Anti-Nutritional Factors and Protein Dispersibility Index as Principal Quality Indicators for Soybean Meal in Diet of Nile Tilapia (Oreochromis niloticus GIFT), a Meta-Analysis.

Soybean meal (SBM) is the most important plant protein source in animal feed. This study investigated the characteristics of different SBMs, produced by soybeans from America and Brazil (SBM-A and SBM-B) in 2017−2021 under the same controlled conditions. The effects of different SBMs on the growth performance of Nile tilapia (Oreochromis niloticus, GIFT) and apparent digestibility coefficients (ADCs) of nutrients and energy were studied. The results showed that protein dispersibility index (PDI), urease activity (UA), glycinin and fiber were the four primary key indicators for distinguishing the characteristics of the tested SBMs. The meta-analysis results suggested that UA, glycinin, and fiber showed a negative effect on the survival rate (SR) and weight gain rate (WGR) of the Nile tilapia, whereas ß-conglycinin, PDI, and nitrogen solubility index (NSI) had a positive effect on the SR and WGR of the fish. The ADCs of dry matter, the gross energy, phosphorus, crude protein, valine (Val), lysine (Lys), histidine (His), serine (Ser), and glutamate (Glu) of the Diet-A group (SBM-A inclusion) were significantly higher than those in the Diet-B group (SBM-B inclusion) (p < 0.05). However, no significant difference was found in ADCs of macro-nutrients between the two SBMs (p > 0.05). Overall, PDI, UA, glycinin, and fiber were the main indicators reflecting the characteristics of the tested SBMs, and UA, glycinin, ß-conglycinin, and PDI had the greatest impact on the growth performance of Nile tilapia in this study. PDI was a more sensitive indicator than NSI for representing the protein quality of SBM.

A new single-cell protein from Clostridium autoethanogenum as a functional protein for largemouth bass (Micropterus salmoides).

Clostridium autoethanogenum protein (CAP) is a new single-cell protein source originating from inactivated bacteria. An in vitro digestion experiment and an 8-wk growth experiment were conducted to evaluate the molecular weight distribution of the CAP hydrolysate, and the effects of dietary CAP levels on the growth performance, plasma parameters, hepatic and intestinal health, and the diversity of gut-adherent microbiota of largemouth bass (Micropterus salmoides). The fish (initial body weight of 47.99 ± 0.01 g) were fed diets where CAP gradually replaced 0% (CAP0), 12.5% (CAP12.5), 25% (CAP25), 37.5% (CAP37.5) and 50% (CAP50) of low-temperature steam dried anchovy fish meal (LTFM) in the diet. Results showed that the content of peptides below 1,000 Da in the CAP hydrolysate (0.56 mg/mL) was higher than that of the LTFM hydrolysate (0.48 mg/mL). Dietary CAP inclusion had no negative effect on growth performance, while whole-body lipid content significantly reduced in the CAP25 and CAP50 groups (P < 0.05). The plasma alanine aminotransferase activities and triglyceride concentrations in the CAP inclusion groups were significantly lower than those in the CAP0 group (P < 0.05). The plasma aspartate aminotransferase activity was significantly reduced in the CAP37.5 group (P < 0.05). The richness and diversity of the gut-adhesive microbiota and the proportion of Clostridium sensu stricto 12 in the CAP50 group were significantly higher than those in the CAP0 group (P < 0.05). Dietary CAP inclusion inhibited inflammatory responses by down-regulating the mRNA levels of interleukin 1ß (IL1ß), IL10 and transforming growth factor ß1 (P < 0.05) in the liver. The mRNA levels of acetyl-CoA carboxylase 1 were significantly down-regulated in the CAP12.5, CAP25 and CAP37.5 groups (P < 0.05), while that of fatty acid synthase was significantly down-regulated in the CAP50 group (P < 0.05). These results demonstrate that dietary CAP inclusion could improve the hepatic and intestinal health of largemouth bass, and can be helpful to further develop CAP as a functional feed ingredient.

Evolutionary History and Functional Diversification of the JmjC Domain-Containing Histone Demethylase Gene Family in Plants.

Histone demethylases containing JumonjiC (JmjC) domains regulate gene transcription and chromatin structure by changing the methylation status of lysine residues and play an important role in plant growth and development. In this study, a total of 332 JmjC family genes were identified from 21 different plant species. The evolutionary analysis results showed that the JmjC gene was detected in each species, that is, the gene has already appeared in algae. The phylogenetic analysis showed that the KDM3/JHDM2 subfamily genes may have appeared when plants transitioned from water to land, but were lost in lycophytes (Selaginella moellendorffii). During the evolutionary process, some subfamily genes may have been lost in individual species. According to the analysis of the conserved domains, all of the plant JmjC genes contained a typical JmjC domain, which was highly conserved during plant evolution. The analysis of cis-acting elements showed that the promoter region of the JmjC gene was rich in phytohormones and biotic and abiotic stress-related elements. The transcriptome data analysis and protein interaction analyses showed that JmjC genes play an important role in plant growth and development. The results clarified the evolutionary history of JmjC family genes in plants and lay the foundation for the analysis of the biological functions of JmjC family genes.

Repairing effects of ICAM-1-expressing mesenchymal stem cells in mice with autoimmune thyroiditis.

The aim of the present study was to determine the repairing effects of intercellular adhesion molecule (ICAM)-1-expressing mesenchymal stem cells (MSCs) in mice with autoimmune thyroiditis. Following induction of an experimental autoimmune thyroiditis (EAT) model, mice were randomly divided into the following groups (n=10 each): i) Normal control; and experimental groups that were subject to EAT induction, including ii) EAT model; and iii) primary MSC; iv) C3H10T1/2/MSC; v) C3H10T1/2-MIGR1/MSC; and vi) C3H10T1/2-MIGR1-ICAM-1/MSC, which were all administered the relevant cells. MSCs were administered via the caudal vein. A blood sample was harvested from the angular vein of each animal 28 days post-treatment and ELISA was used to determine the serum total triiodothyronine, total thyroxine (T4), thyroid-stimulating hormone (TSH), anti-thyroid peroxidase (TPOAb), anti-thyroid microsomal (TMAb) and anti-thyroglobulin (TGAb) antibodies. Hematoxylin and eosin staining was performed to evaluate injury of the thyroid gland by determining the size of the follicle, inflammatory infiltration, colloidal substance retention and epithelial injury. Reverse transcription-quantitative polymerase chain reaction was performed to determine the mRNA expression of interleukin (IL)-4, IL-10, IL-17 and interferon (INF)-γ. Western blot analysis was performed to determine the expression of p38 mitogen-activated protein kinase (p38) and extracellular signal-regulated kinase (ERK). To observe cellular migration in vivo, mice were divided into the following groups, (n=10 each), which were subject to EAT induction: i) CM-DiI-labeled primary MSC; ii) CM-DiI-labeled C3H10T1/2/MSC; iii) CM-DiI-labeled C3H10T1/2-MIGR1/MSC; and iv) CM-DiI-labeled C3H10T1/2-ICAM-1/MSC, which were all administered the relevant cells via the caudal vein. C3H10T1/2-ICAM-1/MSCs were able to ameliorate the expression of T4, TSH, TPOAb, TMAb and TGAb in vivo, attenuate thyroid follicle injury and decrease the splenic index in mice. They were also able to ameliorate the mRNA expression of IL-4, IL-10, IL-17 and INF-γ, and the modulation of the P38 and ERK-signaling pathways in the mouse spleen. Furthermore, ICAM-1 overexpression was able to modulate the nesting of MSCs in the thyroid gland and lung. These findings suggest that C3H10T1/2-ICAM-1/MSC may affect the differentiation, proliferation and migration of immunocytes through modulating the p38 and ERK signaling pathways, and that ICAM-1 may modulate the immunoregulatory effects of MSCs by affecting the migration of MSCs in vivo.

Exenatide exerts direct protective effects on endothelial cells through the AMPK/Akt/eNOS pathway in a GLP-1 receptor-dependent manner.

Glucagon-like peptide-1 (GLP-1) may have direct favorable effects on cardiovascular system. The aim of this study was to investigate the effects of the GLP-1 analog exenatide on improving coronary endothelial function in patients with type 2 diabetes and to investigate the underlying mechanisms. The newly diagnosed type 2 diabetic subjects were enrolled and given either lifestyle intervention or lifestyle intervention plus exenatide treatment. After 12-wk treatment, coronary flow velocity reserve (CFVR), an important indicator of coronary endothelial function, was improved significantly, and serum levels of soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) were remarkably decreased in the exenatide treatment group compared with the baseline and the control group. Notably, CFVR was correlated inversely with hemoglobin A1c (Hb A1c) and positively with high-density lipoprotein cholesterol (HDL-C). In human umbilical vein endothelial cells, exendin-4 (a form of exenatide) significantly increased NO production, endothelial NO synthase (eNOS) phosphorylation, and GTP cyclohydrolase 1 (GTPCH1) level in a dose-dependent manner. The GLP-1 receptor (GLP-1R) antagonist exendin (9-39) or GLP-1R siRNA, adenylyl cyclase inhibitor SQ-22536, AMPK inhibitor compound C, and PI3K inhibitor LY-294002 abolished the effects of exendin-4. Furthermore, exendin-4 reversed homocysteine-induced endothelial dysfunction by decreasing sICAM-1 and reactive oxygen species (ROS) levels and upregulating NO production and eNOS phosphorylation. Likewise, exendin (9-39) diminished the protective effects of exendin-4 on the homocysteine-induced endothelial dysfunction. In conclusion, exenatide significantly improves coronary endothelial function in patients with newly diagnosed type 2 diabetes. The effect may be mediated through activation of AMPK/PI3K-Akt/eNOS pathway via a GLP-1R/cAMP-dependent mechanism.

[Effect of Knockdown of Vascular Cell Adhesion Molecule-1 on the Immunologic Regulation Capacity of Murine Mesenchymal Stem Cells].

OBJECTIVE: To establish the stably lower expression of vascular cell adhesion molecule-1 (VCAM-1) in MSC cell line (C3H10T1/2) by siRNA technology, and explore the effect of knockdown of VCAM-1 on the immunologic regulation capacity of murine MSC. METHODS: The mouse GV118-VCAM-1-RNAi retrovirus vector was constructed by gene recombination technology. The recombinant plasmid was identified by restriction analysis and sequencing, and then the recombinant plasmid GV118-VCAM-1-RNAi was transfected into 293 cells by Lipofectamine, and the supernatant was collected to transfect C3H10T1/2. Moreover, the VCAM-1 lower expression on MSC was evaluated by flow cytometry and fluorescent microscopy. The knockdown VCAM-1 MSC was sorted by flow cytometry. Furthermore, the inhibitory effect of the knockdown VCAM-1 MSC on lymphocyte proliferation was tested by lymphoblast transformation assay (LTT) and mixed lymphocyte reaction assay(MLR). RESULTS: The recombinant retroviral vector of knockdown VCAM-1 (GV118-VCAM-1-RNAi) was successfully constructed and transfected into mouse MSC cell line C3H10T1/2. The knockdown VCAM-1/MSC was obtained by flow cytometric sorting. The LTT and MLR assay showed that the immunosuppressive effect of MSC lower-expressing VCAM-1 dramatically decreased (P<0.05). CONCLUSION: Knockdown VCAM-1 in MSC can significantly down-regulate the inhibitory capability of MSC on the proliferation of T-cells. The data of this study laid an experimental foundation for studying effect of VCAM-1 transfecting into MSC on immune function.

[Effect of Vascular Cell Adhesion Molecule -1 Overexpression on Adipogenic Differentiation of Murine Mesenchymal Stem Cells and Its Mechanism].

OBJECTIVE: To investigate the effect of vascular cell adhesion molecule-1 (VCAM-1) gene overexpression on adipogenic differentiation of mouse mesenchymal stem cells(MSC) and explore its molecular mechanism. METHODS: VCAM-1 overexpression MSC (MIGR1-VCAM-1/MSC) and the empty plasmid transfection MSC (MIGR1/MSC) were induced to adipogenic differentiation, oil-red-O staining and real-time PCR were used to detect the adipogenic differentiation ability and the mRNA expression level of key transcription factors C/EBP α and PPAR γ. The activation of P38, ERK and JNK pathways were analyzed by Western blot. Furthermore, the specific chemical inhibitors of MAPK pathway (SB203580, PD98059 and JNK inhibitor II) were added to the induced culture system and the alteration of the MSC adipogenic differentiation ability were evaluated. RESULTS: no matter in self or induced differentiation groups, the lipid droplets in MIGR1-VCAM-1/MSC became larger, the amount of adipocyte increased than that in MIGR1/MSC (P<0.01), the mRNA expression level of C/EBPα and PPARγ were upregulated, and JNK pathway were down-regulated while the P38 and ERK pathway were significantly up-regulated. The inhibition of JNK pathway of MIGR1-VCAM-1/MSC could lead to increased mRNA expression level of C/EBP α and PPAR γ, the amount of adipocytes increased (P<0.01), however, the inhibition of the P38 and ERK pathway of MIGR1-VCAM-1/MSC could lead to decreased mRNA expression level of C/EBP α and PPAR γ, and the lipid droplets and the number of adipocytes became smaller and less. CONCLUSION: The overexpression of VCAM-1 may promote MSC to differentiate into adipocytes through inhibiting JNK signaling pathway, activating P38 and ERK pathways.