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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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Related in: MedlinePlus

Morphology of MSCs at passage 4. (A) Control, untreated MSCs; (B) SD, serum-deprived MSCs; (C) SD+PGE1, serum-deprived MSCs cultured with 10 ng/ml PGE1. Image visualized under a phase-contrast microscope (magnification, ×100). MSC, mesenchymal stem cells; Con, control; SD, serum deprived; PGE1, prostaglandin E1.
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f1-mmr-12-04-5723: Morphology of MSCs at passage 4. (A) Control, untreated MSCs; (B) SD, serum-deprived MSCs; (C) SD+PGE1, serum-deprived MSCs cultured with 10 ng/ml PGE1. Image visualized under a phase-contrast microscope (magnification, ×100). MSC, mesenchymal stem cells; Con, control; SD, serum deprived; PGE1, prostaglandin E1.

Mentions: MSCs were isolated and expanded from Sprague Dawley rats. The control MSCs were shown to sparsely attach to the culture flasks, and the majority of cells displayed a spindle-like shape (Fig. 1A). In the MSCs cultured with SD medium cells did not display the typical spindle-like shape, and a large number of floating dead cells were observed (Fig. 1B). Following treatment with PGE1, the morphology of the MSCs cultured with SD changed, and the number of floating dead cells was reduced, as compared with the cells cultured with SD alone (Fig. 1C). The MSCs at passage 4 were stably positive for CD90 and CD29 markers, and negative for CD45 and CD11b/c markers.


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)

Morphology of MSCs at passage 4. (A) Control, untreated MSCs; (B) SD, serum-deprived MSCs; (C) SD+PGE1, serum-deprived MSCs cultured with 10 ng/ml PGE1. Image visualized under a phase-contrast microscope (magnification, ×100). MSC, mesenchymal stem cells; Con, control; SD, serum deprived; PGE1, prostaglandin E1.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f1-mmr-12-04-5723: Morphology of MSCs at passage 4. (A) Control, untreated MSCs; (B) SD, serum-deprived MSCs; (C) SD+PGE1, serum-deprived MSCs cultured with 10 ng/ml PGE1. Image visualized under a phase-contrast microscope (magnification, ×100). MSC, mesenchymal stem cells; Con, control; SD, serum deprived; PGE1, prostaglandin E1.
Mentions: MSCs were isolated and expanded from Sprague Dawley rats. The control MSCs were shown to sparsely attach to the culture flasks, and the majority of cells displayed a spindle-like shape (Fig. 1A). In the MSCs cultured with SD medium cells did not display the typical spindle-like shape, and a large number of floating dead cells were observed (Fig. 1B). Following treatment with PGE1, the morphology of the MSCs cultured with SD changed, and the number of floating dead cells was reduced, as compared with the cells cultured with SD alone (Fig. 1C). The MSCs at passage 4 were stably positive for CD90 and CD29 markers, and negative for CD45 and CD11b/c markers.

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