Additional file 2: of Hippocampal CA1 βCaMKII mediates neuroinflammatory responses via COX-2/PGE2 signaling pathways in depression

Table S1. PCR primers used in this study. (DOCX 17 kb

Additional file 1: of Hippocampal CA1 βCaMKII mediates neuroinflammatory responses via COX-2/PGE2 signaling pathways in depression

Figure S1. Depression animal model experimental design: schematic figure of the treatment protocol of rats. (A) CUMS depression model paradigm. (B) LPS-induced depression model paradigm. CUMS, chronic unpredictable mild stress; i.p., intraperitoneal; Cele, celecoxib; FLX, fluoxetine; SPT, sucrose preference test; FST, forced swim test; WB, Western blot; Q-PCR, quantitative real-time PCR; RT-PCR, reverse transcription PCR; ELISA, enzyme-linked immunosorbent assay; IF, immunofluorescence. (TIF 46 kb

Additional file 4: of Hippocampal CA1 βCaMKII mediates neuroinflammatory responses via COX-2/PGE2 signaling pathways in depression

Figure S3. Estimation of βCaMKII knockdown efficiency after viral constructs unilateral injection. (A) Pictures represented coronal brain slices of rats that have received unilateral injection of AAV-βCaMKII RNAi viruses. Left: non-injected side. Right: injected side. (B) Level of knocking down represented by ratio of βCamKII fluorescence signal intensity of the injected and non-injected side. (C) Representative Western blot and quantification of βCaMKII knockdown efficiency. N = 6 per group. Data were presented as the means ± SEM. *P < 0.05, **P < 0.01 CUMS+AAV-βi vs CUMS; #P < 0.05, ##P < 0.01 CUMS+AAV-βi vs CUMS+AAV-control. (AAV-βi, AAV-βCaMKII RNAi). (TIF 1196 kb

Additional file 3: of Hippocampal CA1 βCaMKII mediates neuroinflammatory responses via COX-2/PGE2 signaling pathways in depression

Figure S2. Estimation of βCaMKII overexpression efficiency after viral constructs unilateral injection. (A) Pictures represented coronal brain slices of rats that have received unilateral injection of AAV-βCaMKII viruses. Left: non-injected side. Right: injected side. (B) Level of overexpression represented by ratio of βCamKII fluorescence signal intensity of the injected and non-injected side. (C) Representative Western blot and quantification of βCaMKII overexpression efficiency. N = 6 per group. Data were presented as the means ± SEM. *P < 0.05, **P < 0.01 WT+AAV-βCaMKII vs non-injected side; #P < 0.05. (WT, wild type). (TIF 1360 kb

Data_Sheet_3_Plin4-Dependent Lipid Droplets Hamper Neuronal Mitophagy in the MPTP/p-Induced Mouse Model of Parkinson’s Disease.XLS

Epidemiological studies have shown that both lipid metabolism disorder and mitochondrial dysfunction are correlated with the pathogenesis of neurodegenerative diseases (NDDs), including Parkinson’s disease (PD). Emerging evidence suggests that deposition of intracellular lipid droplets (LDs) participates in lipotoxicity and precedes neurodegeneration. Perilipin family members were recognized to facilitate LD movement and cellular signaling interactions. However, the direct interaction between Perilipin-regulated LD deposition and mitochondrial dysfunction in dopaminergic (DA) neurons remains obscure. Here, we demonstrate a novel type of lipid dysregulation involved in PD progression as evidenced by upregulated expression of Plin4 (a coating protein and regulator of LDs), and increased intracellular LD deposition that correlated with the loss of TH-ir (Tyrosine hydroxylase-immunoreactive) neurons in the MPTP/p-induced PD model mouse mesencephalon. Further, in vitro experiments showed that inhibition of LD storage by downregulating Plin4 promoted survival of SH-SY5Y cells. Mechanistically, reduced LD storage restored autophagy, leading to alleviation of mitochondrial damage, which in turn promoted cell survival. Moreover, the parkin-poly-Ub-p62 pathway was involved in this Plin4/LD-induced inhibition of mitophagy. These findings were further confirmed in primary cultures of DA-nergic neurons, in which autophagy inhibitor treatment significantly countermanded the ameliorations conferred by Plin4 silencing. Collectively, these experiments demonstrate that a dysfunctional Plin4/LD/mitophagy axis is involved in PD pathology and suggest Plin4-LDs as a potential biomarker as well as therapeutic strategy for PD.</p

Data_Sheet_1_Plin4-Dependent Lipid Droplets Hamper Neuronal Mitophagy in the MPTP/p-Induced Mouse Model of Parkinson’s Disease.XLS

Epidemiological studies have shown that both lipid metabolism disorder and mitochondrial dysfunction are correlated with the pathogenesis of neurodegenerative diseases (NDDs), including Parkinson’s disease (PD). Emerging evidence suggests that deposition of intracellular lipid droplets (LDs) participates in lipotoxicity and precedes neurodegeneration. Perilipin family members were recognized to facilitate LD movement and cellular signaling interactions. However, the direct interaction between Perilipin-regulated LD deposition and mitochondrial dysfunction in dopaminergic (DA) neurons remains obscure. Here, we demonstrate a novel type of lipid dysregulation involved in PD progression as evidenced by upregulated expression of Plin4 (a coating protein and regulator of LDs), and increased intracellular LD deposition that correlated with the loss of TH-ir (Tyrosine hydroxylase-immunoreactive) neurons in the MPTP/p-induced PD model mouse mesencephalon. Further, in vitro experiments showed that inhibition of LD storage by downregulating Plin4 promoted survival of SH-SY5Y cells. Mechanistically, reduced LD storage restored autophagy, leading to alleviation of mitochondrial damage, which in turn promoted cell survival. Moreover, the parkin-poly-Ub-p62 pathway was involved in this Plin4/LD-induced inhibition of mitophagy. These findings were further confirmed in primary cultures of DA-nergic neurons, in which autophagy inhibitor treatment significantly countermanded the ameliorations conferred by Plin4 silencing. Collectively, these experiments demonstrate that a dysfunctional Plin4/LD/mitophagy axis is involved in PD pathology and suggest Plin4-LDs as a potential biomarker as well as therapeutic strategy for PD.</p

Data_Sheet_2_Plin4-Dependent Lipid Droplets Hamper Neuronal Mitophagy in the MPTP/p-Induced Mouse Model of Parkinson’s Disease.DOCX

<p>Epidemiological studies have shown that both lipid metabolism disorder and mitochondrial dysfunction are correlated with the pathogenesis of neurodegenerative diseases (NDDs), including Parkinson’s disease (PD). Emerging evidence suggests that deposition of intracellular lipid droplets (LDs) participates in lipotoxicity and precedes neurodegeneration. Perilipin family members were recognized to facilitate LD movement and cellular signaling interactions. However, the direct interaction between Perilipin-regulated LD deposition and mitochondrial dysfunction in dopaminergic (DA) neurons remains obscure. Here, we demonstrate a novel type of lipid dysregulation involved in PD progression as evidenced by upregulated expression of Plin4 (a coating protein and regulator of LDs), and increased intracellular LD deposition that correlated with the loss of TH-ir (Tyrosine hydroxylase-immunoreactive) neurons in the MPTP/p-induced PD model mouse mesencephalon. Further, in vitro experiments showed that inhibition of LD storage by downregulating Plin4 promoted survival of SH-SY5Y cells. Mechanistically, reduced LD storage restored autophagy, leading to alleviation of mitochondrial damage, which in turn promoted cell survival. Moreover, the parkin-poly-Ub-p62 pathway was involved in this Plin4/LD-induced inhibition of mitophagy. These findings were further confirmed in primary cultures of DA-nergic neurons, in which autophagy inhibitor treatment significantly countermanded the ameliorations conferred by Plin4 silencing. Collectively, these experiments demonstrate that a dysfunctional Plin4/LD/mitophagy axis is involved in PD pathology and suggest Plin4-LDs as a potential biomarker as well as therapeutic strategy for PD.</p

Polyurea–Cellulose Composite Aerogel Fibers with Superior Strength, Hydrophobicity, and Thermal Insulation via a Secondary Molding Strategy

Aerogel materials, considered as the “miracle material that can change the world in the 21st century”, owe their transformative potential to their high specific surface area, porosity, and low density. In comparison to commercially available aerogel felt, aerogel particles, and aerogel powder, aerogel fibers not only possess the inherent advantages of aerogel materials but also exhibit exceptional flexibility and design versatility. Therefore, aerogel fibers are expected to be processed into high-performance textiles and smart wearable fabrics to further expand the application field of aerogel materials. However, the aerogel fibers suffer from poor mechanical properties and intricate, time-consuming preparation processes. Herein, a simple and efficient method for crafting polyurea–cellulose composite aerogel fibers (CAFs) with superior mechanical properties is presented. The dried bacterial cellulose (BC) matrix was immersed in a polyurea sol, and the aerogel fibers were prepared via secondary molding, followed by CO2 supercritical drying. In a representative case, the CAFs obtained via secondary molding demonstrate outstanding hydrophobicity with a contact angle of 126°, along with remarkable flexibility. Significantly, the CAFs exhibit excellent mechanical properties, including a tensile strength of 6.4 MPa. Moreover, the CAFs demonstrate superior thermal insulation capabilities, withstanding temperatures ranging from 180 to −40 °C. In conclusion, with the successful fabrication of polyurea–cellulose CAFs, this study introduces a magic approach for producing aerogel fibers endowed with exceptional mechanical properties and thermal insulation. This advancement contributes to the development and application of aerogel materials in various fields

Polyurea–Cellulose Composite Aerogel Fibers with Superior Strength, Hydrophobicity, and Thermal Insulation via a Secondary Molding Strategy

Aerogel materials, considered as the “miracle material that can change the world in the 21st century”, owe their transformative potential to their high specific surface area, porosity, and low density. In comparison to commercially available aerogel felt, aerogel particles, and aerogel powder, aerogel fibers not only possess the inherent advantages of aerogel materials but also exhibit exceptional flexibility and design versatility. Therefore, aerogel fibers are expected to be processed into high-performance textiles and smart wearable fabrics to further expand the application field of aerogel materials. However, the aerogel fibers suffer from poor mechanical properties and intricate, time-consuming preparation processes. Herein, a simple and efficient method for crafting polyurea–cellulose composite aerogel fibers (CAFs) with superior mechanical properties is presented. The dried bacterial cellulose (BC) matrix was immersed in a polyurea sol, and the aerogel fibers were prepared via secondary molding, followed by CO2 supercritical drying. In a representative case, the CAFs obtained via secondary molding demonstrate outstanding hydrophobicity with a contact angle of 126°, along with remarkable flexibility. Significantly, the CAFs exhibit excellent mechanical properties, including a tensile strength of 6.4 MPa. Moreover, the CAFs demonstrate superior thermal insulation capabilities, withstanding temperatures ranging from 180 to −40 °C. In conclusion, with the successful fabrication of polyurea–cellulose CAFs, this study introduces a magic approach for producing aerogel fibers endowed with exceptional mechanical properties and thermal insulation. This advancement contributes to the development and application of aerogel materials in various fields

Polyurea–Cellulose Composite Aerogel Fibers with Superior Strength, Hydrophobicity, and Thermal Insulation via a Secondary Molding Strategy

Aerogel materials, considered as the “miracle material that can change the world in the 21st century”, owe their transformative potential to their high specific surface area, porosity, and low density. In comparison to commercially available aerogel felt, aerogel particles, and aerogel powder, aerogel fibers not only possess the inherent advantages of aerogel materials but also exhibit exceptional flexibility and design versatility. Therefore, aerogel fibers are expected to be processed into high-performance textiles and smart wearable fabrics to further expand the application field of aerogel materials. However, the aerogel fibers suffer from poor mechanical properties and intricate, time-consuming preparation processes. Herein, a simple and efficient method for crafting polyurea–cellulose composite aerogel fibers (CAFs) with superior mechanical properties is presented. The dried bacterial cellulose (BC) matrix was immersed in a polyurea sol, and the aerogel fibers were prepared via secondary molding, followed by CO2 supercritical drying. In a representative case, the CAFs obtained via secondary molding demonstrate outstanding hydrophobicity with a contact angle of 126°, along with remarkable flexibility. Significantly, the CAFs exhibit excellent mechanical properties, including a tensile strength of 6.4 MPa. Moreover, the CAFs demonstrate superior thermal insulation capabilities, withstanding temperatures ranging from 180 to −40 °C. In conclusion, with the successful fabrication of polyurea–cellulose CAFs, this study introduces a magic approach for producing aerogel fibers endowed with exceptional mechanical properties and thermal insulation. This advancement contributes to the development and application of aerogel materials in various fields