11 research outputs found

    Confocal laser microscopic images of immunofluorescence analysis of differentiation of transplanted ADSCs in vivo (n = 12/group).

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    <p>(A and B) Representative images of differentiated cardiomyocytes-like cells using anti-cardiac troponin-I (green, cTnI) revealed significant augmentation of enhanced mRFP (red)/cTnI double positive cardiomyocyte-like cells (white arrow) in Ex-ADSCs group (B) compared with ADSCs group (A). (C) Quantitative analysis of the ratio of differentiated cardiomyocytes-like cells. (D and E) Representative images of differentiated vessel specific cells using anti-α-SMA (green) revealed significant enhancement of mRFP (red)/α-SMA double positive vessel-specific cells (white arrow) in Ex-ADSCs group (E) compared with ADSCs group(D). (F) Quantitative analysis of the ratio of differentiated vessel specific cells. *<i>p</i><0.05. Inset shows the corresponding boxed area magnified.</p

    Exendin-4 restores ROS-induced attenuation of ADSCs adhesion, increases their viability and promotes ADSCs proliferation at 30, 60, 120 min after pretreatment.

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    <p>(A) The effect of Exendin-4 on ADSCs adhesion in the presence of H<sub>2</sub>O<sub>2</sub>. Scale bars = 200 µm. (B) The effects of Exendin-4 on scavenging intracellular ROS of ADSCs which were treated with H<sub>2</sub>O<sub>2</sub> with or without Exendin-4. ROS of ADSCs were detected using DHE reagent. Scale bars = 100 µm. (C) Live/dead staining showed that the effects of Exendin-4 pretreatment on ADSCs viability against H<sub>2</sub>O<sub>2</sub>. Scale bars = 100 µm. (D) Quantification of adhesive ADSCs. (E) Quantification of intracellular ROS. (F) Quantification of viable ADSCs. (G) Quantitative analysis of LDH release in the cell supernatant. (H) Caspase-3 activity determined by using Caspase-3 ELISA kit. (I) MTT assay was performed to analyze the effect of Exendin-4 on viability of ADSCs after H<sub>2</sub>O<sub>2</sub> injury for 6 h. Statistical differences (<i>p</i><0.05) are indicated from Control group(*) and ADSCs+ H<sub>2</sub>O<sub>2</sub> group (#).</p

    Echocardiographic Assessment of Cardiac Function (n = 16/group).

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    <p>(A) Representative M-mode echocardiograms in each group at day 28 after myocardial infarction. (B and C) Quantitative analysis of ejection fraction (B) and fractional shortening (C) by echocardiography. (D and E) Quantitative analysis of hemodynamic parameters LVEDP (D) and dP/dtmax (E). Statistical differences (<i>p</i><0.05) are indicated from the sham (*), PBS (#), and ADSCs ($).</p

    Molecular Imaging of Induced Pluripotent Stem Cell Immunogenicity with <i>In Vivo</i> Development in Ischemic Myocardium

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    <div><p>Whether differentiation of induced pluripotent stem cells (iPSCs) in ischemic myocardium enhances their immunogenicity, thereby increasing their chance for rejection, is unclear. Here, we dynamically demonstrated the immunogenicity and rejection of iPSCs in ischemic myocardium using bioluminescent imaging (BLI). Murine iPSCs were transduced with a tri-fusion (TF) reporter gene consisting of firefly luciferase-red fluorescent protein-truncated thymidine kinase (fluc-mrfp-tTK). Ascorbic acid (Vc) were used to induce iPSCs to differentiate into cardiomyocytes (CM). iPSCs and iPS-CMs were intramyocardially injected into immunocompetent or immunosuppressed allogenic murine with myocardial infarction. BLI was performed to track transplanted cells. Immune cell infiltration was evaluated by immunohistochemistry. Syngeneic iPSCs were also injected and evaluated. The results demonstrated that undifferentiated iPSCs survived and proliferated in allogenic immunocompetent recipients early post-transplantation, accompanying with mild immune cell infiltration. With <i>in vivo</i> differentiation, a progressive immune cell infiltration could be detected. While transplantation of allogenic iPSC-CMs were observed an acute rejection from receipts. In immune-suppressed recipients, the proliferation of iPSCs could be maintained and intramyocardial teratomas were formed. Transplantation of syngeneic iPSCs and iPSC-CMs were also observed progressive immune cell infiltration. This study demonstrated that iPSC immunogenicity increases with <i>in vivo</i> differentiation, which will increase their chance for rejection in iPSC-based therapy.</p></div

    Immune cell infiltration and teratoma formation after allogeneic iPSC transplantation.

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    <p><b>(</b>A) Allogeneic transplantation of iPSCs in immunocompetent allogeneic recipients evoked progressive infiltration of CD3, CD8+ immune cells (Bar = 25 µm); (B) Teratoma formation of iPSCs in immunosuppressed allogeneic recipientts.</p
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