Glia maturation factor-β deficiency improves insulin resistance by promoting CARM1-mediated lipid turnover.

Insulin resistance (IR) is a major factor for obesity-associated type 2 diabetes. The molecular mechanisms of IR and its systemic control remain poorly understood, and pharmacological drugs to ameliorate IR are an unmet need. So finding new therapeutic targets and drugs is important.

Naphthalene Metabolites From Long-Term Environmental Tobacco Smoke Induce the Aging of Retinal Pigment Epithelium.

Tobacco use is the main source of indoor air pollution and contains a variety of toxic components. The smoke from burning cigarettes is a key environmental risk factor that leads to accelerated aging and the occurrence of numerous diseases. Meanwhile, cigarette smoke and aging are both prominent risk factors for age-related macular degeneration (AMD).

Extracellular GMFB activates the non-canonical FAS-FAF1 pathway to induce lysosomal dysfunction in early diabetic retinopathy.

Diabetic retinopathy (DR) is one of the leading causes of blindness in the global working population and involves a pathological microenvironment. In early diabetes, the level of glia maturation factor-β (GMFB) is significantly elevated in the vitreous, which leads to neurodegeneration by inhibiting autophagy in the retinal pigment epithelial (RPE) cells. However, the membrane receptor of extracellular GMFB is unknown.

PHOSPHO1 Suppresses Ferroptosis in Retinal Pigment Epithelial Cells by Reducing the Levels of Phosphatidylethanolamine Molecular Species.

Iron-induced lipid peroxidation of phosphatidylethanolamine (PE) species is a key driver of ferroptosis in retinal pigment epithelial (RPE) cells, a process closely associated with age-related macular degeneration (AMD). The previous studies have demonstrated that induced retinal pigment epithelial (iRPE) cells generated by transcription factor-mediated reprogramming exhibit superior therapeutic efficacy in treating AMD. In this study, it is found that these iRPE cells are resistant to ferroptosis and further identified phosphoethanolamine/phosphocholine phosphatase 1 (PHOSPHO1) as a critical regulator underlying ferroptosis resistance.

Asparagine alleviates naphthalene-induced lens opacity by suppressing ferroptosis.

Cataract, with lens opacity as its feature, often cause vision loss. The main clinical treatment is lens replacement surgery, which usually works well for most of the patients, but not for all. And researching drugs to delay or treat cataracts is also very important socially and scientifically.

DNA-Dependent Protein Kinase Catalytic Subunit Prevents Ferroptosis in Retinal Pigment Epithelial Cells.

Purpose: The purpose of this study was to investigate the activated core kinases involved in the DNA damage responses (DDR) during ferroptosis of retinal pigment epithelial (RPE) cells in vitro and their regulatory effects on ferroptosis.

Methods: Ferroptosis was induced by erastin in induced RPE (iRPE) cells derived from human umbilical cord mesenchymal stem cells (hUCMSCs), hUCMSCs, and induced pluripotent stem cell-derived RPE (iPSC-RPE) cells. CCK8 was employed to measure the cell viability.

Subconjunctival injection of human umbilical cord mesenchymal stem cells alleviates experimental allergic conjunctivitis via regulating T cell response.

Background: T helper 2 (Th2) cells are thought to play critical roles in allergic conjunctivitis (AC). They release inflammatory cytokines to promote an allergic response in AC. Due to individual heterogeneity and long-term chronic management, current therapies do not always effectively control AC.

Local treatment strategies in Stage IVB cervical squamous cell carcinoma and adenocarcinoma.

Objective: To evaluate the effect of different local treatment strategies on survival outcomes in patients with Stage IVB cervical squamous cell carcinoma (SCC) and adenocarcinoma.

Methods: Patients diagnosed with Stage IVB cervical SCC and adenocarcinoma between 2004 and 2015 were included from the Surveillance, Epidemiology, and End Results (SEER) database. Subgroup analysis was performed in those diagnosed between 2010 and 2015 and available for the sites of distant metastases.

CircNCOR1 regulates breast cancer radiotherapy efficacy by regulating CDK2 via hsa-miR-638 binding.

Background: Despite aggressive local and regional therapy, triple-negative breast cancer (TNBC) is characterized by an increased risk of locoregional recurrence. RNA-sequencing data has identified a large number of circRNAs in primary breast cancers, but the role of specific circRNAs in regulating the radiosensitivity of TNBC is not fully understood. This research aimed to investigate the function of circNCOR1 in the radiosensitivity of TNBC.

MOB kinase activator 1A acts as an oncogene by targeting PI3K/AKT/mTOR in ovarian cancer.

Background: To illuminate the precise roles of MOB Kinase Activator 1 A (MOB1A) in the development of ovarian cancer (OC).

Methods: MOB1A expression and clinical data of OC were obtained from the public database on gene expression and proteomics. Meanwhile, verification of expression was carried out in Gene Expression Omnibus, the Human Protein Atlas, and OC cell lines.

The transcriptome profile of RPE cells by the fullerenol against hydrogen peroxide stress.

Age-related macular degeneration (AMD) causes central vision impairment with increased incidence. In the pathogenesis of AMD, reactive oxygen species (ROS) are associated with RPE cell apoptosis. HO is an oxidative toxicant and is used to establish the AMD model.

Induced retinal pigment epithelial cells with anti-epithelial-to-mesenchymal transition ability delay retinal degeneration.

The hostile microenvironment of the retina in patients with age-related macular degeneration (AMD) may trigger epithelial-to-mesenchymal transition (EMT) of grafted retinal pigment epithelial (RPE) cells, thus attenuating the therapeutic outcome. Here, we transformed human dedifferentiated induced pluripotent stem cell-derived RPE (iPSC-RPE) cells into induced RPE (iRPE) cells using a cocktail of four transcription factors (TFs)-CRX, MITF-A, NR2E1, and C-MYC. These critical TFs maintained the epithelial property of iRPE cells by regulating the expression of , forkhead box f2, , and , and conferred resistance to TGF-β-induced EMT in iRPE cells by targeting .

Direct conversion of human umbilical cord mesenchymal stem cells into retinal pigment epithelial cells for treatment of retinal degeneration.

Age-related macular degeneration (AMD) is a major vision-threatening disease. Although mesenchymal stem cells (MSCs) exhibit beneficial neural protective effects, their limited differentiation capacity in vivo attenuates their therapeutic function. Therefore, the differentiation of MSCs into retinal pigment epithelial (RPE) cells in vitro and their subsequent transplantation into the subretinal space is expected to improve the outcome of cell therapy.

Tumor-Suppressor Gene Transmembrane Protein 98 Promotes Proliferation and Inhibits Apoptosis in Ovarian Cancer.

Background: Ovarian cancer (OC) is the most deadly tumor in gynecology and there is no effective biomarker for diagnosis and treatment. The role of Transmembrane Protein 98 (TMEM98) in ovarian cancer is still unclear.

Methods: The expression and prognostic effect of TMEM98 in OC were analyzed using the public database.

Local treatment improves survival in patients with stage IVB cervical cancer.

Objective: To evaluate the value of local treatment in stage IVB cervical cancer (CC).

Methods: Patients diagnosed with stage IVB CC between 2010 and 2015 were included using the data from the Surveillance, Epidemiology, and End Results program. Propensity score matching (PSM) was used to balance the clinicopathological variables of patients.

Chaperone-mediated autophagy plays an important role in regulating retinal progenitor cell homeostasis.

Purpose: To explore the function and regulatory mechanism of IFITM3 in mouse neural retinal progenitor cells (mNRPCs), which was found to be very important not only in the development of the retina in embryos but also in NRPCs after birth.

Methods: Published single-cell sequencing data were used to analyze IFITM3 expression in mNRPCs. RNA interference was used to knock down the expression of IFITM3.

Glia maturation factor-β induces ferroptosis by impairing chaperone-mediated autophagic degradation of ACSL4 in early diabetic retinopathy.

Diabetic retinopathy (DR) is one of the leading causes of blindness in the world, and timely prevention and treatment are very important. Previously, we found that a neurodegenerative factor, Glia maturation factor-β (GMFB), was upregulated in the vitreous at a very early stage of diabetes, which may play an important role in pathogenesis. Here, we found that in a high glucose environment, large amounts of GMFB protein can be secreted in the vitreous, which translocates the ATPase ATP6V1A from the lysosome, preventing its assembly and alkalinizing the lysosome in the retinal pigment epithelial (RPE) cells.

The prognostic effect of residual tumor for advanced epithelial ovarian cancer treated with neoadjuvant chemotherapy or primary debulking surgery.

Purpose: The role of neoadjuvant chemotherapy (NACT) and primary debulking surgery (PDS) in advanced epithelial ovarian cancer (EOC) remains controversial. This study aimed to investigate the prognosis between NACT and PDS in advanced EOC. We also investigated the prognostic effect of the residual tumor (RT) after NACT and PDS.

Enhancing fractalkine/CX3CR1 signalling pathway can reduce neuroinflammation by attenuating microglia activation in experimental diabetic retinopathy.

The concept of diabetic retinopathy (DR) has been extended from microvascular disease to neurovascular disease in which microglia activation plays a remarkable role. Fractalkine (FKN)/CX3CR1 is reported to regulate microglia activation in central nervous system diseases. To characterize the effect of FKN on microglia activation in DR, we employed streptozotocin-induced diabetic rats, glyoxal-treated R28 cells and hypoxia-treated BV2 cells to mimic diabetic conditions and explored retinal neuronal apoptosis, reactive oxygen species (ROS), as well as the expressions of FKN, Iba-1, TSPO, NF-κB, Nrf2 and inflammation-related cytokines.

Silencing Nogo-B improves the integrity of blood-retinal barrier in diabetic retinopathy via regulating Src, PI3K/Akt and ERK pathways.

Objective: To examine the mechanisms of Nogo-B (RTN4B) in the protection of blood-retinal barrier in experimental diabetic retinopathy.

Methods: The level of Nogo-B in vitreous and plasma samples was detected with ELISA. Diabetes was induced in Sprague-Dawley rats with intraperitoneal injection of streptozotocin.

Identification of novel key molecular signatures in the pathogenesis of experimental diabetic retinopathy.

Deep mining of the molecular mechanisms underlying diabetic retinopathy (DR) is critical for the development of novel therapeutic targets. This study aimed to identify key molecular signatures involved in experimental DR on the basis of integrated bioinformatics analysis. Four datasets consisting of 37 retinal samples were downloaded from the National Center of Biotechnology Information Gene Expression Omnibus.

BMSC-derived extracellular vesicles intervened the pathogenic changes of scleroderma in mice through miRNAs.

Background: Systemic sclerosis (SSc) is a disease that features severe fibrosis of the skin and lacks effective therapy. Bone marrow mesenchymal stem cell (BMSC)-derived extracellular vesicles (EVs) are potential stem cell-based tools for the treatment of SSc.

Methods: BMSCs were isolated from the bone marrow of mice and identified with surface markers according to multilineage differentiation.