Gamma-aminobutyric acid enhances miR-21-5p loading into adipose-derived stem cell extracellular vesicles to alleviate myocardial ischemia-reperfusion injury via TXNIP regulation

Figure 5 MicroR-21-5p derived from gamma-aminobutyric acid-induced adipose-derived mesenchymal stem cells from inguinal adipose tissue regulate thioredoxin-interacting protein expression in protein degree. A: Representative immunoblots and quantitative analysis of thioredoxin-interacting protein (TXNIP) at the protein level in neonatal mouse cardiomyocytes (NMCMs) (n = 3); B: Representative micrographs of NMCMs stained with TXNIP antibody (n = 3; scale bars = 200 μm); C: Experiment design. Adipose-derived mesenchymal stem cells (ADSCs) were isolated from both miR-21 KO and miR-21^f/f mice inguinal adipose tissue (IAT), and extracellular vesicles (EVs) were extracted respectively; D: Representative micrographs of NMCMs stained with TXNIP antibody (n = 3; scale bars = 200 μm); E: Representative immunoblots and quantitative analysis of TXNIP at the protein level in NMCMs (n = 3). ^aP < 0.05, ^bP < 0.01, ^cP < 0.001. GABA: Gamma-aminobutyric acid; H/R: Hypoxia and reoxygenation.