Prolonged Button Battery Exposure Leading to Severe Ocular Injury without Heavy Metal Poisoning.

Introduction: Prolonged exposure to a complete button battery can cause severe tissue necrosis in the eye and permanent impairment of visual function. The main mechanism of injury is the current generated by the hydrolysis of tissue fluid at the negative electrode and the production of hydroxide ions. Case Presentation: A 3-year-old girl went to the local hospital because of swelling and pain in her right eye of 12-h duration. The local doctor performed an orbital CT (computed tomography) scan and found a foreign body between the right eyelid and the eyeball. The foreign body was removed immediately under general anesthesia. In addition, it was found that the foreign body was a button battery, but it prolonged 39 h from the onset of the child's symptoms. The child underwent a second operation in our hospital and received amniotic membrane transplantation combined with conjunctival flap coverage. Topical corticosteroid and antibiotic eye ointment were continued for 3 months after surgery. Local pigmentation was seen, there was no symblepharon, but the cornea was still opaque and the visual acuity was only FC (finger count). In this particular case, heavy metal testing conducted on the child's blood fortunately revealed that the levels were within the normal range. Conclusion: Early detection and urgent removal of button battery are crucial in order to minimize exposure time. We should also be concerned about heavy metals in the blood. Children should be kept away from button batteries as much as possible to avoid such injury.

Aeromonas veronii-associated endogenous endophthalmitis: a case report.

BACKGROUND: Aeromonas veronii is a very rare and highly pathogenic microorganism. We investigate the clinical characteristics and significance of endogenous endophthalmitis caused by Aeromonas veronii in our patient. CASE PRESENTATION: A 30-year-old Asian women with systemic lupus erythematosus, uremia, and hypertension developed acute infectious endophthalmitis caused by Aeromonas veronii. After emergency vitrectomy and antibiotic therapy, the clinical condition worsened requiring enucleation. CONCLUSIONS: Aeromonas veronii can cause infection in the human eye, which can manifest as acute endophthalmitis. Early diagnosis and targeted therapy are important for successful treatment.

BMX deletion mitigates neuroinflammation induced by retinal ischemia/reperfusion through modulation of the AKT/ERK/STAT3 signaling cascade.

Aims: Retinal ischemia/reperfusion (I/R) injury is implicated in the etiology of various ocular disorders. Prior research has demonstrated that bone marrow tyrosine kinase on chromosome X (BMX) contributes to the advancement of ischemic disease and inflammatory reactions. Consequently, the current investigation aims to evaluate BMX's impact on retinal I/R injury and clarify its implied mechanism of action. Main methods: This study utilized male and female systemic BMX knockout (BMX-/-) mice to conduct experiments. The utilization of Western blot assay and immunofluorescence labeling techniques was employed to investigate variations in the expression of protein and tissue localization. Histomorphological changes were observed through H&E staining and SD-OCT examination. Visual function changes were assessed through electrophysiological experiments. Furthermore, apoptosis in the retina was identified using the TUNEL assay, as well as the ELISA technique, which has been utilized to determine the inflammatory factors level. Key findings: Our investigation results revealed that the knockdown of BMX did not yield a significant effect on mouse retina. In mice, BMX knockdown mitigated the negative impact of I/R injury on retinal tissue structure and visual function. BMX knockdown effectively reduced apoptosis, suppressed inflammatory responses, and decreased inflammatory factors subsequent to I/R injury. The outcomes of the current investigation revealed that BMX knockdown partially protected the retina through downregulating phosphorylation of AKT/ERK/STAT3 pathway. Significance: Our investigation showed that BMX-/- reduces AKT, ERK, and STAT3 phosphorylation, reducing apoptosis and inflammation. Thus, this strategy protected the retina from structural and functional damage after I/R injury.

BAFF deficiency aggravated optic nerve crush-induced retinal ganglion cells damage by regulating apoptosis and neuroinflammation via NF-κB-IκBα signaling.

Loss of retinal ganglion cells (RGCs) is a primary cause of visual impairment in glaucoma, the pathological process is closely related to neuroinflammation and apoptosis. B-cell activating factor (BAFF) is a fundamental survival factor mainly expressed in the B cell lineage. Evidence suggests its neuroprotective effect, but the expression and role in the retina have not yet been investigated. In this study, we adopt optic nerve crush (ONC) as an in vivo model and oxygen-glucose deprivation/reoxygenation (OGD/R) of RGCs as an in vitro model to investigate the expression and function of BAFF. We found that BAFF and its receptors were abundantly expressed in the retina and BAFF inhibition exacerbated the caspase 3-mediated RGCs apoptosis, glial cell activation and pro-inflammatory cytokines expression, which may be caused by the activation of the NF-κB pathway in vivo. In addition, we found that BAFF treatment could alleviate RGCs apoptosis, pro-inflammatory cytokines expression and NF-κB pathway activation, which could be reversed the effect by blockade of the NF-κB pathway in vitro. Meanwhile, we found that microglia induced to overexpress BAFF in the inflammatory microenvironment in a time-dependent manner. Taken together, our results indicated that BAFF deficiency promoted RGCs apoptosis and neuroinflammation through activation of NF-κB pathway in ONC retinas, suggesting that BAFF may serve as a promising therapeutic target for the treatment of glaucoma.

Setanaxib mitigates oxidative damage following retinal ischemia-reperfusion via NOX1 and NOX4 inhibition in retinal ganglion cells.

Glaucoma, a prevalent cause of permanent visual impairment worldwide, is characterized by the progressive degeneration of retinal ganglion cells (RGCs). NADPH oxidase (NOX) 1 and NOX4 are pivotal nodes in various retinal diseases. Setanaxib, a potent and highly selective inhibitor of NOX1 and NOX4, can impede the progression of various diseases. This study investigated the efficacy of setanaxib in ameliorating retinal ischemia-reperfusion (I/R) injury and elucidated its underlying mechanisms. The model of retinal I/R induced by acute intraocular hypertension and the oxygen-glucose deprivation/reoxygenation (OGD/R) model of primary RGCs were established. By suppressing NOX1 and NOX4 expression in RGCs, setanaxib mitigated I/R-induced retinal neuronal loss, structural disruption, and dysfunction. Setanaxib reduced TUNEL-positive cells, upregulated Bcl-2, and inhibited Bax, Bad, and cleaved-caspase-3 overexpression after I/R injury in vitro and in vivo. Moreover, setanaxib also significantly reduced cellular senescence, as demonstrated by downregulating SA-ß-gal-positive and p16-INK4a expression. Furthermore, setanaxib significantly suppressed ROS production, Hif-1α and FOXO1 upregulation, and NRF2 downregulation in damaged RGCs. These findings highlight that the setanaxib effectively inhibited NOX1 and NOX4, thereby regulating ROS production and redox signal activation. This inhibition further prevents the activation of apoptosis and senescence related factors in RGCs, ultimately protecting them against retinal I/R injury. Consequently, setanaxib exhibits promising potential as a therapeutic intervention for glaucoma.

Application of the suture needle retrograde threading method in scleral fixation of intraocular lenses.

BACKGROUND: Here we described a new threading technique for the universal fixation of any posterior chamber intraocular lens (IOL). METHODS: Twenty-seven eyes of 27 patients whose surgery done by Surgeon A with the needle-guided method or the suture needle retrograde threading (SNRT) method for intrascleral IOL fixation were enrolled in the first group. Thirty-four eyes of 34 patients whose surgery done by Surgeon A, Surgeon B or Surgeon C with the SNRT method for intrascleral IOL fixation were grouped into three sub-groups by surgeon. Information regarding age, sex, best-available visual acuity (BCVA), intraocular pressure (IOP), past ophthalmological history, threading time (from puncturing to externalizing suture) and complications during and after the surgery were gathered. RESULTS: The analysis showed that the threading time was less in the SNRT group than needle-guided group by Surgeon A. There was one eye with suture needle slipping from the guide needle when guiding out of the eye. The threading procedure was completed one time without suture ruptures or loop slippage in the SNRT group operated by Surgeon A. And using the SNRT method, Surgeon A, Surgeon B, and Surgeon C did not show any significant difference in threading time. No complications (e.g., vitreous hemorrhage, hyphemia, retinal detachment, suprachoroidal hemorrhage, or hypotony) were observed during surgery or postoperatively in all cases. No leakage occurred at the site of the puncture after the operation. CONCLUSIONS: The described technique appears to be a safe, simple, easy-to-learn, and universal surgical method, which is suitable for various types of IOLs.

PPAR-γ promotes the polarization of rat retinal microglia to M2 phenotype by regulating the expression of CD200-CD200R1 under hypoxia.

BACKGROUND: Recent reports suggest that peroxisome proliferator-activated receptor-γ (PPAR-γ) could promote microglial M2 polarization to inhibit inflammation. However, the specific molecular mechanisms that trigger PPAR-γ's anti-inflammatory ability in microglia are yet to be expounded. Thus, in this study, we aimed to explore the molecular mechanisms behind the anti-inflammatory effects of PPAR-γ in hypoxia-stimulated rat retinal microglial cells. METHODS AND RESULTS: We used shRNA expressing lentivirus to knock down PPAR-γ and CD200 genes, and we assessed hypoxia-induced polarization markers release - M1 (iNOS, IL-1ß, IL-6, and TNF-α) and M2 (Arg-1, YM1, IL-4, and IL-10) by RT-PCR. We also monitored PPAR-γ-related signals (PPAR-γ, PPAR-γ in cytoplasm or nucleus, CD200, and CD200Rs) by Western blot and RT-PCR. Our results showed that hypoxia enhanced PPAR-γ and CD200 expressions in microglial cells. Moreover, PPAR-γ agonist 15d-PGJ2 elevated CD200 and CD200R1 expressions, whereas sh-PPAR-γ had the opposite effect. Following hypoxia, expressions of M1 markers increased significantly, while those of M2 markers decreased, and the above effects were attenuated by 15d-PGJ2. Conversely, knocking down PPAR-γ or CD200 inhibited the polarization of microglial cells to M2 phenotype. CONCLUSION: Our findings demonstrated that PPAR-γ performed an anti-inflammatory function in hypoxia-stimulated microglial cells by promoting their polarization to M2 phenotype via the CD200-CD200R1 pathway.

RhoA/ROCK Signaling Is Involved in Pathological Retinal Neovascularization.

OBJECTIVE: The aim of the study was to evaluate the effect of the RhoA/ROCK inhibitor Fasudil on retinal neovascularization (NV) in vivo and angiogenesis in vitro. METHODS: C57BL/6 was used to establish an OIR model. First, RhoA/ROCK expression was first examined and compared between OIR and healthy controls. Then, we evaluated the effect of Fasudil on pathological retinal NV. Whole-mount retinal staining was performed. The percentage of NV area, the number of neovascular tufts (NVT), and branch points (BP) were quantified. Finally, human umbilical vein endothelial cells (HUVECs) were used to investigate the effect of Fasudil on angiogenesis. RESULTS: Real-time PCR and Western blotting showed that ROCK expression in retinal tissue was statistically upregulated in OIR. Furthermore, we found that Fasudil attenuated the percentage of NV area, the number of NVT, and BP significantly. In addition, Fasudil could suppress the proliferation and migration of HUVECs induced by VEGF. CONCLUSIONS: RhoA/ROCK might be involved in the pathogenesis of OIR. And its inhibitor Fasudil could suppress retinal NV in vivo and angiogenesis in vitro. Fasudil may be a potential treatment strategy for retinal vascular diseases.

Inhibition of NOX4 with GLX351322 alleviates acute ocular hypertension-induced retinal inflammation and injury by suppressing ROS mediated redox-sensitive factors activation.

Reactive oxygen species (ROS) overproduction plays an essential role in the etiology of ischemic/hypoxic retinopathy caused by acute glaucoma. NADPH oxidase (NOX) 4 was discovered as one of the main sources of ROS in glaucoma. However, the role and potential mechanisms of NOX4 in acute glaucoma have not been fully elucidated. Therefore, the current study aims to investigate the NOX4 inhibitor GLX351322 that targets NOX4 inhibition in acute ocular hypertension (AOH)-induced retinal ischemia/hypoxia injury in mice. Herein, NOX4 was highly expressed in AOH retinas, particularly the retinal ganglion cell layer (GCL). Importantly, the NOX4 inhibitor GLX351322 reduced ROS overproduction, inhibited inflammatory factor release, suppressed glial cell activation and hyperplasia, inhibited leukocyte infiltration, reduced retinal cell senescence and apoptosis in damaged areas, reduced retinal degeneration and improved retinal function. This neuroprotective effect is at least partially associated with mediated redox-sensitive factor (HIF-1α, NF-κB, and MAPKs) pathways by NOX4-derived ROS overproduction. These results suggest that inhibition of NOX4 with GLX351322 attenuated AOH-induced retinal inflammation, cellular senescence, and apoptosis by inhibiting the activation of the redox-sensitive factor pathway mediated by ROS overproduction, thereby protecting retinal structure and function. Targeted inhibition of NOX4 is expected to be a new idea in the treatment of acute glaucoma.

Single­pass four­throw versus traditional knotting pupilloplasty for traumatic mydriasis combined with lens dislocation.

PURPOSE: To compare the use of single­pass four­throw (SFT) and traditional double-pass two-throw knotting (DTT) techniques in pupilloplasty for traumatic mydriasis combined with lens dislocation, and to evaluate the learning curve between the two knotting techniques by wet lab. METHOD: The eyes of 45 patients (45 eyes) were divided into two groups according to the knotting technique used: single­pass four­throw (22 eyes) or traditional double-pass-two-throw knotting (23 eyes). Combined phacoemulsification and pupilloplasty with pars plana vitrectomy were performed in traumatic mydriasis patients with lens dislocation. Preoperative and postoperative corrected distance visual acuity (CDVA), pupil diameter, intraocular pressure (IOP), pupilloplasty time, and complications were compared. Twenty ophthalmology residents were randomized to perform a pupilloplasty suturing exam with or without SFT knotting techniques in porcine eyes. RESULT: All cases had a minimum follow­up period of 6 months (range 6-12 months). There was no significant difference in the CDVA (P = 0.55), postoperative pupil diameter (P = 0.79), IOP (P > 0.05), anterior chamber exudate degree, and loosening or shedding of the line knot between the two groups. The duration of the pupilloplasty was 22.32 ± 4.58 min in the SFT group and 30.35 ± 5.55 min in the traditional group, which was a significant difference (P < 0.01). The residents in the SFT group had higher test scores and fewer surgical mistakes (P < 0.05). CONCLUSION: The SFT knotting technique has a similar treatment effect and safety as the traditional technique but requires a shorter time and is easier to perform in pupilloplasty surgery.

Liquid Metal-Tailored PEDOT:PSS for Noncontact Flexible Electronics with High Spatial Resolution.

Electric field-based noncontact flexible electronics (EF-NFEs) allow people to communicate with intelligent devices through noncontact human-machine interactions, but current EF-NFEs with limited detections (usually <20 cm) distance often lack a high spatial resolution. Here, we report a versatile material for preparing EF-NFE devices with a high spatial resolution to realize everyday human activity detection. Eutectic gallium-indium alloy (EGaIn) was introduced into poly(3,4-ethylenedioxythiophene):poly(styrenesulfonate) (PEDOT:PSS) chains to fabricate this material, named Ga-PP. The introduction of EGaIn successfully regulates the intra- and interchain interactions of PEDOT chains and thus increases the π-electron accumulation on Ga-PP chains, which facilitates improvement of the electron storage of Ga-PP and its noncontact sensing ability. The water solubility of the obtained Ga-PP can reach approximately 15 mg/mL, comparable to that of commercial PEDOT:PSS, thus making Ga-PP suitable for various design strategies to prepare EF-NFE devices. We demonstrate that a conductive textile with a noncontact sensing ability can be achieved by immersing a commercial silk fabric into a Ga-PP solution for 5 min. With a detection distance exceeding 1 m, the prepared Ga-PP-based conductive textile (Ga-PP-CT) possesses outstanding noncontact sensing sensitivity, showing advantages in tracing the locations of signal sources and distinguishing motion states. Surprisingly, even when placed in water, Ga-PP-CT can be used to monitor the movement signals of athletes in different sporting events and output specific noncontact response signals for different sports. Intriguingly, the Ga-PP solution itself can be used to construct noncontact sensing conductive circuits, displaying the potential to be incorporated into smart electronics.

Identification of a novel lipid metabolism-related gene signature for predicting colorectal cancer survival.

Colorectal cancer (CRC) is a common malignant tumor worldwide. Lipid metabolism is a prerequisite for the growth, proliferation and invasion of cancer cells. However, the lipid metabolism-related gene signature and its underlying molecular mechanisms remain unclear. The aim of this study was to establish a lipid metabolism signature risk model for survival prediction in CRC and to investigate the effect of gene signature on the immune microenvironment. Lipid metabolism-mediated genes (LMGs) were obtained from the Molecular Signatures Database. The consensus molecular subtypes were established using "ConsensusClusterPlus" based on LMGs and the cancer genome atlas (TCGA) data. The risk model was established using univariate and multivariate Cox regression with TCGA database and independently validated in the international cancer genome consortium (ICGC) datasets. Immune infiltration in the risk model was developed using CIBERSORT and xCell analyses. A total of 267 differentially expressed genes (DEGs) were identified between subtype 1 and subtype 2 from consensus molecular subtypes, including 153 upregulated DEGs and 114 downregulated DEGs. 21 DEGs associated with overall survival (OS) were selected using univariate Cox regression analysis. Furthermore, a prognostic risk model was constructed using the risk coefficients and gene expression of eleven-gene signature. Patients with a high-risk score had poorer OS compared with patients in the low-risk score group (p = 3.36e-07) in the TCGA cohort and the validationdatasets (p = 4.03e-05). Analysis of immune infiltration identified multiple T cells were associated with better prognosis in the low-risk group, including Th2 cells (p = 0.0208), regulatory T cells (p = 0.0425), and gammadelta T cells (p = 0.0112). A nomogram integrating the risk model and clinical characteristics was further developed to predict the prognosis of patients with CRC. In conclusion, our study revealed that the expression of lipid-metabolism genes were correlated with the immune microenvironment. The eleven-gene signature might be useful for prediction the prognosis of CRC patients.

Ti2C3Tx/Polyurethane Constructed by Gas-Liquid Interface Self-Assembly for Underwater Sensing.

Nowadays, multifunctional, easily prepared, and highly sensitive flexible sensors have attracted extensive attention and are gradually used in various scenarios. Here, we report the design of the Ti2C3Tx/polyurethane composites prepared by a facile gas-liquid interface self-assembly. The obtained flexible sensor has a wide detection range (∼900%), a low-stress detection limit (<1%), a high sensitivity (GF = 1.3, strain from 0 to 100%), and a fast response time (<140 ms). The multifunctional stress sensor can be applied to not only wearable motion monitoring and detection of various signals but also the detection of underwater human motion, as well as different motion states and swimming frequencies of toy fish in water, demonstrating its great prospects in a variety of applications, such as human movement monitoring and marine biological detection and research.

Cavin-1 promotes M2 macrophages/microglia polarization via SOCS3.

PURPOSE: Our study aimed to investigate the function of Cavin-1 and SOCS3 in macrophages/microglia M2 polarization and further explored the relevant mechanism. METHODS: Expression levels of Cavin-1 and SOCS3 in macrophages/microglia were measured by western blotting and RT-PCR, respectively. Then, Cavin-1 or SOCS3 was gene silenced by a siRNA approach, and gene silencing efficiency was determined by western blotting. Next, co-immunoprecipitation (Co-IP) was employed to further analyze the interaction between Cavin-1 and SOCS3. Finally, the activation of STAT6/PPAR-γ signaling was evaluated using western blotting, and the M2 macrophages/microglia polarization was validated by measuring the mRNA expression of M2 markers by RT-PCR. RESULTS: In the polarization process of macrophages/microglia to M2 phenotype, both Cavin-1 and SOCS3 increased synchronously at protein and mRNA level, reached the peak at the 6 h, and then decreased. After Cavin-1 or SOCS3 silencing, the expression of Cavin-1 and SOCS3 declined. These results suggested that Cavin-1 and SOCS3 were positively correlated in macrophages/microglia, and this conjecture was verified by Co-IP. Besides, Cavin-1 silencing not only suppressed the activation of STAT6/PPAR-γ pathway, but also suppressed the release of anti-inflammatory factors. Finally, we found that SOCS3 overexpression reversed the inhibitory effect of Cavin-1 silencing on the release of anti-inflammatory factors in M2 macrophages/microglia. CONCLUSIONS: Cavin-1 and SOCS3 are actively involved in the process of M2 macrophages/microglia polarization. As a SOCS3 interacting protein, Cavin-1 can promote M2 macrophages/microglia polarization via SOCS3.

Loofah Sponge-Derived Hygroscopic Photothermal Absorber for All-Weather Atmospheric Water Harvesting.

The loofah gourd is like a natural water tank that stores underground water and drains it out after aging, leaving only a three-dimensional network consisting of hollow and interconnected fibers. This phenomenon inspired us to fabricate a solar-energy-powered sorption-based atmospheric water harvesting device using a loofah sponge. Herein, moisture absorption and photothermal conversion strategies are rationally designed to fast release the absorbed water. This is accomplished by filling the hollow and connected loofah fiber with LiCl and replacing the original luffa peel with a bacterial cellulose (BC)/carbon nanotube (CNT) photothermal conversion membrane. As a result, loofah/BC/CNT (LBC)@LiCl presents a high water absorption capacity of 2.65 g g-1 at 90% relative humidity (RH) and fast water release performance of 1.33 kg m-2 h-1 under 1.0 sun. Noticeably, ∼1.92-2.40 kg LBC@LiCl can produce daily drinking water for adults (2000-2500 mL) in one night outdoors at ∼66% RH, proving that it is a feasible method to overcome the drinking water shortage of poor and arid areas using cheap and renewable biomass material.

Monomorphic epitheliotropic intestinal T-cell lymphomas: a case report.

BACKGROUND: Monomorphic epitheliotropic intestinal T-cell lymphomas (MEITL) is a rare and aggressive subtype of lymphoma. The most common site of origin is small intestine. Patients are often presented with diagnosis of intestinal perforation with abdominal pain as the main consulting symptoms. Because of the deficiency of specific diagnostic measures and effective management, diagnosis is often confirmed in advanced stage with poor prognosis. CASE PRESENTATION: Here, we introduce a patient who has suffered from abdominal pain and diarrhea, and eventually been diagnosed as Monomorphic epitheliotropic intestinal T-cell lymphomas. CONCLUSION: MEITL is rare in clinical practice with deficiency of early diagnostic measures and poor prognosis. Therefore, any patient with ambiguous gastrointestinal symptoms or perforation of the digestive tract where the primary lesion is difficult to identify should be alert to the possibility of this disease.

Impact of air injection on subretinal fluid following successful scleral buckling surgery for macular-involving retinal detachment.

Air injection is an accessory technique during scleral buckling (SB). Subclinical subretinal fluid (SRF) may presence and persistent after SB. The impact of air injection on SRF is unclear. In the study, we retrospectively enrolled 51 patients with macular-involving RD who had undergone successful SB. They were categorized into Group A (SB without air injection) and Group B (SB with air injection). First, we found that although group B seem to be severer than group A before surgery, Kaplan-Meier graph showed that SRF absorbed more rapidly in group B after surgery, and the incidence of SRF in group B was much lower during the whole follow-up period. Moreover, the cases with superior breaks had the lowest incidence. Second, during the follow-up period, there was no significant difference about postoperative complication between two groups. Lastly, risk factors for persistent SRF were investigated with binary logistic regression, and no risk factor was found. In conclusion, air injection during the SB might accelerate SRF absorption and reduce the incidence of persistent SRF, especially for the longstanding macular-off RD with superior breaks.

Epigenetic Landscape Analysis of the Long Non-Coding RNA and Messenger RNA in a Mouse Model of Corneal Alkali Burns.

Purpose: Corneal alkali burns (CABs) are a common clinical ocular disease, presenting a poor prognosis. Although some long noncoding RNAs (lncRNAs) reportedly play a key role in epigenetic regulation associated with CABs, studies regarding the lncRNA signature in CABs remain rare and elusive. Methods: A CAB model was established in C57BL/6J mice and profiling of lncRNA expressions was performed by RNA-Seq. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted to predicate the related pathological pathways and candidate genes. RT-qPCR was used to verify the expression pattern of lncRNAs and related mRNAs, both in vitro and in vivo. Data were statistically analyzed by GraphPad Prism version 6.0. Results: In all, 4436 aberrantly expressed lncRNAs were identified in CAB mice when compared with control mice. In the top 13 aberrantly expressed lncRNAs, Bc037156 and 4930511E03Rik were confirmed as the most significantly altered lncRNAs. Pathway analysis revealed that mitogen-activated protein kinase (MAPK) signaling pathway was most enriched. Following 4930511E03Rik siRNA treated, Srgn, IL-1ß and Cxcr2 were significant upregulated in corneal epithelial cells, corneal keratocytes, and bone marrow dendritic cells, with NaOH treatment. Moreover, after Bc037156 siRNA treated, expression levels of IL-1ß and Srgn were significantly downregulated in the three cell lines. Conclusions: Our study suggests that Bc037156 and 4930511E03Rik may be involved in inflammation, immune response, and neovascularization by regulating Srgn, IL-1ß, and Cxcr2 expression after CAB. These candidate lncRNAs and mRNAs may be the potential targets for the treatment strategy of the alkali injured cornea.

Fasudil attenuates glial cell-mediated neuroinflammation via ERK1/2 and AKT signaling pathways after optic nerve crush.

To investigate the functional role of fasudil in optic nerve crush (ONC), and further explore its possible molecular mechanism. After ONC injury, the rats were injected intraperitoneally either with fasudil or normal saline once a day until euthanized. RGCs survival was assessed by retrograde labeling with FluoroGold. Retinal glial cells activation and population changes (GFAP, iba-1) were measured by immunofluorescence. The expressions of cleaved caspase 3 and 9, p-ERK1/2 and p-AKT were detected by western blot. The levels of the pro-inflammatory cytokines were determined using real-time polymerase chain reaction. Fasudil treatment inhibited RGCs apoptosis and reduced RGCs loss demonstrated by the decreased apoptosis-associated proteins expression and the increased fluorogold labeling of RGCs after ONC, respectively. In addition, the ONC + fasudil group compared had a significantly lower expression of GFAP and iba1 compared with the ONC group. The levels of pro-inflammatory cytokines were significantly reduced in the ONC + fasudil group than in the ONC group. Furthermore, the phosphorylation levels of ERK1/2 and AKT (p-ERK1/2 and p-AKT) were obviously elevated by the fasudil treatment. Our study demonstrated that fasudil attenuated glial cell-mediated neuroinflammation by up-regulating the ERK1/2 and AKT signaling pathways in rats ONC models. We conclude that fasudil may be a novel treatment for traumatic optic neuropathy.

The expression and role of PIDD in retina after optic nerve crush.

To examine the expression of P53-induced protein with a death domain (PIDD) at retina in animal model of optic nerve crush (ONC) and to investigate the role of PIDD in retinal glial activation and NF-κB activation induced by optic nerve damage, ONC animal model was established in Sprague-Dawley rats. PIDD has three isoforms (Isof); Western blot was performed to examine the expression of PIDD (Isof-1, Isof-2, and Isof-3, respectively) in retina at different time points after ONC. Retinal glial activation is closely associated with retinal neuronal death and is monitored by the expression of GFAP+ glial cells and IBA1+ microglia, then activated microglia leads to inflammatory cytokine production. NF-kB activation in glial cells also can promote neuronal death. In our study, the role of PIDD in retinal glial activation and NF-kB activation was investigated with PIDD inhibition selectively. PIDD expression (Isof-1 and Isof-3) was dramatically increased, and peaked at 3 days after ONC, while Isof-2 did not show any difference. In the ONC animal model, the number of GFAP+ glial cells and IBA1+ microglia in retinal layers was increased significantly, inflammatory cytokine production was upregulated, and NF-κB in glial cell was also activated. Moreover, those responses induced by optic nerve damage were attenuated with PIDD inhibition, which indicated that PIDD could regulate retinal glial activation, neuro-inflammation, and NF-κB activation. These results provided the direct demonstration that the PIDD (Isof-1and Isof-3) was overexpressed in retina after ONC, and PIDD may be involved in retinal neurodegenerative diseases by regulating retinal glial activation and NF-κB activation.