Proteomic Analysis Reveals the Association between the Pathways of Glutathione and α-Linolenic Acid Metabolism and Lanthanum Accumulation in Tea Plants.

Lanthanum can affect the growth and development of the tea plant. Tieguanyin (TGY) and Shuixian (SX) cultivars of Camellia sinensis were selected to explore the mechanism underlying the accumulation of lanthanum (tea plants' most accumulated rare earth element) through proteomics. Roots and fresh leaves of TGY and SX with low- and high-accumulation potential for lanthanum, respectively, were studied; 845 differentially expressed proteins (DEPs) were identified. Gene ontology analysis showed that DEPs were involved in redox processes and related to molecular functions. Kyoto Encyclopedia of Genes and Genomes metabolic pathway analysis showed that DEPs were associated with glutathione (GSH) and α-linolenic acid metabolism, plant pathogen interaction, and oxidative phosphorylation. Thirty-seven proteins in the GSH metabolism pathway showed significant differences, wherein 18 GSH S-transferases showed differential expression patterns in the root system. Compared with the control, expression ratios of GST (TEA004130.1) and GST (TEA032216.1) in TGY leaves were 6.84 and 4.06, respectively, after lanthanum treatment; these were significantly higher than those in SX leaves. The LOX2.1 (TEA011765.1) and LOX2.1 (TEA011776.1) expression ratios in the α-linolenic acid metabolic pathway were 2.44 and 6.43, respectively, in TGY roots, which were significantly higher than those in SX roots. The synthesis of specific substances induces lanthanum-associated defense responses in TGY, which is of great significance for plant yield stability.

Identification, Characterization and Expression Profiling of the RS Gene Family during the Withering Process of White Tea in the Tea Plant (Camellia sinensis) Reveal the Transcriptional Regulation of CsRS8.

Raffinose synthetase (RS) is a key enzyme in the process of raffinose (Raf) synthesis and is involved in plant development and stress responses through regulating Raf content. As a sweetener, Raf makes an important contribution to the sweet taste of white tea. However, studies on the identification, analysis and transcriptional regulation of CsRSs (Camellia sinensis RS genes) are still lacking. In this study, nine CsRSs were identified from the tea plant (Camellia sinensis) genome database. The CsRSs were classified into five groups in the phylogenetic tree. Expression level analysis showed that the CsRSs varied in different parts of the tea plant. Transcriptome data showed that CsRSs could respond to persistent drought and cold acclimation. Except for CsRS5 and CsRS9, the expression pattern of all CsRSs increased at 12 h and decreased at 30 h during the withering process of white tea, consistent with the change trend of the Raf content. Furthermore, combining yeast one-hybrid assays with expression analysis, we found that CsDBB could potentially regulate the expression of CsRS8. Our results provide a new perspective for further research into the characterization of CsRS genes and the formation of the white tea flavour.

Lipoprotein receptor-related protein 6 is required to maintain intercalated disk integrity.

The intercalated disk (ID), a highly organized adhesion structure connecting neighboring cardiomyocytes, fulfills mechanical and electrical signaling communication to ensure normal heart function. Lipoprotein receptor-related protein 6 (LRP6) is a co-receptor inducing canonical Wnt/ß-catenin signaling. It was recently reported that LRP6 deficiency in cardiomyocytes predisposes to arrhythmia independent of Wnt signaling. However, whether LRP6 directly regulates the structure of IDs requires further investigation. The aim of the present study was to explore the role of LRP6 in IDs and the potential underlying mechanisms by inducible cardiac-specific LRP6 knockout mice. The results revealed that LRP6 was predominately expressed in the cell membrane, including the IDs of cardiomyocytes. Tamoxifen-inducible cardiac-specific LRP6 knockout mice displayed overt cardiac dysfunction and disruption of ID structure. Further analysis revealed that cardiac LRP6 deficiency induced the imbalance of ID component proteins, characterized by the sharply decreased expression of connexin 43 (Cx43) and the significantly increased expression of N-cadherin, desmoplakin and γ-catenin in tissue lysates or membrane fraction from the left ventricle. STRING database analysis indicated that ß-catenin, but no other ID-associated proteins, interacted with LRP6. Our immunoprecipitation analysis demonstrated that LRP6 strongly interacted with Cx43, N-cadherin and γ-catenin, and weakly interacted with ß-catenin, whereas there was no association with desmoplakin. In response to LRP6 deficiency, the recruitment of ß- or γ-catenin to N-cadherin was increased, but they displayed little interaction with Cx43. In conclusion, LRP6 is required to maintain the integrity of ID structure and the balance of ID proteins, and the interaction between LRP6 and Cx43, N-cadherin and γ-catenin may be involved in this process.

Cardiac-specific LRP6 knockout induces lipid accumulation through Drp1/CPT1b pathway in adult mice.

We recently reported low-density lipoprotein receptor-related protein 6 (LRP6) decreased in dilated cardiomyopathy hearts, and cardiac-specific knockout mice displayed lethal heart failure through activation of dynamin-related protein 1 (Drp1). We also observed lipid accumulation in LRP6 deficiency hearts, but the detailed molecular mechanisms are unclear. Here, we detected fatty acids components in LRP6 deficiency hearts and explored the potential molecular mechanisms. Fatty acid analysis by GC-FID/MS revealed cardiac-specific LRP6 knockout induced the higher level of total fatty acids and some medium-long-chain fatty acids (C16:0, C18:1n9 and C18:2n6) than in control hearts. Carnitine palmitoyltransferase 1b (CPT1b), a rate-limiting enzyme of mitochondrial ß-oxidation in adult heart, was sharply decreased in LRP6 deficiency hearts, coincident with the activation of Drp1. Drp1 inhibitor greatly improved cardiac dysfunction and attenuated the increase in total fatty acids and fatty acids C16:0, C18:1n9 in LRP6 deficiency hearts. It also greatly inhibited the decrease in the cardiac expression of CPT1b and the transcriptional factors CCCTC-binding factor (CTCF) and c-Myc induced by cardiac-specific LRP6 knockout in mice. C-Myc but not CTCF was identified to regulate CPT1b expression and lipid accumulation in cardiomyocytes in vitro. The present study indicated cardiac-specific LRP6 knockout induced lipid accumulation by Drp1/CPT1b pathway in adult mice, and c-Myc is involved in the process. It suggests that LRP6 regulates fatty acid metabolism in adult heart.

Mechanical stresses induce paracrine ß-2 microglobulin from cardiomyocytes to activate cardiac fibroblasts through epidermal growth factor receptor.

By employing a proteomic analysis on supernatant of mechanically stretched cardiomyocytes, we found that stretch induced a significantly high level of ß-2 microglobulin (ß2M), a non-glycosylated protein, which is related to inflammatory diseases but rarely known in cardiovascular diseases. The present data showed that serum ß2M level was increased in patients with hypertension and further increased in patients with chronic heart failure (HF) as compared with control group, and the high level of serum ß2M level correlated to cardiac dysfunction in these patients. In pressure overload mice model by transverse aortic constriction (TAC), ß2M levels in serum and heart tissue increased progressively in a time-dependent manner. Exogenous ß2M showed pro-fibrotic effects in cultured cardiac fibroblasts but few effects in cardiomyocytes. Adeno-associated virus 9 (AAV9)-mediated knockdown of ß2M significantly reduced cardiac ß2M level and inhibited myocardial fibrosis and cardiac dysfunction but not cardiac hypertrophy at 4 weeks after TAC. In vitro, mechanical stretch induced the rapid secretion of ß2M mainly from cardiomyocytes by activation of extracellular-regulated protein kinase (ERK). Conditional medium (CM) from mechanically stretched cardiomyocytes activated cultured cardiac fibroblasts, and the effect was partly abolished by CM from ß2M-knockdown cardiomyocytes. In vivo, knockdown of ß2M inhibited the increase in phosphorylation of epidermal growth factor receptor (EGFR) induced by TAC. In cultured cardiac fibroblasts, inhibition of EGFR significantly attenuated the ß2M-induced the activation of EGFR and pro-fibrotic responses. The present study suggests that ß2M is a paracrine pro-fibrotic mediator and associated with cardiac dysfunction in response to pressure overload.

Ryanodine Receptor Type 2 Plays a Role in the Development of Cardiac Fibrosis under Mechanical Stretch Through TGFß-1.

Ryanodine receptor type 2 (RyR-2), the main Ca2+ release channel from sarcoplasmic reticulum in cardiomyocytes, plays a vital role in the regulation ofmyocardial contractile function and cardiac hypertrophy. However, the role of RyR-2 in cardiac fibrosis during the development of cardiac hypertrophy remains unclear.In this study, we examined whether RyR-2 regulates TGFß1, which is secreted from cardiomyocytes and exerts on cardiac fibrosis using cultured cardiomyocytes and cardiac fibroblasts of neonatal rats. The expression of RyR-2 was found only in cardiomyocytesbut not in cardiac fibroblasts. Mechanical stretch induced upregulation of TGFß1 in cardiomyocytes and RyR-2 knockdown significantly suppressed the upregulation of TGFß1 expression. The transcript levels of collagen genes were also decreased in fibroblasts compare with wild type, although the expression of both two kinds was higher than those in stationary cardiomyocytes (non-stretch). With the inhibition of the TGFß1-neutralizing antibody, the expression of collagen genes has no significant difference between the mechanically stretched cardiomyocytes and non-stretchedones. These results indicate that RyR-2 regulated TGFß1 expression in mechanically stretched cardiomyocytes and TGFß1 promoted collagen formation of cardiac fibroblasts by a paracrine mechanism.RyR-2 in mechanical stretch could promote the development of cardiac fibrosis involving TGFß1-dependent paracrine mechanism. Our findings provided more insight into comprehensively understanding the molecular role of RyR-2 in regulating cardiac fibrosis.

Pharmaceutical composition and drug effect of synthetic Bacopa monnieri L. health promoting agent from the perspective of resistance fatigue.

Bacopa monnieri has effect on the nervous system, digestive system and blood circulation systems. In this paper, the authors conducted pharmacological analysis on Bacopa monniera and its innovative pharmaceutical preparation of promote motor function. The extract of the drug has some effect on relieving the fatigue and providing the movement function. By analyzing the composition and efficacy of Chinese herbal extracts, it can be seen that these drugs have obvious effect on improving immunity. Experimental results show that the agent can increase the liver glycogen energy reserves, reduce Bla and BUN levels, balance and energy metabolism of muscle cells in the environment, it plays a positive role to improve the exercise capacity and exercise fatigue.

Nucleosome Assembly Protein 1-Like 1 (Nap1l1) Regulates the Proliferation of Murine Induced Pluripotent Stem Cells.

BACKGROUND/AIMS: To investigate whether nucleosome assembly protein 1-like 1 (Nap1l1) regulates the proliferation of induced pluripotent stem cells (iPSC) and the potential mechanisms. METHODS: Nap1l1-knockdown-iPSC and Nap1l1-overexpression-iPSC were constructed by transfection of lentiviral particles. The proliferation of iPSC was detected by MTT analysis, and cell cycle was analyzed by flow cytometry. RESULTS: Nap1l1 overexpression promoted iPSC proliferation and induced G2/M transition compared to their control iPSC while Nap1l1-knockdown-iPSC dramatically displayed the reduced proliferation and accumulated G2/M phase cells. Further analysis showed that Nap1l1 overexpression in iPSC increased the expression of cyclin B1, downregulated the expression of p21 and p27, while knockdown of Nap1l1 showed the opposite effects. In addition, overexpression of Nap1l1 promoted the phosphorylation of AKT and ERK in iPSC, while knockdown of Nap1l1 inhibited the effects. However, these effects displayed in Nap1l1-overexpression-iPSC were greatly suppressed by the inhibition of AKT or ERK signaling. CONCLUSIONS: The results indicate that Nap1l1 promotes the proliferation of iPSC attributable to G2/M transition caused by downregulation of p27 and p21, and upregulation of cyclin B1, the activation of AKT or ERK is involved in the process. The present study has revealed a novel molecular mechanism involved in the proliferation of iPSC.

Identification of Amino Acid Residues in Angiotensin II Type 1 Receptor Sensing Mechanical Stretch and Function in Cardiomyocyte Hypertrophy.

BACKGROUND/AIMS: Angiotensin II (AngII) type 1 receptor (AT1R) could be activated by mechanical stress without the involvement of AngII during the development of cardiac hypertrophy. We aimed to identify sensing sites of AT1R for activation by mechanical stretch. METHODS: We constructed several site-directed mutations of AT1R (AT1R(K199Q), AT1R(L212F), AT1R(Q257A) and AT1R(C289A)), transfected them respectively into COS7 cells or angiotensinogen knockout cardiomyocytes (ATG(−/−)-CMs), and observed cellular events after mechanical stretch. RESULTS: AngII-induced phosphorylation of ERKs and Jak2, and redistribution of Gαq11 in AT1R(WT)- COS7 or -ATG(−/−)-CMs were dramatically decreased in AT1R(K199Q)- or AT1R(Q257A)- COS7 cells or -ATG(−/−)- CMs, while those effects induced by mechanical stretch were greatly suppressed in COS7 cells or ATG(−/−)-CMs expressing AT1R(L212F), AT1R(Q257A) or AT1R(C289A) compared with these cells expressing AT1R(WT). AngII-induced hypertrophic responses (the increase in hypertrophic genes expression and cross-sectional area) in AT1R(WT)- ATG(−/−)-CMs were partly abolished in AT1R(K199Q)-ATG(−/−)- CMs or AT1R(Q257A) -ATG(−/−)-CMs, while these responses induced by mechanical stretch were greatly inhibited in ATG(−/−)-CMs overexpressing AT1R(L212F), AT1R(Q257A )or AT1R(C289A). CONCLUSION: These results indicated that Leu212, Gln257 and Cys289 in AT1R are not only sensing sites for mechanical stretch but also functional amino residues for activation of the receptor and cardiomyocytes hypertrophy induced by mechanical stretch.

Knockdown of nucleosome assembly protein 1-like 1 induces mesoderm formation and cardiomyogenesis via notch signaling in murine-induced pluripotent stem cells.

Low efficiency of cardiomyocyte differentiation from induced pluripotent stem cells (iPSCs) hinders the clinical application of iPSC technology for cardiac repair strategy. Recently, we screened out nucleosome assembly protein 1-like 1 (Nap1l1), which was downregulated during the differentiation of P19CL6 cells into cardiomyocytes. Here, we attempted to study the role of Nap1l1 in cardiomyogenesis of iPSC. Nap1l1 was downregulated during the differentiation of iPSC. Knockdown of Nap1l1 dramatically enhanced the differentiation of iPSC into functional cardiomyocytes while overexpression of Nap1l1 sharply lowered the differentiation. Moreover, although Nap1l1-knockdown had little effect on endoderm differentiation, the Nap1l1 modulation significantly accelerated mesoderm development. Re-expressing Nap1l1 in Nap1l1-knockdown-iPSC rescued the effects of Nap1l1. Inducibly overexpressing Nap1l1 at early stage of differentiation greatly inhibited mesoderm induction and cardiogenesis of iPSC. However, mesoderm stem cells (Flk-1-positive cells) originated from Nap1l1-knockdown- or -overexpression-iPSC showed no difference in further cardiomyocyte differentiation compared with that of control-iPSC. Further study revealed that Nap1l1-overexpression increased γ-secretase activity and the expression of Notch intracellular domain (NICD) and downstream genes during the differentiation of iPSC. γ-Secretase inhibitor DAPT (N-[N-(3,5-difluorophenacetyl)-L-alanyl]-S-phenylglycinet-butyl ester) greatly suppressed the production of NICD and abolished the inhibitory effects of Nap1l1-overexpression on mesoderm induction and cardiogenesis. These findings demonstrate that downregulation of Nap1l1 significantly enhances mesodermal induction and subsequent cardiogenesis of murine iPSC via inhibition of γ-secretase-regulated Notch signaling, which would facilitate the application of iPSC in heart diseases.

Urotensin II Protects Cardiomyocytes from Apoptosis Induced by Oxidative Stress through the CSE/H2S Pathway.

Plasma urotensin II (UII) has been observed to be raised in patients with acute myocardial infarction; suggesting a possible cardiac protective role for this peptide. However, the molecular mechanism is unclear. Here, we treated cultured cardiomyocytes with H2O2 to induce oxidative stress; observed the effect of UII on H2O2-induced apoptosis and explored potential mechanisms. UII pretreatment significantly reduced the number of apoptotic cardiomyocytes induced by H2O2; and it partly abolished the increase of pro-apoptotic protein Bax and the decrease of anti-apoptotic protein Bcl-2 in cardiomyocytes induced by H2O2. SiRNA targeted to the urotensin II receptor (UT) greatly inhibited these effects. Further analysis revealed that UII increased the production of hydrogen sulfide (H2S) and the level of cystathionine-γ-lyase (CSE) by activating the ERK signaling in H2O2-treated-cardiomyocytes. Si-CSE or ERK inhibitor not only greatly inhibited the increase in CSE level or the phosphorylation of ERK induced by UII but also reversed anti-apoptosis of UII in H2O2-treated-cadiomyocytes. In conclusion, UII rapidly promoted the phosphorylation of ERK and upregulated CSE level and H2S production, which in turn activated ERK signaling to protect cardiomyocytes from apoptosis under oxidative stress. These results suggest that increased plasma UII level may protect cardiomyocytes at the early-phase of acute myocardial infarction in patients.

Urotensin II inhibited the proliferation of cardiac side population cells in mice during pressure overload by JNK-LRP6 signalling.

Cardiac side population cells (CSPs) are promising cell resource for the regeneration in diseased heart as intrinsic cardiac stem cells. However, the relative low ratio of CSPs in the heart limited the ability of CSPs to repair heart and improve cardiac function effectively under pathophysiological condition. Which factors limiting the proliferation of CSPs in diseased heart are unclear. Here, we show that urotensin II (UII) regulates the proliferation of CSPs by c-Jun N-terminal kinase (JNK) and low density lipoprotein receptor-related protein 6 (LRP6) signalling during pressure overload. Pressure overload greatly upregulated UII level in plasma, UII receptor (UT) antagonist, urantide, promoted CSPs proliferation and improved cardiac dysfunction during chronic pressure overload. In cultured CSPs subjected to mechanical stretch (MS), UII significantly inhibited the proliferation by UT. Nanofluidic proteomic immunoassay showed that it is the JNK activation, but not the extracellular signal-regulated kinase signalling, that involved in the UII-inhibited- proliferation of CSPs during pressure overload. Further analysis in vitro indicated UII-induced-phospho-JNK regulates phosphorylation of LRP6 in cultured CSPs after MS, which is important in the inhibitory effect of UII on the CSPs during pressure overload. In conclusion, UII inhibited the proliferation of CSPs by JNK/LRP6 signalling during pressure overload. Pharmacological inhibition of UII promotes CSPs proliferation in mice, offering a possible therapeutic approach for cardiac failure induced by pressure overload.

Transcriptome and metabolome reveal the effects of ABA promotion and inhibition on flavonoid and amino acid metabolism in tea plant.

Flavonoids (especially anthocyanins and catechins) and amino acids represent a high abundance of health-promoting metabolites. Although we observed abscisic acid accumulation in purple leaves and low levels in albino tea leaves, the specific mechanism behind its impact on flavor compounds remains unclear. In this study, we treated tea leaves with exogenous abscisic acid and abscisic acid biosynthesis inhibitors (Flu), measured physiological indicators and conducted comprehensive transcriptomic and metabolomic analyses to elucidate the potential mechanisms underlying color change. Our results demonstrate that abscisic acid treatment induces purple coloration, while Flu treatment causes discoloration in tea leaves. Metabolomic analysis revealed higher levels of four anthocyanins and six catechins in the group treated with abscisic acid in comparison with the control group. Additionally, there was a notable increase in 15 amino acids in the Flu-treated group. Notably, the levels of flavonoids and amino acids showed an inverse relationship between the two treatments. Transcriptomic comparison between the treatments and the control group revealed upregulation of differentially expressed genes encoding dihydroflavonol reductase and uridine diphosphate-glycose flavonoid glycosyltransferase in the abscisic acid-treated group, leading to the accumulation of identified anthocyanins and catechins. In contrast, differentially expressed genes encoding nitrate reductase and nitrate transporter exhibited elevated expression in the group treated with Flu, consequently facilitating the accumulation of amino acids, specifically L-theanine and L-glutamine. Furthermore, our co-expression network analysis suggests that MYB and bHLH transcription factors may play crucial roles in regulating the expression of differentially expressed genes involved in the biosynthesis of flavonoids and amino acids. This study provides insights for targeted genetic engineering to enhance the nutritional and market value of tea, together with the potential application of purple and albino tea leaves as functional beverages. It also offers guidance for future breeding programs and production.

High Light Intensity Triggered Abscisic Acid Biosynthesis Mediates Anthocyanin Accumulation in Young Leaves of Tea Plant (Camellia sinensis).

There is increasing interest in the production and consumption of tea (Camellia sinensis L.) processed from purple-leaved cultivar due to their high anthocyanin content and health benefits. However, how and why seasonal changes affect anthocyanin accumulation in young tea leaves still remains obscured. In this study, anthocyanin and abscisic acid (ABA) contents in young leaves of Zifuxing 1 (ZFX1), a cultivar with new shoots turning to purple in Wuyi Mountain, a key tea production region in China, were monitored over four seasons. Young leaves produced in September were highly purplish, which was accompanied with higher anthocyanin and ABA contents. Among the environmental factors, the light intensity in particular was closely correlated with anthocyanin and ABA contents. A shade experiment also indicated that anthocyanin content significantly decreased after 168 h growth under 75% shade, but ABA treatment under the shade conditions sustained anthocyanin content. To confirm the involvement of ABA in the modulation of anthocyanin accumulation, anthocyanin, carotenoids, chlorophyll, ABA, jasmonic acid (JA), and salicylic acid (SA) in the young leaves of four cultivars, including ZFX1, Zijuan (ZJ), wherein leaves are completely purple, Rougui (RG) and Fudingdabaicha (FDDB) wherein leaves are green, were analyzed, and antioxidant activities of the leaf extracts were tested. Results showed that ABA, not other tested hormones, was significantly correlated with anthocyanin accumulation in the purple-leaved cultivars. Cultivars with higher anthocyanin contents exhibited higher antioxidant activities. Subsequently, ZFX1 plants were grown under full sun and treated with ABA and fluridone (Flu), an ABA inhibitor. ABA treatment elevated anthocyanin level but decreased chlorophyll contents. The reverse was true to those treated with Flu. To pursue a better understanding of ABA involvement in anthocyanin accumulation, RNA-Seq was used to analyze transcript differences among ABA- or Flu-treated and untreated ZFX1 plants. Results indicated that the differentially expressed genes in ABA or Flu treatment were mainly ABA signal sensing and metabolism-related genes, anthocyanin accumulation-related genes, light-responsive genes, and key regulatory MYB transcription factors. Taking all the results into account, a model for anthocyanin accumulation in ZFX1 cultivar was proposed: high light intensity caused reactive oxygen stress, which triggered the biosynthesis of ABA; ABA interactions with transcription factors, such as MYB-enhanced anthocyanin biosynthesis limited chlorophyll and carotenoid accumulation; and transport of anthocyanin to vacuoles resulting in the young leaves of ZFX1 with purplish coloration. Further research is warranted to test this model.

Association of Stat3 with HSF1 plays a critical role in G-CSF-induced cardio-protection against ischemia/reperfusion injury.

Granulocyte colony-stimulating factor (G-CSF) has been shown to be cardio-protective against ischemia through activating Jak2/Stat3 pathway, however, the mechanism is unclear. Heat shock transcription factor 1 (HSF1), a definite endogenous protective protein in cardiomyocytes, may interact with Stat family under stress conditions. We hypothesized that G-CSF could induce cardio-protection against ischemia/reperfusion (I/R) through association of HSF1 with Stat3. To test the hypothesis, we built cardiac I/R injury model with HSF1 knockout (KO) mice and wild type (WT) mice by occlusion of the left anterior descending (LAD) coronary artery for 30min and subsequent release of the occlusion for 24h. These mice were administered with G-CSF (100µg/kg/day) or vehicle subcutaneously for 3days before surgery. As expected, G-CSF induced significant cardio-protections against I/R injury, characterized by higher ejection fraction (EF%), lower left ventricular end diastolic pressure (LVEDP), increased dp/dt value and decreased infarct area as compared with the vehicle treatment in WT mice. In HSF1-KO mice, however, these cardio-protections induced by G-CSF were greatly attenuated. Inhibition of oxidative stress-induced cardiomyocyte apoptosis by G-CSF also disappeared due to the deficiency of HSF1 in vitro and in vivo. Furthermore, G-CSF increased the phosphorylation and the association of Stat3 with HSF1, which enhanced transcriptional activity of HSF1. Inhibition of either Stat3 or HSF1 by pharmacological agents suppressed G-CSF-induced association of the two proteins and anti-apoptotic effect on cardiomyocytes. Our data suggest that G-CSF stimulates phosphorylation and association of Stat3 with HSF1 and therefore enhances transcriptional activity of HSF1, leading to the cardio-protection against I/R injury.

Widely Targeted Metabolomics Analysis Reveals the Differences of Nonvolatile Compounds in Oolong Tea in Different Production Areas.

The flavor differences in Oolong tea from different producing areas are caused by its complex differential compounds. In this study, representative samples of Oolong tea from four countries were collected, and their differential nonvolatile compounds were analyzed by a combination of widely targeted metabolomics, chemometrics, and quantitative taste evaluation. A total of 801 nonvolatile compounds were detected, which could be divided into 16 categories. We found that the difference in these compounds' content among Oolong teas from three producing areas in China was the largest. There were 370 differential compounds related to the producing areas of Oolong tea, which were mainly distributed in 67 Kyoto Encyclopedia of Genes and Genomes (KEGG) metabolic pathways. In total, 81 differential nonvolatile compounds made important contributions to the taste differences in Oolong tea from different producing areas, among which the number of flavonoids was the largest. Finally, the characteristic compounds of Oolong tea in six producing areas were screened. This study comprehensively identifies the nonvolatile compounds of Oolong tea in different producing areas for the first time, which provides a basis for the analysis of flavor characteristics, quality directional control, and the identification and protection of geographical landmark agricultural products of Oolong tea from different producing areas.

Combined analysis of lipidomics and transcriptomics revealed the key pathways and genes of lipids in light-sensitive albino tea plant (Camellia sinensis cv. Baijiguan).

Currently, the mechanism by which light-sensitive albino tea plants respond to light to regulate pigment synthesis has been only partially elucidated. However, few studies have focused on the role of lipid metabolism in the whitening of tea leaves. Therefore, in our study, the leaves of the Baijiguan (BJG) tea tree under shade and light restoration conditions were analyzed by a combination of lipidomics and transcriptomics. The leaf color of BJG was regulated by light intensity and responded to light changes in light by altering the contents and proportions of lipids. According to the correlation analysis, we found three key lipid components that were significantly associated with the chlorophyll SPAD value, namely, MGDG (36:6), DGDG (36:6) and DGDG (34:3). Further weighted gene coexpression network analysis (WGCNA) showed that HY5 TF and GLIP genes may be hub genes involved lipid regulation in albino tea leaves. Our results lay a foundation for further exploration of the color changes in albino tea leaves.

Willingness of Tea Farmers to Adopt Ecological Agriculture Techniques Based on the UTAUT Extended Model.

Ecological agricultural technology is the key method for making the transition from traditional agriculture to ecological agriculture, and is also the basic measure for promoting the transformation and upgrading of the tea industry and sustainable development. This study explores the influencing factors and mechanisms of tea farmers' adoption of ecological agricultural technology by using the extended model of the unified theory of technology adoption and use (UTAUT) based on perceived value. The analysis results, using the partial least squares structural equation model (PLS-SEM), show that: the positive impact of perceived value on willingness to use not only makes the explanatory power of the extended model greater than that of the original model but also expands the UTAUT model into a full mediating model, in which performance expectation has the greatest impact on behavioral intention through the implemented value. Effect expectation, social influence and factoring factors following, then the four intermediary paths have significant positive effects on behavioral intention. This study improves on the limitations of the UTAUT theoretical model through the theory of perceived value, and provides a reference for research on the same topic. At the same time, the government should provide tea farmers with enhanced subsidies, skills training and communication platforms.

Interplay of Ecological Opportunities and Functional Traits Drives the Evolution and Diversification of Millettiod Legumes (Fabaceae).

Understanding the striking diversity of the angiosperms is a paramount issue in biology and of interest to biologists. The Millettiod legumes is one of the most hyper-diverse groups of the legume family, containing many economically important medicine, furniture and craft species. In the present study, we explore how the interplay of past climate change, ecological opportunities and functional traits' evolution may have triggered diversification of the Millettiod legumes. Using a comprehensive species-level phylogeny from three plastid markers, we estimate divergence times, infer habit shifts, test the phylogenetic and temporal diversification heterogeneity, and reconstruct ancestral biogeographical ranges. We found that three dramatic accumulations of the Millettiod legumes occurred during the Miocene. The rapid diversification of the Millettiod legumes in the Miocene was driven by ecological opportunities created by the emergence of new niches and range expansion. Additionally, habit shifts and the switch between biomes might have facilitated the rapid diversification of the Millettiod legumes. The Millettiod legumes provide an excellent case for supporting the idea that the interplay of functional traits, biomes, and climatic and geographic factors drives evolutionary success.

Relationship between the Grade and the Characteristic Flavor of PCT (Panyong Congou Black Tea).

Panyong Congou black tea (PCT) is one of the most representative and historically famous Congou black teas in China and has been gaining more and more attention for its beneficial health properties. Currently, four grades of PCT are available, based on the raw leaf materials and consumer palatability. The chemical profiles distinguishing different grades of PCT are yet to be defined, nor has the relationship with grade been evaluated. In the present study, chemometric analysis showed that epigallocatechin (EGC), catechin (C), polyphenols, gallic acid (GA), and free amino acids are grade related bio-markers of PCT. These compounds are associated with the sweet and mellow aftertaste of PCT. A total of 34 volatile components were identified, of which the three component types with the highest relative percentages were alcohols (51.34-52.51%), ketones (27.31-30.28%), and aldehydes (12.70-13.18%). Additionally, our results revealed that sweet floral and fruity aromas were positively correlated with six volatile organic compounds (VOCs), 1-pentanol, propyl hexanoate, linalool, cyclohexanone, hexanal, and 2,5-dimethylpyrazine. Clear discrimination was achieved using orthogonal projections to latent structures discriminant analysis (OPLS-DA). The findings provide vital information on the characteristic flavor of each grade of PCT.