Targeting autophagy in ischemic stroke: From molecular mechanisms to clinical therapeutics.

Progress in targeting PTEN/PI3K/Akt axis in glioblastoma therapy: Revisiting molecular interactions.

Ischemia-reperfusion injury (IRI)-induced acute kidney injury (AKI) is a life-threatening disease. The activation of mitophagy was previously identified to play an important role in IRI. Maternally expressed 3 (MEG3) can promote cerebral IRI and hepatic IRI. The present study was designed to study the role of MEG3 in renal IRI. Renal IRI mice models were established, and HK-2 cells were used to construct the in vitro models of IRI. Hematoxylin-eosin staining assay was applied to reveal IRI-triggered tubular injury. MitoTracker Green FM staining and an ALP kit were employed for detection of mitophagy. TdT-mediated dUTP-biotin nick-end labeling assay was used to reveal cell apoptosis. The results showed that renal cortex of IRI mice contained higher expression of MEG3 than that of sham mice. MEG3 expression was also elevated in HK-2 cells following IRI, suggesting that MEG3 might participate in the development of IRI. Moreover, downregulation of MEG3 inhibited the apoptosis of HK-2 cells after IRI. Mitophagy was activated by IRI, and the inhibition of MEG3 can restore mitophagy activity in IRI-treated HK-2 cells. Mechanistically, we found that MEG3 can bind with miR-145-5p in IRI-treated cells. In addition, rhotekin (RTKN) was verified to serve as a target of miR-145-5p. MEG3 upregulated RTKN expression by binding with miR-145-5p. Further, MEG3 activated the Wnt/β-catenin pathway by upregulation of RTKN. The downstream effector of Wnt/β-catenin pathway, c-MYC, served as the transcription factor to activate MEG3. In conclusion, the positive feedback loop of MEG3/miR-145-5p/RTKN/Wnt/β-catenin/c-MYC promotes renal IRI by activating mitophagy and inducing apoptosis, which might offer a new insight into the therapeutic methods for renal IRI in the future.

/pdf/c-myc-induced-long-noncoding-rna-meg3-aggravates-kidney-87bmnpau4z.pdf

c-MYC-induced long noncoding RNA MEG3 aggravates kidney ischemia-reperfusion injury through activating mitophagy by upregulation of RTKN to trigger the Wnt/β-catenin pathway

This paper reports on an aluminum nitride (AlN) piezoelectric micromachined ultrasound transducer (PMUT) array for photoacoustic (PA) imaging, where the high-order resonance modes of the PMUT are utilized to improve imaging resolution. A flexural vibration mode (FVM) PMUT is fabricated and applied in a photoacoustic imaging (PAI) system. Specifically, the microelectromechanical system (MEMS)-based PMUT is suitable for PA endoscopic imaging of blood vessels and bronchi due to its miniature size and high sensitivity. More importantly, AlN is a nontoxic material, which makes it harmless for biomedical applications. In the PAI system, the AlN PMUT array is used to detect PA signals, and the acousto-mechanical response is designed and optimized at the PMUT's fundamental resonance. In this work, we focus on the high-order resonance performance of the PMUT PAI beyond the fundamental resonance. The acoustic and electrical responses of the PMUT's high-order resonance modes are characterized and analyzed. The fundamental and three high-order resonance bandwidths are 2.2, 8.8, 18.5, and 48.2 kHz. Compared with the resolution at the fundamental resonance mode, the resolutions at third- and fourth-order resonance modes increase by 38.7% and 76.9% in a phantom experiment. The high-order resonance modes of the AlN PMUT sensor array provide higher central frequency and wider bandwidth for PA signal detection, which increase the resolution of PAI compared to the PMUT working at the fundamental resonance mode. 

/pdf/beyond-fundamental-resonance-mode-high-order-multi-band-aln-2gkvsog9.pdf

Beyond fundamental resonance mode: high-order multi-band ALN PMUT for in vivo photoacoustic imaging

Ischemic stroke is one of the leading causes of global mortality and disability. It is a multi-factorial disease involving multiple factors, and gene dysregulation is considered as the major molecular mechanisms underlying disease progression. Angiogenesis can promote collateral circulation, which helps the restoration of blood supply in the ischemic area and reduces ischemic necrosis following ischemic injury. Aberrant expression of long non-coding RNAs (lncRNAs) in ischemic stroke is associated with various biological functions of endothelial cells and serves essential roles on the angiogenesis of ischemic stroke. The key roles of lncRNAs on angiogenesis suggest their potential as novel therapeutic targets for future diagnosis and treatment. This review elucidates the detailed regulatory functions of lncRNAs on angiogenesis following ischemic stroke through numerous mechanisms, such as interaction with target microRNAs, downstream signaling pathways and target molecules.

/pdf/the-regulatory-functions-of-lncrnas-on-angiogenesis-4jzquha10j.pdf

The Regulatory Functions of lncRNAs on Angiogenesis Following Ischemic Stroke.

Role of long noncoding RNA MEG3/miR-378/GRB2 axis in neuronal autophagy and neurological functional impairment in ischemic stroke.

Glioblastoma has been identified as the most common and aggressive primary brain tumor in adults. Recently, it has been found that cisplatin (DDP) treatment is a common chemotherapeutic method for GBM patients. Circ_PTN (ID number: hsa_circ_0003949) is a newly found circular (circRNA) which has been proved to be highly expressed in GBM cells while its role in GBM remains unclear. Therefore, our study focused on investigating the role of circ_PTN in the DDP resistance of GBM cells. The expression of circ_PTN in DDP-sensitive and DDP-resistant GBM cells was detected in our assay. Functional experiments were utilized to unveil the effects of circ_PTN on the DDP resistance of GBM cells. Moreover, mechanism assays were conducted to confirm the mechanism of how circ_PTN affected the DDP resistance of GBM cells. According to the results, we found that circ_PTN promoted the DDP resistance of GBM cells through activating PI3K/AKT pathway. Moreover, circ_PTN silencing inhibited the DDP resistance of GBM tumors in vivo. To conclude, our study unveiled the influence of circ_PTN on the DDP resistance of GBM cells, which might provide a therapeutic target for GBM treatment via DDP.

Circ_PTN contributes to the cisplatin-resistance of glioblastoma cells via stimulating PI3K/AKT signaling through miR-542-3p/PIK3R3 pathway

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Role of long noncoding RNA MEG3/miR-378/GRB2 axis in neuronal autophagy and neurological functional impairment in ischemic stroke.

Circ_PTN contributes to the cisplatin-resistance of glioblastoma cells via stimulating PI3K/AKT signaling through miR-542-3p/PIK3R3 pathway