GLORIA

GEOMAR Library Ocean Research Information Access

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Qi, Renli  (10)
  • 2015-2019  (10)
Material
Publisher
Language
Years
  • 2015-2019  (10)
Year
Subjects(RVK)
  • 1
    Online Resource
    Online Resource
    Wiley ; 2018
    In:  Journal of Cellular Physiology Vol. 233, No. 2 ( 2018-02), p. 1236-1246
    In: Journal of Cellular Physiology, Wiley, Vol. 233, No. 2 ( 2018-02), p. 1236-1246
    Abstract: Tumor necrosis factor (TNF) α can induce cell apoptosis and activate nuclear transcription (NF)‐κB in different cell types. Activated NF‐κB further promotes or suppresses cellular apoptosis in different cases. The present study explored the effect of activated NF‐κB on adipocyte apoptosis induced by TNFα and which microRNAs (miRNAs) were involved in the process. Our findings demonstrated that treatment of differentiated 3T3‐L1 adipocytes with TNFα (20 ng/mL) rapidly activated NF‐κB and induced moderate apoptosis. Pyrrolidinedithiocarbamic acid (PDTC, 60 µM), a specific NF‐κB inhibitor, abated NF‐κB activation that rendered the adipocytes vulnerable to TNFα‐induced apoptosis. Dozens of miRNAs exhibited significant expression changes following TNFα treatment and the addition of PDTC. In which, miRNA‐224‐5p (miR‐224) was up‐regulated by TNFα exposure but down‐regulated by PDTC addition. Furthermore, over‐expression of miR‐224 promoted NF‐κB activation and prevented the adipocyte apoptosis induced by TNFα, while miR‐224 deficiency showed the opposite effects. The TRAF‐associated NF‐κB activator ( TANK ) gene was identified as a direct target of miR‐224 by computational and luciferase reporter assays. Additionally, silencing the TANK gene by the small interfering RNA similarly promoted NF‐κB activation and attenuated the cellular apoptosis. In conclusion, these findings demonstrate that miR‐224 plays an essential role in adipocyte apoptosis caused by TNFα through control of NF‐κB activation via targeting the TANK gene.
    Type of Medium: Online Resource
    ISSN: 0021-9541 , 1097-4652
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2018
    detail.hit.zdb_id: 1478143-8
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 2
    Online Resource
    Online Resource
    Elsevier BV ; 2019
    In:  Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids Vol. 1864, No. 5 ( 2019-05), p. 744-755
    In: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids, Elsevier BV, Vol. 1864, No. 5 ( 2019-05), p. 744-755
    Type of Medium: Online Resource
    ISSN: 1388-1981
    RVK:
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2019
    detail.hit.zdb_id: 2209502-0
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 3
    Online Resource
    Online Resource
    Wiley ; 2019
    In:  Journal of Animal Physiology and Animal Nutrition Vol. 103, No. 6 ( 2019-11), p. 1908-1918
    In: Journal of Animal Physiology and Animal Nutrition, Wiley, Vol. 103, No. 6 ( 2019-11), p. 1908-1918
    Abstract: This study investigated the effect of Lactobacillus plantarum strain 299v on gut health in suckling piglets. Sixty newborn piglets were assigned to control and probiotic treatments, with three litters per treatment (ten piglets/litter). From days 1 to 20 of life, piglets were orally administered a placebo of 0.1% peptone or 1.0 ×  10 10  CFU L. plantarum 299v daily. Six piglets per treatment were sacrificed on day 20, and intestinal tissues (including duodenum, jejunum, ileum and colon) and the intestinal contents from colon segments were collected. The results demonstrated that piglets treated with L. plantarum 299v had a lower diarrhoea incidence than the controls. L. plantarum 299v administration significantly increased the ratio of the villus height to the crypt depth in the jejunum and ileum, as well as the mRNA expression of jejunal occludin and ileal zonula occludens 1 ( ZO‐1 ). The L. plantarum treatment also increased the mRNA abundance of porcine β‐defensin 2 ( pBD2 ) and pBD3 in the jejunum and ileum and of toll‐like receptors (TLRs), such as TLR2 , TLR4 , TLR6 and TLR9 in the ileum, and significantly upregulated the mRNA abundances of ileal pBD1 and colonic TLR4 . Additionally, the L. plantarum 299v treatment significantly changed the structure of the colonic microbiota, as evidenced by the obvious increases in the relative abundances of the phyla Firmicutes and Actinobacteria and of the genus Lactobacillus . Our findings indicate that L. plantarum 299v facilitates the gut health of suckling piglets, probably by improving the intestinal morphology and intestinal barrier function and by modifying the structure of the gut microbiota.
    Type of Medium: Online Resource
    ISSN: 0931-2439 , 1439-0396
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 2020405-X
    SSG: 12
    SSG: 21
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 4
    Online Resource
    Online Resource
    S. Karger AG ; 2017
    In:  Cellular Physiology and Biochemistry Vol. 44, No. 6 ( 2017), p. 2467-2475
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 44, No. 6 ( 2017), p. 2467-2475
    Abstract: Background/Aims: Myoblasts and muscle satellite cells have the potential to transdifferentiate into adipocytes or adipocyte-like cells. Previous studies suggest that mitogen-activated protein kinase (MAPK) is critical to adipogenic trans-differentiation of muscle cells. ERK1/2, P38 and JNK are three major MAPK family members; their activation and regulatory functions during adipogenic trans-differentiation of myoblasts are investigated. Methods: C2C12 myoblasts were cultured and induced for adipogenic trans-differentiation. Activation patterns of MAPKs were assayed using protein microarray and Western blot. Three specific MAPK blockers, U0126, SB20358 and SP600125, were used to block ERK1/2, P38 and JNK during trans-differentiation. Cellular adipogenesis was measured using staining and morphological observations of cells and expression changes in adipogenic genes. Results: Inhibitors reduced phosphorylation of corresponding MAPK and produced unique cellular effects. Suppressing P38 promoted adipogenic trans-differentiation and intensified adipolytic metabolism in differentiated cells. However, inhibition of ERK1/2 had the opposite effects on adipogenesis and no effect on adipolysis. Blocking JNK weakly blocked trans-differentiation but stimulated adipolysis and induced apoptosis. Conclusion: Three MAPKs participate in the regulation of myoblast adipogenic trans-differentiation by controlling adipogenic and adipolysis metabolism.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2017
    detail.hit.zdb_id: 1482056-0
    SSG: 12
    SSG: 15,3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 5
    Online Resource
    Online Resource
    S. Karger AG ; 2016
    In:  Cellular Physiology and Biochemistry Vol. 40, No. 3-4 ( 2016), p. 668-680
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 40, No. 3-4 ( 2016), p. 668-680
    Abstract: Background/Aims: Conjugated linoleic acids (CLAs) are known to induce apoptosis in adipocytes; however, the cellular mechanisms involved remained illdefined. We explored the different apoptotic induction effects of two CLA isomers on adipocytes and then investigated the expression and function of microRNAs (miRNAs) related to the apoptosis. Methods: TUNEL and FCM assays were used to detect CLAs-induced adipocyte apoptosis. Microarrays were used to compare the differential expression of miRNAs. MiR-23a, a miRNA that showed significant changes in expression in the CLA-treated cells, was selected for the subsequent functional studies via over-expression and knock down in in vivo and in vitro experiments. Results: C9, t11-CLA exhibited a stronger induction of apoptosis in the differentiated 3T3-L1 adipocytes than t10, c12-CLA. However, t10, c12-CLA could rapidly activate NF-κB, which may have caused their different apoptotic effects. MiR-23a was markedly down-regulated by the CLAs treatment and miR-23a over-expression attenuated CLA-induced apoptosis. Apoptosis protease-activating factor 1 (APAF1) was identified as a target gene of miR-23a. In an in vivo experiment endogenous miR-23a was down-regulated in mice fed with a mixture of both CLAs. The mice also exhibited less fat deposition and more apoptotic fat cells in adipose tissue. Moreover, endogenous miR-23a was suppressed in mice via intravenous injection with an antagomir which resulted in decreased body weight, increased number of apoptotic fat cells and increased APAF1 expression in adipose tissue. Conclusion: Taken together, our results suggest that miR-23a plays a critical role in CLA-induced apoptosis in adipocytes via controlling APAF1 expression.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2016
    detail.hit.zdb_id: 1482056-0
    SSG: 12
    SSG: 15,3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 6
    In: Genes, MDPI AG, Vol. 7, No. 10 ( 2016-10-24), p. 92-
    Type of Medium: Online Resource
    ISSN: 2073-4425
    Language: English
    Publisher: MDPI AG
    Publication Date: 2016
    detail.hit.zdb_id: 2527218-4
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 7
    In: Genes, MDPI AG, Vol. 8, No. 10 ( 2017-10-13), p. 271-
    Type of Medium: Online Resource
    ISSN: 2073-4425
    Language: English
    Publisher: MDPI AG
    Publication Date: 2017
    detail.hit.zdb_id: 2527218-4
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 8
    Online Resource
    Online Resource
    MDPI AG ; 2019
    In:  International Journal of Molecular Sciences Vol. 20, No. 15 ( 2019-07-30), p. 3725-
    In: International Journal of Molecular Sciences, MDPI AG, Vol. 20, No. 15 ( 2019-07-30), p. 3725-
    Abstract: Myoblasts could transdifferentiate into adipocytes or adipocyte-like cells, which have the capability of producing and storing intracellular lipids. Long-chain non-coding RNAs (lncRNAs) have many important physiological functions in eukaryotes, which include regulating gene expression, chromosome silencing, and nuclear transport. However, changes in the expression of lncRNAs in muscle cells during adipogenic transdifferentiation have not been investigated to date. Here, C2C12 myoblasts were seeded and then induced to undergo myogenic and adipogenic transdifferentiation. The expression profiles of lncRNAs in various differentiated cells were analyzed and then compared by digital gene expression (DGE) RNA sequencing. A total of 114 core lncRNAs from 836 differentially expressed lncRNAs in adipogenic cells were identified. Further investigation by in silico analysis revealed that the target genes of core lncRNAs significantly enriched various signaling pathways that were related to glucose and lipid metabolism and muscle growth. The lncRNA-GM43652 gene was a potential regulator of adipogenesis in muscle cells. It showed the highest levels of expression in adipogenic cells, and the knocking down lncRNA-GM43652 negatively influenced lipid deposition in transdifferentiated myoblasts. This study has identified the novel candidate regulators that may be assessed in future molecular studies on adipogenic conversion of muscle cells.
    Type of Medium: Online Resource
    ISSN: 1422-0067
    Language: English
    Publisher: MDPI AG
    Publication Date: 2019
    detail.hit.zdb_id: 2019364-6
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 9
    In: Gene, Elsevier BV, Vol. 618 ( 2017-06), p. 49-56
    Type of Medium: Online Resource
    ISSN: 0378-1119
    RVK:
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2017
    detail.hit.zdb_id: 1491012-3
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 10
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 39, No. 3 ( 2016), p. 1087-1097
    Abstract: Background/Aims: Muscle cells are able to trans-differentiate into adipocytes with adipogenesis induction. MicroRNAs (miRNAs), a class of small non-coding RNAs, widely participate in the regulation of growth and development of cells. However, the expression and regulatory role of miRNAs in the trans-differentiation of muscle cell are largely unknown. Methods: C2C12 myoblasts were inducted to adipogenesis trans-differentiation and microarrays were used to assay the changes of expression profile of miRNAs. MiR-199a, a miRNA showed significant change in the trans-differentiation, was selected for the subsequent function study via over- expression and knock down. Results: Dozens of miRNAs showed different changes followed the adipogenesis trans-differentiation of C2C12 cells. In which, miR-199a was decreased in the adipogenic cells and miR-199a over-expression inhibited the trans-differentiation and decreased lipid accumulation in the cells. Moreover, Fatty acid transport protein 1 (Fatp1), a major regulator of trans-membrane transportation and the oxidative metabolism of free fatty acids, was showed to be a target of miR-199a by computational and luciferase reporter assays. Additionally, Fatp1 knock-down by small interfering RNA had similar inhibitory effects on the trans-differentiation in C2C12 cells. Conclusion: Our study reveals an important role for miR-199a in the regulation of adipogenic trans-differentiation in muscle cells via suppression of Fatp1 gene.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2016
    detail.hit.zdb_id: 1482056-0
    SSG: 12
    SSG: 15,3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...