Journal: Materials Today Bio

Article Title: Extracellular biogenic nanoscale mitochondria reprogram the wound microenvironment via ROS scavenging independent of cellular uptake

doi: 10.1016/j.mtbio.2026.103023

Figure Lengend Snippet: MSC-mt alleviates oxidative stress and promote tissue regeneration during wound healing (A) In vivo imaging showing the spatial–temporal persistence of fluorescently labeled MSC-mt (mtH) at the wound site at indicated time point, indicating transient but sustained early presence after topical application. (B) Measurement of ATP levels in peri-wound tissues on PWD8 showed enhanced local metabolic activity following mtH treatment. n = 5 ∼ 6 per group. (C) Quantification of malondialdehyde (MDA) levels in peri-wound tissues on PWD8 indicated reduced lipid peroxidation and oxidative stress in both MSC-mt–treated wounds. n = 5 ∼ 6 per group. (D) Laser speckle contrast imaging of blood perfusion at the wound site on PWD8 showed improved microvascular perfusion following mtH treatment. n = 5 per group. (E) Representative immunofluorescence images and quantification of CD31 expression in peri-wound tissues on PWD8, indicating enhanced angiogenesis in mtH–treated wounds. n = 6 per group. (F) Quantitative PCR analysis of angiogenesis-related gene expression in peri-wound tissues on PWD8, indicating transcriptional activation of pro-angiogenic programs following mtH treatment. n = 3 ∼ 5 per group. (G-H) Representative immunohistochemical staining and quantification of Col1a1 in wound tissues on PWD8, showing increased collagen synthesis and matrix remodeling in mtH–treated wounds. n = 6 per group. Scale bar = 100 μm. (I-J) Representative immunofluorescence staining and quantification of Vimentin and TUNEL in wound tissues on PWD8, indicating reduced fibroblast apoptosis following mtH treatment. n = 6 per group. Scale bar = 20 μm. (K-L) Representative immunofluorescence staining and quantification of Vimentin and 8-hydroxyguanosine (8-OHG) in wound tissues on PWD8, indicating attenuated oxidative DNA damage in fibroblasts following mtH treatment. n = 6 per group. Scale bar = 20 μm. Data are presented as mean ± SEM. ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001; ns, not significant.

Article Snippet: For immunohistochemistry, Col1a1 expression was evaluated using a rabbit anti-Col1a1 antibody (CST, Cat# 72026, 1:200), followed by HRP-conjugated secondary antibody and DAB chromogen development.

Techniques: In Vivo Imaging, Labeling, Activity Assay, Imaging, Immunofluorescence, Expressing, Real-time Polymerase Chain Reaction, Gene Expression, Activation Assay, Immunohistochemical staining, Staining, TUNEL Assay

Journal: iScience

Article Title: Human iPSC cardiomyocyte patch transplantation modifies extracellular matrix and fibroblast behavior after myocardial infarction

doi: 10.1016/j.isci.2026.115341

Figure Lengend Snippet: TGF-β secreted from the hiPSC-derived CM patch induced Col1a1 expression but not Col3a1 (A) Schematic representation of the co-culture system. hiPSC-derived CMs were seeded on the upper chamber, whereas the cardiac fibroblasts isolated from mice heart were cultured at the lower chamber in the presence and absence of SB431542, a TGF-β receptor inhibitor. (B) RT-qPCR analysis of Col1a1 , Col3a1 , and Pai1 in the cultured cardiac fibroblasts. Two-way ANOVA (co-culture × inhibitor) with interaction; Tukey-adjusted post hoc tests on estimated marginal means. Data represent mean ± SEM. N = 3–6, one-way ANOVA followed by Tukey’s HSD test, p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

Article Snippet: Then proteins were analyzed using primary antibodies for Col1a1 (R1038, OriGene, Rockville, MD), Col3a1(ab6310, Abcam, Cambridge, UK) and Gapdh (AM4300, Thermo Fisher Scienctific, Waltham, MA), respectively on Amersham Imager 600 (GE Healthcare, Chicago, IL).

Techniques: Derivative Assay, Expressing, Co-Culture Assay, Isolation, Cell Culture, Quantitative RT-PCR