayed. Numerous approaches have been developed to slow down facial skin aging process as it is of interest to stake holders in the beauty and fashion world as well as to plastic surgeons. Adipose-derived stem cell [ADSC] and mesenchymal stem cell [MSC] as potential anti-aging agents to some extent have provided a promising and effective alternative in managing skin and facial skin aging. Furthermore, bone marrow-derived mesenchymal stem cells [BMMSC] have exhibited similar ability to rejuvenate aged skin. This review is aimed at giving a comprehensive account of the application of stem cells especially ADSCs and MSCs to reduce or slow down the rate of facial skin aging process.

scholarly journals NADPH Oxidase Signaling Pathway Mediates Mesenchymal Stem Cell-Induced Inhibition of Hepatic Stellate Cell Activation

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Haowen Qiao ◽  
Yu Zhou ◽  
Xingping Qin ◽  
Jing Cheng ◽  
Yun He ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Liver Fibrosis ◽  
Nadph Oxidase ◽  
Signaling Pathway ◽  
Cell Activation ◽  
Stellate Cell ◽  
Smooth Muscle Actin ◽  
Alpha Smooth Muscle Actin

Background. Bone marrow-derived mesenchymal stem cells (BMSCs) have blossomed into an effective approach with great potential for the treatment of liver fibrosis. The aim of this study was to investigate the underlying antifibrosis mechanisms by which the BMSC inhibit activated hepatic stellate cells (HSCs) in vivo and in vitro. Methods. To study the effect of human bone marrow-derived mesenchymal stem cells (hBM-MSCs) on activated HSCs, we used HSCs and the coculture systems to evaluate the inhibition of activated HSCs from the aspects of the apoptosis of activated HSCs. In addition, activation of NADPH oxidase pathway and the changes in liver histopathology were tested by using the carbon tetrachloride- (CCl4-) induced liver fibrosis in mice. Results. Introduction of hBM-MSCs significantly inhibited the proliferation of activated HSCs by inducing the apoptosis process of activated HSCs. The effect of hBM-MSCs reduced the signaling pathway of NADPH oxidase in activated HSCs. Besides, the signaling pathway of NADPH oxidase mediated hBM-MSC upregulation of the expression of the peroxisome proliferator-activated receptor γ and downregulation of the expression of α1(I) collagen and alpha-smooth muscle actin (α-SMA) in activated HSCs. Moreover, the hBM-MSC-induced decrease in the signaling pathway of NADPH oxidase was accompanied by the decrease of the activated HSC number and liver fibrosis in a mouse model of CCl4-induced liver fibrosis. Conclusion. The hBM-MSCs act as a promising drug source against liver fibrosis development with respect to hepatopathy as a therapeutic target.

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