Elevated ATG13 in serum of patients with ME/CFS stimulates oxidative stress response in microglial cells via activation of receptor for advanced glycation end products (RAGE)

Magnetoelectric stimulation is a promising therapy for various disorders due to its high efficacy and safety. To explore its potential in chronic skin wound treatment, we developed a magnetoelectric dressing, CFO@CTAB/PVDF (CCP), by electrospinning cetyltrimethylammonium bromide-modified CoFe2O4 (CFO) particles with polyvinylidene fluoride. Cetyltrimethylammonium bromide (CTAB) serves as a dispersion surfactant for CFO, with its quaternary ammonium cations imparting antibacterial and hydrophilic properties to the dressing. Electrospinning polarizes polyvinylidene fluoride (PVDF) molecules and forms a fibrous membrane with flexibility and breathability. With a wearable electromagnetic induction device, a dynamic magnetic field is established to induce magnetostrictive deformation of CFO nanoparticles. Consequently, a piezoelectric potential is generated on the surface of PVDF nanofibers to enhance the endogenous electrical field in the wound, achieving a cascade coupling of electric-magnetic-mechanical-electric effects. Bacteria and cell cultures show that 2% CTAB effectively balances antibacterial property and fibroblast activity. Under dynamic magnetoelectric stimulation, the CCP dressing demonstrates significant upregulation of TGF-β, FGF, and VEGF, promoting L929 cell adhesion and proliferation. Moreover, it facilitates the healing of diabetic rat skin wounds infected with Staphylococcus aureus within 2 weeks. Histological and molecular biology evaluations confirm the anti-inflammatory effect of CTAB and the accelerated formation of collagen and vessel by electrical stimulation. This work provides insights into the application of magnetoelectric stimulation in the healing of chronic wounds.

Wearable Magnetoelectric Stimulation for Chronic Wound Healing by Electrospun CoFe2O4@CTAB/PVDF Dressings.

Antiviral responses of ATG13 to the infection of peste des petits ruminants virus through activation of interferon response.

Bacteria-infected wounds pose challenges to healing due to persistent infection and associated damage to nerves and vessels. Although sonodynamic therapy can help kill bacteria, it is limited by the residual oxidative stress, resulting in prolonged inflammation. To tackle these barriers, novel 4 octyl itaconate-coated Li-doped ZnO/PLLA piezoelectric composite microfibers are developed, offering a whole-course "targeted" treatment under ultrasound therapy. The inclusion of Li atoms causes the ZnO lattice distortion and increases the band gap, enhancing the piezoelectric and sonocatalytic properties of the composite microfibers, collaborated by an aligned PLLA conformation design. During the infection and inflammation stages, the piezoelectric microfibers exhibit spatiotemporal-dependent therapeutic effects, swiftly eliminating over 94.2 % of S. aureus within 15 min under sonodynamic therapy. Following this phase, the microfibers capture reactive oxygen species and aid macrophage reprogramming, restoring mitochondrial function, achieving homeostasis, and shortening inflammation cycles. As the wound progresses through the healing stages, bioactive Zn2+ and Li + ions are continuously released, improving cell recruitment, and the piezoelectrical stimulation enhances wound recovery with neuro-vascularization. Compared to commercially available dressings, our microfibers accelerate the closure of rat wounds (Φ = 15 mm) without scarring in 12 days. Overall, this "one stone, four birds" wound management strategy presents a promising avenue for infected wound therapy. 

Ultrasound-responsive Microfibers Promoted Infected Wound Healing with Neuro-vascularization by Segmented Sonodynamic Therapy and Electrical Stimulation

An instructional design strategy for optimization of GelMA hydrogels material properties

Revolutionizing wound healing: Ultrashort pulse electric fields in seconds for highly aligned extracellular matrix and efficient cell migration

Dear Editor, Autophagy is an intracellular degradation pathway regulated by the orchestrated action of the autophagy‐related (ATG) proteins. ATG proteins traditionally have been studied for their roles in autophagy, but they have increasingly demonstrated functions other than cel‐ lular self‐eating.1 The non‐autophagic functions of autophagy pro‐ teins include cell survival and apoptosis, modulation of cellular traffic, protein secretion, cell signalling, transcription, translation and membrane reorganization.2 The ATG12‐ATG5 conjugate nega‐ tively modulated immunostimulatory RNA (isRNA)‐generated type I IFN production by sequestration of CARD proteins.3 The direct antiviral activity of IFNγ against murine norovirus in macrophages required nondegradative role of ATG5‐ATG12, ATG7 and ATG16L1.4 Intriguingly, ATG5‐ATG12 positively regulated antiviral NF‐κB and IRF3 signalling during foot‐and‐mouth disease virus infection.5 Moreover, Mauthe et al conduct an unbiased RNA interference screen approach to explore unconventional functions of ATG pro‐ teins during viral infections. They revealed that ATG13 and FIP200 act independently of the ULK complex to modify picornaviral repli‐ cation outside the context of autophagy.6‐8 Previous study suggest that ATG13 had both autophagic and nonautophagic functions and that the latter were essential for cardiac development.9 Targeting the ATG101‐ATG13 interaction showed the strongest autophagy‐in‐ hibitory effect.10 However, the role of ATG13 in innate antiviral im‐ mune signalling remains to be elucidated. In order to identify possible roles for ATG13 in antiviral immunity, we transfected human embryonic kidney cells HEK293T (293T cells) with an IFN‐sensitive response element (ISRE) luciferase reporter, which was an interferon regulatory factor 3 (IRF3)‐dependent pro‐ moter, and the internal control renilla luciferase, as well as expression vectors containing ATG13. Then we treated the cells intracellularly with the synthetic nucleic acid duplex poly(I:C)/ poly(dA:dT) or in‐ fected with vesicular stomatitis virus (VSV) for 12 hours to trigger type I interferon signalling. The ISRE‐Luc activity induced by intracel‐ lular poly(I:C)/ poly(dA:dT) or VSV infection was greatly enhanced by HA‐ATG13 overexpression (Figure 1A). These results indicated that ATG13 may be a positive regulator of the type I interferon response. Next, we co‐transfected ATG13 with signalling proteins involved in innate antiviral response and determined the activation of ISRE or nuclear factor kappa B (NF‐κB) promoters. The overexpression of ATG13 with the retinoic acid‐inducible gene‐I (RIG‐I)‐like receptors (RLRs) signalling proteins, including RIG‐I, melanoma differentia‐ tion‐associated antigen 5 (MDA5), mitochondrial antiviral signalling (MAVS), tumor necrosis factor (TNF) receptor associated factor (TRAF) family member associated NF‐κB activator (TANK) binding kinase 1 (TBK1), inhibitor of NF‐κB kinase subunit epsilon (IKKi), IRF3 and stimulator of interferon genes, additively activated ISRE luciferase activity (Figure 1B). However, overexpression of ATG13 with RIG‐I and MDA5, but not TRAF6 and MAVS, additively acti‐ vated NF‐κB luciferase activity (Figure 1C). Intriguingly, ATG13 itself can activate ISRE and NF‐κB luciferase activity in a dose‐dependent manner (Figure 1D). To demonstrate a link between the enhanced type I interferon response and antiviral immunity of ATG13 gene, we overexpressed ATG13 in 293T cells and then infected the cells with VSV tagged with enhanced green fluorescent protein (VSV‐eGFP) at a multiplicity of infection of 0.1. Overexpression of ATG13 ren‐ dered the cells resistant to viral infection and resulted in consider‐ ably fewer GFP+ (virus‐infected) cells than among cells transfected with empty vector (Figure 1E). Besides, we performed RT‐qPCR to quantify VSV replication over a time course manner (Figure S1). Then we determined whether specific knockdown of endog‐ enous ATG13 would decrease IFN‐β expression under physiolog‐ ical conditions. We used three ATG13‐specific short hairpin RNA (shRNA) constructs to knock down the expression of ATG13. All three efficiently inhibited the expression of endogenous ATG13 in mRNA level and transfected ATG13 in protein level in 293T cells (Figure 1F). With the ISRE luciferase reporter assay, we found that knockdown of ATG13 resulted in much less activity of the ISRE lu‐ ciferase reporter triggered by intracellular poly(I:C), poly(dA:dT) or VSV‐eGFP in 293T cells (Figure 1G). Consistent with that, knock‐ down of ATG13 also resulted in lower expression of IFN‐β and IFN‐α mRNA with intracellular poly(I:C) or poly(dA:dT) treatment (Figure 1H). Several interferon‐stimulated genes (ISG), including ISG54 and ISG56, were down‐regulated by ATG13 knockdown with the same treatment (Figure 1I). For rescue experiment, ISRE luciferase activity recovered to some extent with ATG13 re‐expres‐ sion after knockdown under intracellular poly(I:C) or poly(dA:dT) treatment (Figure 1J). For 293T‐TLR3 cells (293T cells that express TLR3) treated with poly(I:C), no significant difference was observed in ISRE activity with ATG13 knockdown (Figure 1K). It suggest that

ATG13 restricts viral replication by induction of type I interferon.

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Revolutionizing wound healing: Ultrashort pulse electric fields in seconds for highly aligned extracellular matrix and efficient cell migration

ATG13 restricts viral replication by induction of type I interferon.