Helix B Surface Peptide Protects Cardiomyocytes From Hypoxia/Reoxygenation-induced Autophagy Through the PI3K/Akt Pathway.

BACKGROUND: Helix B surface peptide (HBSP) is a newly discovered tissue-protective erythropoietin derivative that provides benefits after myocardial ischemia/reperfusion. This study explores the cardioprotective effects of HBSP in myocardial cells in response to hypoxia/reoxygenation injury and its potential mechanism. METHODS: In this study, rat ventricular (H9c2) cell cultures were established and pretreated with HBSP. H9c2 cardiomyocytes were randomly assigned to the control, H/R, H/R + LY294002 (a PI3K inhibitor), HBSP + H/R, and HBSP + H/R + LY294002 groups. The pretreated cardiomyocytes underwent H/R, and the cardiomyocytes were monitored for viability through a CCK-8 assay, whereas flow cytometry was used to test cell apoptosis. Orgotein Superoxide Dismutase (SOD) and lactate dehydrogenase (LDH) expression were monitored by SOD and LDH kits, respectively. The expression of LC3 autophagosomes was determined by immunocytochemistry. The expression of LC3II/LC3I, p-Mammalian Target of Rapamycin (mTOR) mTOR, mTOR, Beclin 1, p-PI3K, PI3K p-Akt, and Akt was determined by Western blotting. RESULTS: HBSP increased cell viability and reduced SOD and LDH production, and it also reduced H/R-induced cell apoptosis. Moreover, the expression of the autophagy-related proteins (LC3II/LC3I) was inhibited by HBSP, whereas the expression of p-PI3K, p-Akt, and p-mTOR was enhanced. However, the PI3K inhibitor (LY294002) notably abolished these effects in H9c2 cells. CONCLUSIONS: HBSP inhibits excessive autophagy and apoptosis induced by H/R by activating the PI3K/Akt pathway. HBSP may potentially be a therapeutic intervention for myocardial ischemia/reperfusion injury.

Fingerprint-Inspired Strain Sensor with Balanced Sensitivity and Strain Range Using Laser-Induced Graphene.

Sensitivity and strain range are two mutually exclusive features of strain sensors, where a significant improvement in flexibility is usually accompanied by a reduction in sensitivity. The skin of a human fingertip, due to its undulating fingerprint pattern, can easily detect environmental signals and enhances sensitivity without losing elasticity. Inspired by this characteristic, laser-induced graphene (LIG) with a fingerprint structure is prepared in one step on a polyimide (PI) film and transferred into an Ecoflex substrate to assemble resistive strain sensors. Experimentally, the fingerprint-inspired strain sensor exhibits a superfast response time (∼70 ms), balanced sensitivity and strain range (a gauge factor of 191.55 in the 42-50% strain range), and good reliability (>1500 cycles). Self-organized microcracks, initiated in weak mechanical areas, cause prominent resistance changes during reconnection/disconnection but irreversibly fail after excessive stretching. The robust function of fingerprint-inspired sensors is further demonstrated by real-time monitoring of tiny pulses, large body movements, gestures, and voice recognition.

Erythropoietin helix B surface peptide modulates miR-21/Atg12 axis to alleviates cardiomyocyte hypoxia-reoxygenation injury.

BACKGROUND: The erythropoietin helix B surface peptide (HBSP) has been shown to have neuroprotective and repair-damaging myocardium effects similar to erythropoietin (EPO). However, the protective mechanism of HBSP on cardiomyocyte hypoxia-reoxygenation (H/R) injury is not clear. METHODS: H9C2 cells were pretreated with HBSP and subjected to hypoxia/reoxygenation (H/R), changes in cell function, autophagy and apoptosis were assessed, respectively. Cells were transfected with miR-21 mimic and miR-NC, and the relative expression of miR-21 and Atg12 were detected by qRT-PCR. The target role of miR-21 and Atg12 was evaluated by dual-luciferase reporter. After transfected with si-Atg12 and si-NC, western blot was used to assess autophagy and apoptosis proteins, flow cytometry assay was used to detect apoptosis rate. RESULTS: We found the expression of miR-21 was significantly down-regulated, accompanied by remarkably activated of autophagy and apoptosis in H9C2 cells during H/R injury. Pleasantly, HBSP pretreatment has a similar effect as transfection of miR-21 mimic, which is to evidently inhibit autophagy and apoptosis by up-regulating miR-21 expression. Moreover, Bioinformatics analysis and luciferase reporter assay revealed that Atg12 was directly bond to miR-21. To further understand whether Atg12 is involved in the process of miR-21 regulating autophagy, si-Atg12 and si-NC were transfected into H9C2 cell, the results showed that knockdown of Atg12 enhances the inhibition autophagy and apoptosis effect of HBSP. CONCLUSION: These results demonstrate that HBSP inhibits myocardial H/R injury induced by autophagy over-activation and apoptosis via miR-21/Atg12 axis.