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Protective effects of hiPSC-EV treatment on structural integrity and viability of hAO during IRI. (A) Experimental timeline. (B-E) Representative bright-field images (4x magnifications, EVOS microscope) of hAO pre-ischemia, post-ischemia (16 hours) and different reperfusion phases, show onset of cellular degeneration (black arrows). The bottom row of each image highlights morphological damage. (F) Label-free imaging of hAO pre-ischemia and different reperfusion phases (6 and 24 hours) performed using <t>multiphoton</t> microscopy. (G) hAO viability assessed by cellular ATP-dependent luminescence (RLU) at each time point. Data are mean ± SD (n = 3). Samples without hiPSC-EV treatment: w/o hiPSC-EV. Samples with hiPSC-EV treatment: with hiPSC-EV. *p < 0.05 versus pre-ischemia (control); # p < 0.05 versus IRI without hiPSC-EV.
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Protective effects of hiPSC-EV treatment on structural integrity and viability of hAO during IRI. (A) Experimental timeline. (B-E) Representative bright-field images (4x magnifications, EVOS microscope) of hAO pre-ischemia, post-ischemia (16 hours) and different reperfusion phases, show onset of cellular degeneration (black arrows). The bottom row of each image highlights morphological damage. (F) Label-free imaging of hAO pre-ischemia and different reperfusion phases (6 and 24 hours) performed using <t>multiphoton</t> microscopy. (G) hAO viability assessed by cellular ATP-dependent luminescence (RLU) at each time point. Data are mean ± SD (n = 3). Samples without hiPSC-EV treatment: w/o hiPSC-EV. Samples with hiPSC-EV treatment: with hiPSC-EV. *p < 0.05 versus pre-ischemia (control); # p < 0.05 versus IRI without hiPSC-EV.
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Protective effects of hiPSC-EV treatment on structural integrity and viability of hAO during IRI. (A) Experimental timeline. (B-E) Representative bright-field images (4x magnifications, EVOS microscope) of hAO pre-ischemia, post-ischemia (16 hours) and different reperfusion phases, show onset of cellular degeneration (black arrows). The bottom row of each image highlights morphological damage. (F) Label-free imaging of hAO pre-ischemia and different reperfusion phases (6 and 24 hours) performed using <t>multiphoton</t> microscopy. (G) hAO viability assessed by cellular ATP-dependent luminescence (RLU) at each time point. Data are mean ± SD (n = 3). Samples without hiPSC-EV treatment: w/o hiPSC-EV. Samples with hiPSC-EV treatment: with hiPSC-EV. *p < 0.05 versus pre-ischemia (control); # p < 0.05 versus IRI without hiPSC-EV.
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Protective effects of hiPSC-EV treatment on structural integrity and viability of hAO during IRI. (A) Experimental timeline. (B-E) Representative bright-field images (4x magnifications, EVOS microscope) of hAO pre-ischemia, post-ischemia (16 hours) and different reperfusion phases, show onset of cellular degeneration (black arrows). The bottom row of each image highlights morphological damage. (F) Label-free imaging of hAO pre-ischemia and different reperfusion phases (6 and 24 hours) performed using <t>multiphoton</t> microscopy. (G) hAO viability assessed by cellular ATP-dependent luminescence (RLU) at each time point. Data are mean ± SD (n = 3). Samples without hiPSC-EV treatment: w/o hiPSC-EV. Samples with hiPSC-EV treatment: with hiPSC-EV. *p < 0.05 versus pre-ischemia (control); # p < 0.05 versus IRI without hiPSC-EV.
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Image Search Results


Protective effects of hiPSC-EV treatment on structural integrity and viability of hAO during IRI. (A) Experimental timeline. (B-E) Representative bright-field images (4x magnifications, EVOS microscope) of hAO pre-ischemia, post-ischemia (16 hours) and different reperfusion phases, show onset of cellular degeneration (black arrows). The bottom row of each image highlights morphological damage. (F) Label-free imaging of hAO pre-ischemia and different reperfusion phases (6 and 24 hours) performed using multiphoton microscopy. (G) hAO viability assessed by cellular ATP-dependent luminescence (RLU) at each time point. Data are mean ± SD (n = 3). Samples without hiPSC-EV treatment: w/o hiPSC-EV. Samples with hiPSC-EV treatment: with hiPSC-EV. *p < 0.05 versus pre-ischemia (control); # p < 0.05 versus IRI without hiPSC-EV.

Journal: International Journal of Biological Sciences

Article Title: Extracellular Vesicles from Human Induced Pluripotent Stem Cells Reduce Lung Ischemia-Reperfusion Injury via Cytoprotective Mechanisms in both 2D Cultures and a Human Airway Organoid Model

doi: 10.7150/ijbs.134686

Figure Lengend Snippet: Protective effects of hiPSC-EV treatment on structural integrity and viability of hAO during IRI. (A) Experimental timeline. (B-E) Representative bright-field images (4x magnifications, EVOS microscope) of hAO pre-ischemia, post-ischemia (16 hours) and different reperfusion phases, show onset of cellular degeneration (black arrows). The bottom row of each image highlights morphological damage. (F) Label-free imaging of hAO pre-ischemia and different reperfusion phases (6 and 24 hours) performed using multiphoton microscopy. (G) hAO viability assessed by cellular ATP-dependent luminescence (RLU) at each time point. Data are mean ± SD (n = 3). Samples without hiPSC-EV treatment: w/o hiPSC-EV. Samples with hiPSC-EV treatment: with hiPSC-EV. *p < 0.05 versus pre-ischemia (control); # p < 0.05 versus IRI without hiPSC-EV.

Article Snippet: Label-free imaging of hAO was also performed using a multiphoton microscopy Leica Stellaris DIVE 8 (Leica Microsystems, Germany), enabling visualization of cellular structures and intrinsic properties while maintaining the native organoid environment.

Techniques: Microscopy, Label-free Imaging, Control