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Prostaglandin E₁ protects bone marrow-derived mesenchymal stem cells against serum deprivation-induced apoptosis.

Zeng K, Deng BP, Jiang HQ, Wang M, Hua P, Zhang HW, Deng YB, Yang YQ - Mol Med Rep (2015)

Bottom Line: Prostaglandin E1 (PGE1) is known to have anti‑inflammatory and anti‑apoptotic effects on the myocardium.The results of the present study demonstrated that SD induced apoptosis of MSCs, and that treatment with PGE1 attenuated the morphological changes characteristic of apoptosis.Furthermore, treatment with PGE1 significantly reduced SD‑induced apoptosis, decreased the protein expression levels of Bax and caspase‑3, and increased the expression levels of Bcl‑2.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiac Surgery, Sun Yat‑sen Memorial Hospital, Sun Yat‑sen University, Guangzhou, Guangdong 510120, P.R. China.

ABSTRACT
Mesenchymal stem cells (MSCs) have become a recent focus of experimental and clinical research regarding myocardial regeneration. However, the therapeutic potential of these cells is limited by poor survival. Prostaglandin E1 (PGE1) is known to have anti‑inflammatory and anti‑apoptotic effects on the myocardium. The aim of the present study was to determine whether PGE1 could protect MSCs against serum deprivation (SD)‑induced apoptosis. An SD model was used to induce apoptosis in MSCs in vitro. Apoptotic morphological changes were detected by Hoechst 33258 fluorescent nuclear staining; and Annexin V‑fluorescein isothiocyanate/propidium iodide (PI) double staining and flow cytometry was used to quantify the rate of apoptosis. Western blot analysis was used to detect the expression levels of the apoptosis‑associated proteins Bcl‑2, Bax and caspase‑3. The results of the present study demonstrated that SD induced apoptosis of MSCs, and that treatment with PGE1 attenuated the morphological changes characteristic of apoptosis. Annexin V/PI staining showed that the rate of apoptosis gradually increased with the duration of ischemia. Furthermore, treatment with PGE1 significantly reduced SD‑induced apoptosis, decreased the protein expression levels of Bax and caspase‑3, and increased the expression levels of Bcl‑2. These data suggest that PGE1 is able to influence the survival of MSCs under certain conditions. These results may aid in improving the therapeutic efficacy of MSC transplantation used to treat chronic ischemic heart disease.

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Western blot analysis of Bax, Bcl-2 and caspase-3 following 24 h of serum deprivation with or without PGE1 preconditioning. Control, untreated MSCs; SD, serum-deprived MSCs; SD+PGE1, serum-deprived MSCs cultured with 10 ng/ml PGE1. MSCs were cultured at 37°C in a humidified atmosphere containing 5% CO2. Protein expression levels of (A) Bax and Bcl-2, and (B) caspase-3. GAPDH was used as a loading control, and the expression levels of the target proteins were determined relative to the levels of GAPDH. Blots are shown from at least three independent experiments. The data are presented as the mean ± standard error (n=5). *P<0.01, as compared with the control group; #P<0.05, ##P<0.01, as compared with the SD group. MSC, mesenchymal stem cells; Con, control; SD, serum deprived; PGE1, prostaglandin E.
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f4-mmr-12-04-5723: Western blot analysis of Bax, Bcl-2 and caspase-3 following 24 h of serum deprivation with or without PGE1 preconditioning. Control, untreated MSCs; SD, serum-deprived MSCs; SD+PGE1, serum-deprived MSCs cultured with 10 ng/ml PGE1. MSCs were cultured at 37°C in a humidified atmosphere containing 5% CO2. Protein expression levels of (A) Bax and Bcl-2, and (B) caspase-3. GAPDH was used as a loading control, and the expression levels of the target proteins were determined relative to the levels of GAPDH. Blots are shown from at least three independent experiments. The data are presented as the mean ± standard error (n=5). *P<0.01, as compared with the control group; #P<0.05, ##P<0.01, as compared with the SD group. MSC, mesenchymal stem cells; Con, control; SD, serum deprived; PGE1, prostaglandin E.

Mentions: Treatment with PGE1 significantly reduced SD-induced Bax protein expression levels and increased the protein expression levels of Bcl-2 (Fig. 4A). PGE1 also reduced the protein expression levels of cleaved caspase-3 in the MSCs (Figure 4B). These results indicate that PGE1 was able to attenuate SD-induced apoptosis though activation of Bax and deactivation of Bcl-2, thus reducing the expression of cleaved caspase-3.


Prostaglandin E₁ protects bone marrow-derived mesenchymal stem cells against serum deprivation-induced apoptosis.

Zeng K, Deng BP, Jiang HQ, Wang M, Hua P, Zhang HW, Deng YB, Yang YQ - Mol Med Rep (2015)

Western blot analysis of Bax, Bcl-2 and caspase-3 following 24 h of serum deprivation with or without PGE1 preconditioning. Control, untreated MSCs; SD, serum-deprived MSCs; SD+PGE1, serum-deprived MSCs cultured with 10 ng/ml PGE1. MSCs were cultured at 37°C in a humidified atmosphere containing 5% CO2. Protein expression levels of (A) Bax and Bcl-2, and (B) caspase-3. GAPDH was used as a loading control, and the expression levels of the target proteins were determined relative to the levels of GAPDH. Blots are shown from at least three independent experiments. The data are presented as the mean ± standard error (n=5). *P<0.01, as compared with the control group; #P<0.05, ##P<0.01, as compared with the SD group. MSC, mesenchymal stem cells; Con, control; SD, serum deprived; PGE1, prostaglandin E.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4581785&req=5

f4-mmr-12-04-5723: Western blot analysis of Bax, Bcl-2 and caspase-3 following 24 h of serum deprivation with or without PGE1 preconditioning. Control, untreated MSCs; SD, serum-deprived MSCs; SD+PGE1, serum-deprived MSCs cultured with 10 ng/ml PGE1. MSCs were cultured at 37°C in a humidified atmosphere containing 5% CO2. Protein expression levels of (A) Bax and Bcl-2, and (B) caspase-3. GAPDH was used as a loading control, and the expression levels of the target proteins were determined relative to the levels of GAPDH. Blots are shown from at least three independent experiments. The data are presented as the mean ± standard error (n=5). *P<0.01, as compared with the control group; #P<0.05, ##P<0.01, as compared with the SD group. MSC, mesenchymal stem cells; Con, control; SD, serum deprived; PGE1, prostaglandin E.
Mentions: Treatment with PGE1 significantly reduced SD-induced Bax protein expression levels and increased the protein expression levels of Bcl-2 (Fig. 4A). PGE1 also reduced the protein expression levels of cleaved caspase-3 in the MSCs (Figure 4B). These results indicate that PGE1 was able to attenuate SD-induced apoptosis though activation of Bax and deactivation of Bcl-2, thus reducing the expression of cleaved caspase-3.

Bottom Line: Prostaglandin E1 (PGE1) is known to have anti‑inflammatory and anti‑apoptotic effects on the myocardium.The results of the present study demonstrated that SD induced apoptosis of MSCs, and that treatment with PGE1 attenuated the morphological changes characteristic of apoptosis.Furthermore, treatment with PGE1 significantly reduced SD‑induced apoptosis, decreased the protein expression levels of Bax and caspase‑3, and increased the expression levels of Bcl‑2.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiac Surgery, Sun Yat‑sen Memorial Hospital, Sun Yat‑sen University, Guangzhou, Guangdong 510120, P.R. China.

ABSTRACT
Mesenchymal stem cells (MSCs) have become a recent focus of experimental and clinical research regarding myocardial regeneration. However, the therapeutic potential of these cells is limited by poor survival. Prostaglandin E1 (PGE1) is known to have anti‑inflammatory and anti‑apoptotic effects on the myocardium. The aim of the present study was to determine whether PGE1 could protect MSCs against serum deprivation (SD)‑induced apoptosis. An SD model was used to induce apoptosis in MSCs in vitro. Apoptotic morphological changes were detected by Hoechst 33258 fluorescent nuclear staining; and Annexin V‑fluorescein isothiocyanate/propidium iodide (PI) double staining and flow cytometry was used to quantify the rate of apoptosis. Western blot analysis was used to detect the expression levels of the apoptosis‑associated proteins Bcl‑2, Bax and caspase‑3. The results of the present study demonstrated that SD induced apoptosis of MSCs, and that treatment with PGE1 attenuated the morphological changes characteristic of apoptosis. Annexin V/PI staining showed that the rate of apoptosis gradually increased with the duration of ischemia. Furthermore, treatment with PGE1 significantly reduced SD‑induced apoptosis, decreased the protein expression levels of Bax and caspase‑3, and increased the expression levels of Bcl‑2. These data suggest that PGE1 is able to influence the survival of MSCs under certain conditions. These results may aid in improving the therapeutic efficacy of MSC transplantation used to treat chronic ischemic heart disease.

Show MeSH
Related in: MedlinePlus