The protective effect of 17β-estradiol against hydrogen peroxide-induced apoptosis on mesenchymal stem cell

Chen, Haiying; Zhang, Xian; Chen, Shuangfeng; Zhang, Yingxin; Liu, Yihua; Ma, Lei; Wang, Lexin

doi:10.1016/j.biopha.2011.11.014

Cited by 34 publications

(21 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…H 2 O 2 can easily penetrate the cell membrane, and form hydroxyl radicals with intracellular metal ions. Treatment with H 2 O 2 results in cytosolic release of cytochrome c as well as activating caspase-9 and caspase-3 and works through the intrinsic/mitochondrial apoptotic pathway in several cell types, including MSCs [90,91,92,93,94,95]. And hence, H 2 O 2 scavenging is likely more dependent on GSH, rather than BR and BV.…”

Section: Resultsmentioning

confidence: 99%

Curcumin-Induced Heme Oxygenase-1 Expression Prevents H2O2-Induced Cell Death in Wild Type and Heme Oxygenase-2 Knockout Adipose-Derived Mesenchymal Stem Cells

Cremers

Lundvig

Dalen

et al. 2014

IJMS

View full text Add to dashboard Cite

Mesenchymal stem cell (MSC) administration is a promising adjuvant therapy to treat tissue injury. However, MSC survival after administration is often hampered by oxidative stress at the site of injury. Heme oxygenase (HO) generates the cytoprotective effector molecules biliverdin/bilirubin, carbon monoxide (CO) and iron/ferritin by breaking down heme. Since HO-activity mediates anti-apoptotic, anti-inflammatory, and anti-oxidative effects, we hypothesized that modulation of the HO-system affects MSC survival. Adipose-derived MSCs (ASCs) from wild type (WT) and HO-2 knockout (KO) mice were isolated and characterized with respect to ASC marker expression. In order to analyze potential modulatory effects of the HO-system on ASC survival, WT and HO-2 KO ASCs were pre-treated with HO-activity modulators, or downstream effector molecules biliverdin, bilirubin, and CO before co-exposure of ASCs to a toxic dose of H2O2. Surprisingly, sensitivity to H2O2-mediated cell death was similar in WT and HO-2 KO ASCs. However, pre-induction of HO-1 expression using curcumin increased ASC survival after H2O2 exposure in both WT and HO-2 KO ASCs. Simultaneous inhibition of HO-activity resulted in loss of curcumin-mediated protection. Co-treatment with glutathione precursor N-Acetylcysteine promoted ASC survival. However, co-incubation with HO-effector molecules bilirubin and biliverdin did not rescue from H2O2-mediated cell death, whereas co-exposure to CO-releasing molecules-2 (CORM-2) significantly increased cell survival, independently from HO-2 expression. Summarizing, our results show that curcumin protects via an HO-1 dependent mechanism against H2O2-mediated apoptosis, and likely through the generation of CO. HO-1 pre-induction or administration of CORMs may thus form an attractive strategy to improve MSC therapy.

show abstract

Section: Resultsmentioning

confidence: 99%

Curcumin-Induced Heme Oxygenase-1 Expression Prevents H2O2-Induced Cell Death in Wild Type and Heme Oxygenase-2 Knockout Adipose-Derived Mesenchymal Stem Cells

Cremers

Lundvig

Dalen

et al. 2014

IJMS

View full text Add to dashboard Cite

show abstract

“…Less injury and inflammation is found in female patients compared to males after acute cardiac injuries. Estradiol contributes by decreasing the expression of the Bcl-2 family of genes and JNK pathways 158 .…”

Section: Introductionmentioning

confidence: 99%

Use of Mesenchymal Stem Cells for Therapy of Cardiac Disease

Karantalis

Hare

2015

Circulation Research

372

332

View full text Add to dashboard Cite

Despite substantial clinical advances over the past 65 years, cardiovascular disease remains the leading cause of death in America. The past 15 years has witnessed major basic and translational interest in the use of stem and/or precursor cells as a therapeutic agent for chronically injured organs. Among the cell types under investigation, adult mesenchymal stem cells (MSCs) are widely studied and in early stage clinical studies show promise for repair and regeneration of cardiac tissues. The ability of MSCs to differentiate into mesoderm and non-mesoderm derived tissues, their immunomodulatory effects, their availability and their key role in maintaining and replenishing endogenous stem cell niches have rendered them one of the most heavily investigated and clinically tested type of stem cell. Accumulating data from preclinical and early phase clinical trials document their safety when delivered as either autologous or allogeneic forms in a range of cardiovascular diseases, but also importantly define parameters of clinical efficacy that justify further investigation in larger clinical trials. Here, we review the biology of MSCs, their interaction with endogenous molecular and cellular pathways, and their modulation of immune responses. Additionally, we discuss factors that enhance their proliferative and regenerative ability and factors that may hinder their effectiveness in the clinical setting.

show abstract

“…After transplantation, BMSCs face hostile microenvironments in the ischemic brain, including oxidative stress, hypoxia and inflammatory reactions, which promote cell apoptosis. [2][3][4] Oxidative stress results in an excessive accumulation of reactive oxygen species (ROS), which is a major detrimental factor for the survival of engrafted BMSCs during stroke treatment. Therefore, a strategy that promotes the survival of BMSCs in ischemic microenvironments may augment the effectiveness of BMSC transplantation therapy.…”

mentioning

confidence: 99%

Tetramethylpyrazine Protects Bone Marrow-Derived Mesenchymal Stem Cells against Hydrogen Peroxide-Induced Apoptosis through PI3K/Akt and ERK1/2 Pathways

Yan

Chu

et al. 2017

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

Bone marrow-derived mesenchymal stem cells (BMSCs) transplantation is one of the new therapeutic strategies for treating ischemic stroke. However, the poor survival rate of transplanted BMSCs in ischemic tissue limits the therapeutic efficacy of this approach. Oxidative stress is a major mechanism underlying the pathogenesis of brain ischemia and has a negative impact on the survival of transplanted BMSCs. Tetramethylpyrazine (TMP) has been reported to possess potent antioxidant activity. In the present study, we aimed to investigate the protective effects of TMP pretreatment on BMSCs survival of hydrogen peroxide (H 2 O 2 )-induced apoptosis in vitro and to elucidate the potential antiapoptotic mechanisms of TMP pretreatment on BMSCs. BMSCs were pretreated with TMP (10, 25, 50, 100, and 200 µmol/L) for 24 h and then exposed to 500 µmol/L of H 2 O 2 for 24 h. We found that TMP pretreatment significantly increased cell viability and decreased cell apoptosis and intracellular reactive oxygen species (ROS) generation. Furthermore, the protective effects of TMP were related to increased Bcl-2 expression, attenuated Bax expression, and enhanced levels of phosphorylated Akt (p-Akt) and extracellular regulated protein kinases1/2 (p-ERK1/2). Further studies found that these beneficial effects of TMP were significantly blocked by wortmannin (an inhibitor of phosphoinositide-3 kinase (PI3K)) or PD98059 (an inhibitor of ERK1/2). In conclusion, our results confirm that TMP protects BMSCs against H 2 O 2 -induced apoptosis by regulating the PI3K/Akt and ERK1/2 signaling pathways, suggesting that TMP may be used in combination with BMSCs to improve cell survival for the treatment of ischemic stroke.Key words tetramethylpyrazine; bone marrow-derived mesenchymal stem cell; apoptosis; oxidative stress; phosphoinositide 3-kinase/Akt (PI3K/Akt); extracellular regulated protein kinases1/2 (ERK1/2) Ischemic stroke is one of leading causes of death and disability worldwide. Recently, basic and clinical studies have found that the transplantation of bone marrow-derived mesenchymal stem cells (BMSCs) is a promising therapeutic strategy for brain tissue repair following brain ischemia.

show abstract

The protective effect of 17β-estradiol against hydrogen peroxide-induced apoptosis on mesenchymal stem cell

Cited by 34 publications

References 21 publications

Curcumin-Induced Heme Oxygenase-1 Expression Prevents H2O2-Induced Cell Death in Wild Type and Heme Oxygenase-2 Knockout Adipose-Derived Mesenchymal Stem Cells

Curcumin-Induced Heme Oxygenase-1 Expression Prevents H2O2-Induced Cell Death in Wild Type and Heme Oxygenase-2 Knockout Adipose-Derived Mesenchymal Stem Cells

Use of Mesenchymal Stem Cells for Therapy of Cardiac Disease

Tetramethylpyrazine Protects Bone Marrow-Derived Mesenchymal Stem Cells against Hydrogen Peroxide-Induced Apoptosis through PI3K/Akt and ERK1/2 Pathways

Contact Info

Product

Resources

About