Animal Cells Research Articles

Industrial Research and Development on the Production Process and Quality of Cultured Meat Hold Significant Value: A Review.

Cultured meat has been gaining popularity as a solution to the increasing problem of food insecurity. Although research on cultured meat started later compared to other alternative meats, the industry is growing rapidly every year, with developed products evaluated as being most similar to conventional meat. Studies on cultured meat production techniques, such as culturing new animal cells and developing medium sera and scaffolds, are being conducted intensively and diversely. However, active in-depth research on the quality characteristics of cultured meat, including studies on the sensory and storage properties that directly influence consumer preferences, is still lacking. Additionally, studies on the combination or ratio of fat cells to muscle cells and on the improvement of microbiota, protein degradation, and fatty acid degradation remain to be conducted. By actively investigating these research topics, we aim to verify the quality and safety of cultured meats, ultimately improving the consumer preference for cultured meat products.

Investigating the Impact of Hydrocephalus on Epiplexus Cells of the Choroid Plexus

Hydrocephalus is characterized by accumulation of cerebrospinal fluid (CSF) in the brain, resulting from over-production, under-absorption, or blockage of the flow of CSF. Current treatments are limited to surgically placed shunts that often require follow-up procedures. The goal of this research group is to understand the mechanisms of hydrocephalus with the aim of finding effective pharmacological treatments. The animal model used exhibits a mutation in the transmembrane 67 (Tmem67) gene. Homozygous recessive animals present with ventriculomegaly at birth and severe hydrocephalus by postnatal day 15 (P15). Experiments in this study compare tissue obtained from wildtype animals and homozygous mutant animals. The choroid plexus (CP) is the main producer of CSF, making it a target structure in hydrocephalus research. It is a branched tissue that includes a stroma with fenestrated capillaries, wrapped by a tightly regulated barrier epithelium. Choroid plexus epithelial cells (CPe) are multiciliated cells that strictly regulate the osmotic balance of CSF. Epiplexus cells are poorly understood immune cells localized on the apical (CSF-facing) side of the CPe. These cells are believed to share functional characteristics with microglia and macrophages. Microglia are the innate immune cells of the central nervous system; a specialized type of glial cell that interact with neurons, and aid in the structure and immunosurveillance of the brain. Macrophages originate from monocytes and reside in most tissues of the body, responding to cellular signals of injury and infection. Macrophages can be found free-roaming in tissues or associated to epithelial cells, known as border-associated macrophages (BAMs). Due to their association with the CPe, epiplexus cells are considered BAMs. Beyond their apparent similarities to other immune cells, little else is known about the properties and functions of epiplexus cells or their interaction with the CPe or CSF, nor if they play a role in the development of hydrocephalus. This study furthers the understanding of epiplexus cells, specifically how they impact, or are impacted by hydrocephalus. Rat pups (P15) were terminally anesthetized, perfused with 1x PBS, and fixed with 4% PFA. In the lateral ventricle CP, we have visualized CPe-associated cells with morphology consistent with epiplexus cells. These cells are labeled with microglial/macrophage/epiplexus cell markers: allograft inflammatory factor1/ionized calcium-binding adaptor molecule 1 (Iba1), macrosialin (CD68), and mannose receptor type C-1 lectin (CD206). Iba1 is thought to play a role in restructuring the actin cytoskeleton in cells of monocyte lineage (macrophages and microglia), resulting in morphological differences across levels of activation. CD68 is a transmembrane protein commonly expressed in macrophages and monocytes, supposedly related to the oxidized low-density lipoprotein (OxLDL) pathway, which is involved in exacerbating oxidative stress. CD206 is a transmembrane protein that may aid in the roles of detecting pathogens, removing proteins, and sending waste through lymphatic system. Confocal analysis combining cell morphology and immunohistochemical labeling will be used to quantify CPe-associated epiplexus cells in wildtype and hydrocephalic animals. The results will be substantiated using quantitative real-time PCR. Funding: United States Department of Defense Congressionally Directed Medical Research Program Award; Hydrocephalus Association. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Dapagliflozin suppresses diabetes-induced oxidative DNA damage and hypermethylation in mouse somatic cells

Diabetes mellitus is a complex metabolic disorder resulting from the interplay of environmental, genetic, and epigenetic factors that increase the risk of cancer development. However, it is unclear whether the increased cancer risk is due to poor glycemic control or the use of some antidiabetic medications. Therefore, we investigated the genetic and epigenetic changes in somatic cells in a mouse model of diabetes and studied whether multiple exposures to the antidiabetic medication dapagliflozin influence these changes. We also elucidated the mechanism(s) of these ameliorations. The micronucleus test and modified comet assay were used to investigate bone marrow DNA damage and methylation changes. These assays revealed that dapagliflozin is non-genotoxic in the tested regimen, and oxidative DNA damage and hypermethylation were significantly higher in diabetic mice. Spectrophotometry also evaluated oxidative DNA damage and global DNA methylation, revealing similar significant alterations induced by diabetes. Conversely, the dapagliflozin-treated diabetic animals significantly reduced these changes. The expression of some genes involved in DNA repair and DNA methylation was disrupted considerably in the somatic cells of diabetic animals. In contrast, dapagliflozin treatment significantly restored these disruptions and enhanced DNA repair. The simultaneous effects of decreased oxidative DNA damage and hypermethylation levels suggest that dapagliflozin can be used as a safe antidiabetic drug to reduce DNA damage and hypermethylation in diabetes, demonstrating its usefulness in patients with diabetes to control hyperglycemia and decrease the development of its subsequent complications.

Creative Visual Arts and Biology Processes: Examining Emergent Bi/Multilingual High Schoolers Meanings

This case study research examines how emergent bilingual and multilingual high school students construct meanings while engaging with objects during a biology lesson that integrates visual arts. Drawing on the theoretical framework of Symbolic Interactionism (SI), the study focuses on "Artistic Reformatting to Represent Interdependence among the Structures and Functions of an Animal Cell." By investigating the connections between the students' interests, beliefs, memories, and objects, as well as their social interactions with peers, friends, family, and others, the research uncovers the ways in which meanings are constructed. While visual arts integration is common in academic content, little attention has been given to its potential to support meaning-making among emergent bilingual and multilingual students. The findings of this study highlight the importance of adopting a holistic approach to visual arts education that emphasizes contemporary strategies, enduring ideas, and social interaction in engaging with content. These insights suggest that educators can enhance their teaching methods and create meaningful learning experiences for bi/multilingual students by incorporating these approaches. The study underscores the significance of visual arts in fostering personal connections and deeper comprehension of academic content among diverse student populations, ultimately promoting a more inclusive and effective educational environment.

Bioactivity of <i>Lantana camara</i> Flowers: Antilithiatic and Nephroprotective Implications in Male Wistar Rats

Lantana camara is a well-known medicinal plant with various reported therapeutic compounds. This study explores the antilithiatic and nephroprotective effects of Lantana camara flower hydroalcoholic extract. Using animal models and cell culture, we assessed its impact on ethylene glycol-induced nephrolithiasis and gentamicin-induced nephrotoxicity. The ethylene glycol-induced nephrolithiasis model revealed elevated levels of calcium, phosphate, and oxalate, indicating the formation of calculi. Treatment with the hydroalcoholic extract resulted in a significant decrease in uric acid levels, reducing the likelihood of calculi formation. Additionally, the animals treated with the extract showed reduced levels of urea, and creatinine, indicating improved kidney function. The results highlighted the notable difference between the preventive and curative treatments. In the HEK-293 cell culture, the hydroalcoholic extract demonstrated a significant inhibition of abnormal cell morphology induced by gentamicin, a nephrotoxic drug. The extract also exhibited a marked improvement in cell growth compared to the standard treatment. The findings of this study provide substantial evidence supporting the antilithiatic and nephroprotective effects of the hydroalcoholic extract of Lantana camara flowers. The extract effectively reduced the risk of calculi formation, improved renal parameters, and demonstrated potential in mitigating drug-induced nephrotoxicity. These results validate the traditional claims regarding the efficacy of Lantana camara as a therapeutic agent for kidney-related disorders. The hydroalcoholic extract of Lantana camara flowers could serve as a valuable alternative treatment option, offering potential benefits in the management of lithiasis and nephrotoxicity.

Edible mycelium as proliferation and differentiation support for anchorage-dependent animal cells in cultivated meat production

Cultivated meat production requires bioprocess optimization to achieve cell densities that are multiple orders of magnitude higher compared to conventional cell culture techniques. These processes must maximize resource efficiency and cost-effectiveness by attaining high cell growth productivity per unit of medium. Microcarriers, or carriers, are compatible with large-scale bioreactor use, and offer a large surface-area-to-volume ratio for the adhesion and proliferation of anchorage-dependent animal cells. An ongoing challenge persists in the efficient retrieval of cells from the carriers, with conflicting reports on the effectiveness of trypsinization and the need for additional optimization measures such as carrier sieving. To surmount this issue, edible carriers have been proposed, offering the advantage of integration into the final food product while providing opportunities for texture, flavor, and nutritional incorporation. Recently, a proof of concept (POC) utilizing inactivated mycelium biomass derived from edible filamentous fungus demonstrated its potential as a support structure for myoblasts. However, this POC relied on a model mammalian cell line combination with a single mycelium species, limiting realistic applicability to cultivated meat production. This study aims to advance the POC. We found that the species of fungi composing the carriers impacts C2C12 myoblast cell attachment—with carriers derived from Aspergillus oryzae promoting the best proliferation. C2C12 myoblasts effectively differentiated on mycelium carriers when induced in myogenic differentiation media. Mycelium carriers also supported proliferation and differentiation of bovine satellite cells. These findings demonstrate the potential of edible mycelium carrier technology to be readily adapted in product development within the cultivated meat industry.

IMPORTANCE OF PHYTOTHERAPY IN CHRONIC NON-INFECTIOUS DISEASES OF THE LIVER

Currently, in the countries of Central Asia, as in most countries, 15-20% of the adult population suffers from acute and chronic liver pathology. Today, non-alcoholic fatty liver disease (NAFLD) is the most common non-communicable liver disease, accounting for approximately 70% of all chronic liver diseases. The complexity and versatility of the pathogenetic mechanisms of lipid metabolism disorders in the body requires effective pharmacological correction aimed at normalizing the composition, structure and ratio of various classes of lipoproteins. In this regard, the most harmless and therapeutically effective herbal remedies of natural origin, metabolic products of plant and animal cells, which have low toxicity and a wide spectrum of action, are of great importance. The advantage of phytotherapy is that it allows the use of plants for a long time without significant side effects, due to their compatibility with many drugs and with each other. KEYWORDS: phytotherapy, herbal remedies, lipid metabolism.

A high dose KRP203 induces cytoplasmic vacuoles associated with altered phosphoinositide segregation and endosome expansion

In animal cells, vacuoles are absent, but can be induced by diseases and drugs. While phosphoinositides are critical for membrane trafficking, their role in the formation of these vacuoles remains unclear. The immunosuppressive KRP203/Mocravimod, which antagonizes sphingosine-1-phosphate receptors, has been identified as having novel multimodal activity against phosphoinositide kinases. However, the impact of this novel KRP203 activity is unknown. Here, we show that KRP203 disrupts the spatial organization of phosphoinositides and induces extensive vacuolization in tumor cells and immortalized fibroblasts. The KRP203-induced vacuoles are primarily from endosomes, and augmented by inhibition of PIKFYVE and VPS34. Conversely, overexpression of PTEN decreased KRP203-induced vacuole formation. Furthermore, V-ATPase inhibition completely blunted KRP203-induced vacuolization, pointing to a critical requirement of the endosomal maturation process. Importantly, nearly a half of KRP203-induced vacuoles are significantly decorated with PI4P, a phosphoinositide typically enriched at the plasma membrane and Golgi. These results suggest a model that noncanonical spatial reorganization of phosphoinositides by KRP203 alters the endosomal maturation process, leading to vacuolization. Taken together, this study reveals a previously unrecognized bioactivity of KRP203 as a vacuole-inducing agent and its unique mechanism of phosphoinositide modulation, providing a new insight of phosphoinositide regulation into vacuolization-associated diseases and their molecular pathologies.

Ameliorative Effect of Natural Sesquiterpene Alcohol Cedrol Against Cerebral Ischemia Infarction-In Vitro and In Vivo Studies.

Cedrol is a major bioactive compound present in the Cedrus atlantica with numerous biological properties. In this study, we elucidated the neuroprotective properties of cedrol against ischemic infarction in animal and in vitro studies. A cerebral ischemic/reperfusion model was induced in adult Wistar rats, and oxygen-glucose deprivation/reperfusion was induced in SH-SY5Y neuronal cells and treated with different concentrations of cedrol. The percentage of water content, cerebral infarct, and neurological deficit score was assessed in experimental rats. The acetylcholinesterase activity and inflammatory cytokines were quantified to analyze the anti-inflammatory potency of cedrol. Oxidative stress marker malondialdehyde and antioxidants were quantified to evaluate the antioxidant potency of cedrol in an ischemic condition. The neuroprotective potency of cedrol was confirmed by histopathological analysis of the brain tissue of cedrol-treated I/R-induced rats. In in vitro studies, the MTT and LDH assays were performed in cedrol-treated OGD/R SH-SY5Y cells to analyze the cytoprotective effect of cedrol. The anti-inflammatory property of cedrol was confirmed by quantifying the pro-inflammatory cytokine levels in OGD/R-induced cedrol-treated SH-SY5Y cells. The results obtained prove that cedrol significantly prevents brain edema, neurological deficits, acetylcholinesterase activity, and oxidative damage in ischemic-induced rats. It inhibited neuroinflammation in ischemic-induced rats and also in in vitro models. The neuroprotective effect of cedrol during an ischemic condition was authentically established with histological analysis in an animal model and cell survival assays in an in vitro model. Overall, our results confirm that cedrol is a potent alternative drug to treat cerebral ischemia in the future.

Evaluation of the effects of zinc oxide (ZnO NPs) nanoparticles synthesized by green synthesis on Caenorhabditis elegans.

In recent years, the rapid development of nanotechnology has caused the products obtained with this technology to be used more daily. Information on the effects of these products, which provide great advantages in every respect, on human health and the environment is insufficient. It has been suggested that these nanoparticles may have toxic effects on living things, mostly in animal experiments and cell cultures. In this paper, the organism Caenorhabditis elegans (C. elegans), which contains a genome and biochemical ways highly similar to humans, is used to understand and reveal the metabolism of Zinc oxide nanoparticles (ZnO NPs) toxicological effects. The toxicological effects of ZnO NPs on C. elegans organisms were investigated and the results were evaluated in terms of environment and human health. C. elegans was exposed to commercial ZnO NPs and green synthesized ZnO NPs from Olea europaea (olive tree, OLE). LC50 values were determined by probit analysis (green synthesized ZnO NP LC5024h = 84.97mg/L, LC5072h = 33.27mg/L, commercial ZnO NPs LC5024h = 5.75mg/L, LC5072h = 1.91mg/L). When the survival times of C. elegans were evaluated by the Kaplan-Meier method, it was seen that commercial ZnO NPs were more toxic than green synthesized ZnO NPs. In MTT tests, it was clearly seen that commercial ZnO NPs and green synthesized ZnO NPs entered the cell and caused different cytotoxicity. While there was a difference between control and 0.5, 2.5, 5, 10, 25, and 50mg/L doses in commercial ZnO NP applications, there were significant differences between control and 25, 50mg/L concentrations in green synthesized ZnO NP applications.

Damage-repair events increase the instability of cortical microtubules in Arabidopsis.

Microtubules rely on dynamic assembly and disassembly for their functions. Increasing evidences support that the damage-repair of microtubule lattices can affect microtubule dynamics in vitro and in animal cells. Here we successfully established a way for visualizing damage-repair sites on microtubule lattices in plant cells, via labeling the tubulin proteins with the photoconvertible fluorescent protein mEOS3.2. We observed that the crossovers of the microtubule lattice were more prone to be damaged and repaired, with the frequency of damage-repair events positively correlated with the crossing angle between microtubules. The microtubules with damage-repair events displayed shorter lifespans and significantly increased severing frequency compared with the undamaged microtubules. These observations suggested that the damage-repair events promoted instability of cortical microtubules in plant cells.

NBR1-dependent autophagy activation protects against environmental cadmium-evoked placental trophoblast senescence

Cadmium (Cd), a well-established developmental toxicant, accumulates in the placentae and disrupts its structure and function. Population study found adverse pregnancy outcomes caused by environmental Cd exposure associated with cell senescence. However, the role of autophagy activation in Cd-induced placental cell senescence and its reciprocal mechanisms are unknown. In this study, we employed animal experiments, cell culture, and case-control study to investigate the above mentioned. We have demonstrated that exposure to Cd during gestation induces placental senescence and activates autophagy. Pharmacological and genetic interventions further exacerbated placental senescence induced by Cd through the suppression of autophagy. Conversely, activation of autophagy ameliorated Cd-induced placental senescence. Knockdown of NBR1 exacerbated senescence in human placental trophoblast cells. Further investigations revealed that NBR1 facilitated the degradation of p21 via LC3B. Our case-control study has demonstrated a positive correlation between placental senescence and autophagy activation in all-cause fetal growth restriction (FGR). These findings offer a novel perspective for mitigating placental aging and placental-origin developmental diseases induced by environmental toxicants.

Regulatory role of PDK1 via integrated gene analysis of mitochondria-immune response in periodontitis

AimsTo investigate the association between mitochondrial events and immune response in periodontitis and related regulatory genes. Main methodsGene expression profiles in gingival tissues were retrieved from the Gene Expression Omnibus. Mitochondria-immune response-related differentially expressed genes (MIR-DEGs) between the healthy and periodontitis samples were determined. WGCNA, GO, and KEGG were used to investigate the function and the enriched pathways of MIR-DEGs. The correlation between MIR-DEGs expression and clinical probing pocket depth was analyzed. The MIR-DEGs were further identified and verified in animal samples. A periodontitis model was established in C57BL/6 mice with silk ligation. Micro-computed tomography was used to assess alveolar bone loss. Western blot, quantitative real-time polymerase chain reaction, and immunohistochemical analyses further validated the differential expression of the MIR-DEGs. Key findingsA total of ten MIR-DEGs (CYP24A1, PRDX4, GLDC, PDK1, BCL2A1, CBR3, ARMCX3, BNIP3, IFI27, and UNG) were identified, the expression of which could effectively distinguish patients with periodontitis from the healthy controls. Enhanced immune response was detected in the periodontitis group with that in the healthy controls, especially in B cells. PDK1 was a critical MIR-DEG correlated with B cell immune response and clinical periodontal probing pocket depth. Both animal and clinical periodontal samples presented higher gene and protein expression of PDK1 than the control samples. Additionally, PDK1 colocalized with B cells in both animal and clinical periodontal tissues. SignificanceMitochondria participate in the regulation of the immune response in periodontitis. PDK1 may be the key mitochondria-related gene regulating B-cell immune response in periodontitis.

Lutein Suppresses the Maturation and Function of Bone Marrow-Derived Dendritic Cells

Lutein, nonivamide, and baicalein, organic compounds found in a variety of plants, are known to exert anti-inflammatory effects in animal cells. Dendritic cells (DCs) are professional antigen-presenting cells (APCs) and link the innate and adaptive immune systems. DCs can be directed into fully mature APCs by exposure to bacterial or viral components, resulting in inflammatory situations. The manipulation of DC maturation provides a strategy for the treatment of allergic and inflammatory diseases. In this study, we evaluated the effects of lutein, nonivamide, and baicalein on the maturation and activation of DCs. Compared to nonivamide and baicalein, lutein significantly and dose-dependently reduced the levels of maturation-associated cell surface markers, including CD40, co-stimulatory molecule CD86, and major histocompatibility complex class II (I-Ab) molecule in lipopolysaccharide (LPS)-stimulated DCs. Lutein also decreased IL-12p40 and IL-6 gene expression and secretion in LPS-stimulated DCs. Furthermore, lutein significantly enhanced the endocytic ability of LPS-stimulated DCs. These results demonstrated that lutein may exhibit immunosuppressive activity by inhibiting the phenotypic and functional maturation of DCs, and provide new evidence for the value of lutein in the search for novel therapeutic agents in the treatment of inflammatory diseases.

Compartmental neuronal degeneration in the ventral striatum induced by status epilepticus in young rats' brain in comparison with adults.

According to experimental and clinical studies, status epilepticus (SE) causes neurodegenerative morphological changes not only in the hippocampus and other limbic structures, it also affects the thalamus and the neocortex. In addition, several studies reported atrophy, metabolic changes, and neuronal degeneration in the dorsal striatum. The literature lacks studies investigating potential neuronal damage in the ventral component of the striatopallidal complex (ventral striatum [VS] and ventral pallidum) in SE experimentations. To better understand the development of neuronal damage in the striatopallidal complex associated with SE, the detected neuronal degeneration in the compartments of the VS, namely, the nucleus accumbens (NAc) and the olfactory tubercle (OT), was analyzed. The experiments were performed on Wistar rats at age of 25-day-old pups and 3-month-old adult animals. Lithium-pilocarpine model of SE was used. Lithium chloride (3mmol/kg, ip) was injected 24 h before administering pilocarpine (40 mg/kg, ip). This presented study demonstrates the variability of post SE neuronal damage in 25-day-old pups in comparison with 3-month-old adult rats. The NAc exhibited small to moderate number of Fluoro-Jade B (FJB)-positive neurons detected 4 and 8h post SE intervals. The number of degenerated neurons in the shell subdivision of the NAc significantly increased at survival interval of 12 h after the SE. FJB-positive neurons were evidently more prominent occupying the whole anteroposterior and mediolateral extent of the nucleus at longer survival intervals of 24 and 48 h after the SE. This was also the case in the bordering vicinity between the shell and the core compartments but with clusters of degenerating cells. The severity of damage of the shell subdivision of the NAc reached its peak at an interval of 24 h post SE. Isolated FJB-positive neurons were detected in the ventral peripheral part of the core compartment. Degenerated neurons persisted in the shell subdivision of the NAc 1 week after SE. However, the quantity of cell damage had significantly reduced in comparison with the aforementioned shorter intervals. The third layer of the OT exhibited more degenerated neurons than the second layer. The FJB-positive cells in the young animals were higher than in the adult animals. The morphology of those cells was identical in the two age groups except in the OT.

Activation of skeletal carbohydrate-response element binding protein (ChREBP)-mediated de novo lipogenesis increases intramuscular fat content in chickens

The intracellular lipids in muscle cells of farm animals play a crucial role in determining the overall intramuscular fat (IMF) content, which has a positive impact on meat quality. However, the mechanisms underlying the deposition of lipids in muscle cells of farm animals are not yet fully understood. The purpose of this study was to determine the roles of carbohydrate-response element binding protein (ChREBP) and fructose in IMF deposition of chickens. For virus-mediated ChREBP overexpression in tibialis anterior (TA) muscle of chickens, seven 5-d-old male yellow-feather chickens were used. At 10 d after virus injection, the chickens were slaughtered to obtain TA muscles for analysis. For fructose administration trial, sixty 9-wk-old male yellow-feather chickens were randomly divided into 2 groups, with 6 replicates per group and 5 chickens per replicate. The chickens were fed either a basal diet or a basal diet supplemented with 10% fructose (purity ≥ 99%). At 4 wk later, the chickens were slaughtered, and breast and thigh muscles were collected for analysis. The results showed that the skeletal ChREBP mRNA levels were positively associated with IMF content in multiple species, including the chickens, pigs, and mice (P < 0.05). ChREBP overexpression increased lipid accumulation in both muscle cells in vitro and the TA muscles of mice and chickens in vivo (P < 0.05), by activation of the de novo lipogenesis (DNL) pathway. Moreover, activation of ChREBP by dietary fructose administration also resulted in increased IMF content in mice and notably chickens (P < 0.05). Furthermore, the lipidomics analysis revealed that ChREBP activation altered the lipid composition of chicken IMF and tented to improve the flavor profile of the meat. In conclusion, this study found that ChREBP plays a pivotal role in mediating the deposition of fat in chicken muscles in response to fructose-rich diets, which provides a novel strategy for improving meat quality in the livestock industry.

Tb-doped strontium aluminate nanophosphor: Cytotoxicity, phytotoxicity, and bioimaging in plant cells

This study explores the novel application of terbium-doped strontium aluminate nanoparticles for fluorescence imaging in plant cells. The study encompasses microwave assisted solid state synthesis as well as the structural and optical characterization of terbium-doped strontium aluminate nanophosphors, their toxicity studies in plant and animal cells and their use as a fluorescent dye for plant imaging. The X-ray diffraction pattern analysis, along with Rietveld refinement studies, show the formation of SrAl2O4 as a dominant crystalline phase. Photoluminescence investigations demonstrate green emission from Tb3+ transition levels. In vitro biocompatibility of terbium-doped strontium aluminate nanophosphors was studied using L929 fibroblast cells. The plant Clitoria ternatea was used to examine phytotoxicity. The samples' potential for bioimaging was further investigated. Our findings reveal improved growth of seedlings, positioning these nanoparticles as promising tools in plant-related research. This study advances our understanding of nanoparticle-plant interactions and holds potential for transformative applications in agriculture.

In vivo SPECT imaging of Tc-99m radiolabeled exosomes from human umbilical-cord derived mesenchymal stem cells in small animals

Extracellular vesicles derived from human umbilical cord-derived mesenchymal stem cells (UCMSC-EVs) have been postulated to have therapeutic potential for various diseases. However, the biodistribution and pharmacokinetics of these vesicles are still unclear. For a better understanding of the in vivo properties of UCMSC-EVs, in the present study, these vesicles were first radiolabeled with Technetium-99m (99mTc-UCMSC-EVs) and evaluated using in vivo single photon emission computed tomography (SPECT) imaging and biodistribution experiments. SPECT images demonstrated that the liver and spleen tissues mainly took up the 99mTc-UCMSC-EVs. The biodistribution study observed slight uptake in the thyroid and stomach, indicating that 99mTc-UCMSC-EVs was stable at 24 h in vivo. The pharmacokinetic analyses of the blood half-life demonstrated the quick distribution phase (0.85 ± 0.28 min) and elimination phase (25.22 ± 20.76 min) in mice. This study provides a convenient and efficient method for 99mTc-UCMSC-EVs preparation without disturbing their properties. In conclusion, the biodistribution, quick elimination, and suitable stability in vivo of 99mTc-UCMSC-EVs were quantified by the noninvasive imaging and pharmacokinetic analyses, which provides useful information for indication selection, dosage protocol design, and toxicity assessment in future applications.

Hypoxia preconditioning increases Notch1 activity by regulating DNA methylation in vitro and in vivo.

Our previous research has demonstrated that hypoxic preconditioning (HPC) can improve spatial learning and memory abilities in adult mice. Adult hippocampal neurogenesis has been associated with learning and memory. The Neurogenic locus notch homolog protein (Notch) was involved in adult hippocampal neurogenesis, as well as in learning and memory. It is currently unclear whether the Notch pathway regulates hippocampal neuroregeneration by modifying the DNA methylation status of the Notch gene following HPC. The HPC animal model and cell model were established through repeated hypoxia exposure using mice and the mouse hippocampal neuronal cell line HT22. Step-down test was conducted on HPC mice. Real-time PCR and Western blot analysis were used to assess the mRNA and protein expression levels of Notch1 and hairy and enhancer of split1 (HES1). The presence of BrdU-positive cells and Notch1 expression in the hippocampal dental gyrus (DG) were examined with confocal microscopy. The methylation status of the Notch1 was analyzed using methylation-specific PCR (MS-PCR). HT22 cells were employed to elucidate the impact of HPC on Notch1 in vitro. HPC significantly improved the step-down test performance of mice with elevated levels of mRNA and protein expression of Notch1 and HES1 (P < 0.05). The intensities of the Notch1 signal in the control group, the H group and the HPC group were 2.62 ± 0.57 × 107, 2.87 ± 0.84 × 107, and 3.32 ± 0.14 × 107, respectively, and the number of BrdU (+) cells in the hippocampal DG were 1.83 ± 0.54, 3.71 ± 0.64, and 7.29 ± 0.68 respectively. Compared with that in C and H group, the intensity of the Notch1 signal and the number of BrdU (+) cells increased significantly in HPC group (P < 0.05). The methylation levels of the Notch1 promoter 0.82 ± 0.03, 0.65 ± 0.03, and 0.60 ± 0.02 in the C, H, and HPC groups, respectively. The methylation levels of Notch1 decreased significantly (P < 0.05). The effect of HPC on HT22 cells exhibited similarities to that observed in the hippocampus. HPC may confer neuroprotection by activating the Notch1 signaling pathway and regulating its methylation level, resulting in the regeneration of hippocampal neurons.

Disease Mechanisms and Therapeutic Approaches in SMARD1-Insights from Animal Models and Cell Models.

Spinal muscular atrophy with respiratory distress type 1 (SMARD1) is a fatal childhood motoneuron disease caused by mutations in the IGHMBP2 gene. It is characterized by muscle weakness, initially affecting the distal extremities due to the degeneration of spinal α-motoneurons, and respiratory distress, due to the paralysis of the diaphragm. Infantile forms with a severe course of the disease can be distinguished from juvenile forms with a milder course. Mutations in the IGHMBP2 gene have also been found in patients with peripheral neuropathy Charcot-Marie-Tooth type 2S (CMT2S). IGHMBP2 is an ATP-dependent 5'→3' RNA helicase thought to be involved in translational mechanisms. In recent years, several animal models representing both SMARD1 forms and CMT2S have been generated to initially study disease mechanisms. Later, the models showed very well that both stem cell therapies and the delivery of the human IGHMBP2 cDNA by AAV9 approaches (AAV9-IGHMBP2) can lead to significant improvements in disease symptoms. Therefore, the SMARD1 animal models, in addition to the cellular models, provide an inexhaustible source for obtaining knowledge of disease mechanisms, disease progression at the cellular level, and deeper insights into the development of therapies against SMARD1.