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Wang, Haixia,Shi, Xin,Cheng, Longlong,Han, Jie,Mu, Jianjun The Korean Society of Pharmacology 2021 The Korean Journal of Physiology & Pharmacology Vol.25 No.3
The present study explored the therapeutic potential of hydrogen sulfide (H2S) in restoring aging-induced loss of cardioprotective effect of remote ischemic preconditioning (RIPC) along with the involvement of signaling pathways. The left hind limb was subjected to four short cycles of ischemia and reperfusion (IR) in young and aged male rats to induce RIPC. The hearts were subjected to IR injury on the Langendorff apparatus after 24 h of RIPC. The measurement of lactate dehydrogenase, creatine kinase and cardiac troponin served to assess the myocardial injury. The levels of H2S, cystathionine β-synthase (CBS), cystathionine γ-lyase (CSE), nuclear factor erythroid 2-related factor 2 (Nrf2), and hypoxia-inducible factor (HIF-1α) were also measured. There was a decrease in cardioprotection in RIPC-subjected old rats in comparison to young rats along with a reduction in the myocardial levels of H2S, CBS, CSE, HIF-1α, and nuclear: cytoplasmic Nrf2 ratio. Supplementation with sodium hydrogen sulfide (NaHS, an H2S donor) and l-cysteine (H2S precursor) restored the cardioprotective actions of RIPC in old hearts. It increased the levels of H2S, HIF-1α, and Nrf2 ratio without affecting CBS and CSE. YC-1 (HIF-1α antagonist) abolished the effects of NaHS and l-cysteine in RIPC-subjected old rats by decreasing the Nrf2 ratio and HIF-1α levels, without altering H2S. The late phase of cardioprotection of RIPC involves an increase in the activity of H2S biosynthetic enzymes, which increases the levels of H2S to upregulate HIF-1α and Nrf2. H2S has the potential to restore aging-induced loss of cardioprotective effects of RIPC by upregulating HIF-1α/Nrf2 signaling.
Photonic Microcavity-Enhanced Magnetic Plasmon Resonance of Metamaterials for Sensing Applications
Chen, Jing,Peng, Cheng,Qi, Shibin,Zhang, Qian,Tang, Chaojun,Shen, Xueyang,Da, Haixia,Wang, Lianhui,Park, Gun-Sik IEEE 2019 IEEE Photonics Technology Letters Vol.31 No.2
<P>We first investigate numerically photonic microcavity-enhanced magnetic plasmon (MP) resonance in metamaterials for high-quality refractive index sensing. The metamaterials consist of a top periodic array of U-shaped metallic split-ring resonators (SRRs), a middle dielectric layer, and a bottom metallic backed plate. The top metallic SRRs that are placed at about Bragg distance above the bottom metallic plate constitute a photonic microcavity. Because the MP resonance excited in metallic SRRs is coupled to the photonic microcavity mode supported by the photonic microcavity, the radiative damping of the MP resonance is strongly reduced, and consequently, its linewidth is decreased dramatically. Benefiting from the narrow linewidth, large modulation depth, and giant magnetic field enhancement at the MP resonance, the cavity-coupled metamaterial sensor has very high sensitivity ( <TEX>$\text {S}= 400$</TEX> nm/RIU and <TEX>$\text {S}^{\ast } = 26$</TEX>/RIU) and figure of merit ( <TEX>$\text {FOM}= 33$</TEX> and FOM* = 4215), which suggests that the proposed metamaterials have potential in applications of plasmonic biosensors.</P>
LncRNA-IMAT1 Promotes Invasion of Meningiomas by Suppressing KLF4/hsa-miR22-3p/Snai1 Pathway
Tao Zhang,Yu Ge,Daijun Wang,Qin Liu,Shuchen Sun,Lingyang Hua,Jiaojiao Deng,Shihai Luan,Haixia Cheng,Qing Xie,Ye Gong,Tao Zhang 한국분자세포생물학회 2022 Molecules and cells Vol.45 No.6
Malignant meningiomas often show invasive growth that makes complete tumor resection challenging, and they are more prone to recur after radical resection. Invasive meningioma associated transcript 1 (IMAT1) is a long noncoding RNA located on Homo sapiens chromosome 17 that was identified by our team based on absolute expression differences in invasive and non-invasive meningiomas. Our studies indicated that IMAT1 was highly expressed in invasive meningiomas compared with non-invasive meningiomas. In vitro studies showed that IMAT1 promoted meningioma cell invasion through the inactivation of the Krüppel-like factor 4 (KLF4)/hsa-miR22-3p/Snai1 pathway by acting as a sponge for hsa-miR22-3p, and IMAT1 knockdown effectively restored the tumor suppressive properties of KLF4 by preserving its tumor suppressor pathway. In vivo experiments confirmed that IMAT1 silencing could significantly inhibit the growth of subcutaneous tumors and prolong the survival period of tumor-bearing mice. Our findings demonstrated that the high expression of IMAT1 is the inherent reason for the loss of the tumor suppressive properties of KLF4 during meningioma progression. Therefore, we believe that IMAT1 may be a potential biological marker and treatment target for meningiomas.