首页期刊导航|Cell biology international.
期刊信息/Journal information
Cell biology international.
John Wiley & Sons,
Cell biology international.

John Wiley & Sons,

1065-6995

Cell biology international./Journal Cell biology international.
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    2页
      原文链接:
    • NSTL

    The role of metal ions in the Golgi apparatus

    Jiayin GaoAnbo GaoHong ZhouLinxi Chen...
    11页
    查看更多>>摘要：Abstract The Golgi apparatus is a membrane‐bound organelle that functions as a central role in the secretory pathway. Since the discovery of the Golgi apparatus, its structure and function have attracted ever‐increasing attention from researchers. Recently, it has been demonstrated that metal ions are necessary for the Golgi apparatus to maintain its proper structure and functions. Given that metal ions play an important role in various biological processes, their abnormal homeostasis is related to many diseases. Therefore, in this paper, we reviewed the uptake and release mechanisms of the Golgi apparatus Ca2+, Cu, and Zn2+. Furthermore, we describe the diseases associated with Golgi apparatus Ca2+, Cu, and Zn2+ imbalance.
      原文链接:
    • NSTL
    • Wiley

    siRNA‐based nanotherapeutics as emerging modalities for immune‐mediated diseases: A preliminary review

    Saman SargaziRabia ArshadReza GhamariAbbas Rahdar...
    25页
    查看更多>>摘要：Abstract Immune‐mediated diseases (IMDs) are chronic conditions that have an immune‐mediated etiology. Clinically, these diseases appear to be unrelated, but pathogenic pathways have been shown to connect them. While inflammation is a common occurrence in the body, it may either stimulate a favorable immune response to protect against harmful signals or cause illness by damaging cells and tissues. Nanomedicine has tremendous promise for regulating inflammation and treating IMIDs. Various nanoparticles coated with nanotherapeutics have been recently fabricated for effective targeted delivery to inflammatory tissues. RNA interference (RNAi) offers a tremendous genetic approach, particularly if traditional treatments are ineffective against IMDs. In cells, several signaling pathways can be suppressed by using RNAi, which blocks the expression of particular messenger RNAs. Using this molecular approach, the undesirable effects of anti‐inflammatory medications can be reduced. Still, there are many problems with using short‐interfering RNAs (siRNAs) to treat IMDs, including poor localization of the siRNAs in target tissues, unstable gene expression, and quick removal from the blood. Nanotherapeutics have been widely used in designing siRNA‐based carriers because of the restricted therapy options for IMIDs. In this review, we have discussed recent trends in the fabrication of siRNA nanodelivery systems, including lipid‐based siRNA nanocarriers, liposomes, and cationic lipids, stable nucleic acid‐lipid particles, polymeric‐based siRNA nanocarriers, polyethylenimine (PEI)‐based nanosystems, chitosan‐based nanoformulations, inorganic material‐based siRNA nanocarriers, and hybrid‐based delivery systems. We have also introduced novel siRNA‐based nanocarriers to control IMIDs, such as pulmonary inflammation, psoriasis, inflammatory bowel disease, ulcerative colitis, rheumatoid arthritis, etc. This study will pave the way for new avenues of research into the diagnosis and treatment of IMDs.
      原文链接:
    • NSTL
    • Wiley

    tert‐Butylhydroquinone‐induced formation of high‐molecular‐weight p62: A novel mechanism in the activation of Nrf2‐Keap1

    Yunfang ChenHua CaoWan HeXi Zhang...
    10页
    查看更多>>摘要：Abstract The respiratory system is always exposed to air and is most vulnerable to attack by environmental free radicals. The nuclear factor E2‐related factor 2–Kelch‐like ECH‐associated protein 1–antioxidant response element (Nrf2‐Keap1‐ARE) pathway and p62 are both involved in the oxidative stress response. However, the interplay between these two systems remains largely unknown. This study shows that treatment of L2 cells with tert‐Butylhydroquinone (tBHQ) generates a high‐molecular‐weight (HMW) form of p62, leading to activation of the Nrf2‐Keap1‐ARE pathway. The levels of HMW‐p62 increased as the tBHQ concentration increased, with concomitant decreases seen in the classical form of p62. Moreover, small interfering RNA targeting p62 increases Keap1 protein levels and inactivates the Nrf2‐Keap1‐ARE pathway. These results demonstrate that the Nrf2‐Keap1 pathway is partially regulated by p62. tBHQ‐induced HMW‐p62 production may be a novel mechanism in the activation of the Nrf2‐Keap1‐ARE pathway.
      原文链接:
    • NSTL
    • Wiley

    Hydrogen sulfide prevents arecoline‐induced neurotoxicity via promoting leptin/leptin receptor signaling pathway

    Xiang ChengJia‐Mei JiangChun‐Yan WangWei Zou...
    12页
    查看更多>>摘要：Abstract Arecoline, a major alkaloid of the areca nut, has potential toxicity to the nervous system. Our previous study reveals that the neurotoxicity of arecoline involves in?inhibited endogenous hydrogen sulfide (H2S) generation. Therefore, the present study investigated whether exogenous H2S protects against arecoline‐induced neurotoxicity and further explore the underlying mechanisms focusing on leptin/leptin receptor signaling pathway. The cell viability was measured by CCK‐8 kit. The apoptosis were detected by Hoechst 33258 and Annexin V/PI (propidium iodide) staining. The protein expressions were determined by Western blot analysis. Our results demonstrated that NaHS, an exogenous H2S donor, significantly increases the cell viability, decreases apoptosis ratio, and reduces caspase‐3 activity as well as Bax/Bcl‐2 ratio in PC12 cells exposed to arecoline, indicating the protection of H2S against arecoline‐induced cytotoxicity and apoptosis. Also, NaHS attenuated arecoline‐induced endoplasmic reticulum (ER) stress, as evidenced by the decreases in the expressions of glucose‐regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), and Cleaved caspase‐12. Meanwhile, NaHS promoted leptin/leptin receptor signaling pathway in arecoline‐exposed PC12 cells, as illustrated by upregulations of leptin and leptin receptor expressions. Furthermore, leptin tA, an antagonist of leptin receptor, obviously abolished the inhibitory effects of NaHS on arecoline‐induced cytotoxicity, apoptosis, and ER stress in arecoline‐exposed PC12 cells. Taken together, these results suggested that H2S prevents arecoline‐induced neurotoxicity via enhancing the leptin/leptin receptor signaling pathway.
      原文链接:
    • NSTL
    • Wiley

    Calycosin suppresses colorectal cancer progression by targeting ERβ, upregulating PTEN, and inhibiting PI3K/Akt signal pathway

    Lin ZhuSha LiuYi‐Fan LiaoYan‐Mei Sheng...
    11页
    查看更多>>摘要：Abstract High intake of phytoestrogen has been reported to be associated with the prevention of colorectal cancer (CRC). Calycosin belongs to the phytoestrogen that has been shown to suppress CRC cells in our previous study. However, its anticancer activity and molecular mechanisms have not been elucidated. In this study, we analyzed the effect of calycosin on the viability and apoptosis of human CRC HCT116 and SW480 cells via MTT assay, flow cytometry assay, and caspase‐3/7 activity assay. The protein expressions of estrogen receptor β (ERβ), PTEN, and PI3K/Akt signal pathways were determined by Western blot analysis. And then, the alterations of biological behavior in CRC cells transfected with ERβ siRNA were analyzed. Mouse xenograft models were further performed to detect the antitumor effect in vivo.?The results show that calycosin reduces CRC cell viability, induces cell apoptosis, and suppresses xenograft tumor growth. The protein expressions of ERβ and PTEN are significantly upregulated following calycosin treatment, whereas p‐AKT/AKT ratio and Bcl‐2 level are downregulated. Suppressing ERβ with siRNA partially attenuates the reduction in viability and apoptosis induced by calycosin. Our results indicate that calycosin shows inhibitory effects on CRC cells, which might be obtained by targeting ERβ, upregulating PTEN, and inhibiting the PI3K/Akt signal pathway.
      原文链接:
    • NSTL
    • Wiley

    Potential proteomic alteration in the brain of Tg(SOD1*G93A)1Gur mice: A new pathogenesis insight of amyotrophic lateral sclerosis

    Chunyan TangWeiming GanRenshi XuJie Zhang...
    21页
    查看更多>>摘要：Abstract The pathogenesis of amyotrophic lateral sclerosis (ALS) remains unclear. The recent studies have suggested that the protein abnormalities could play some important roles in ALS because several protein mutations were found in individuals with this disease. However, proteins that are currently known to be associated with ALS only explain the pathogenesis of this disease in a minority of cases, thus, further screening is needed to identify other ALS‐related proteins. In this study, we systematically analyzed and compared the brain proteomic alterations between a mouse model of ALS, the Tg(SOD1*G93A)1Gur model, and wild‐type mice using isobaric tags for relative and absolute quantitation (iTRAQ) as well as bioinformatics methods. The results revealed some significant up‐ and downregulated proteins at the different developmental stages in the ALS‐like mice as well as the possibly related cellular components, molecular functions, biological processes, and pathways in the development of ALS. Our results identified some possible proteins that participate in the pathogenesis of ALS as well as the cellular components that are damaged by these proteins, we additionally identified the molecular functions, the biological processes, and the pathways of these proteins as well as the molecules that are associated with these pathways. This study represents an important preliminary investigation of the role of proteomic abnormalities in the pathogenesis of ALS, both in human patients and other animal models. We present some novel findings that may serve as a basis for further investigation of abnormal proteins that are involved in the pathogenesis of ALS.
      原文链接:
    • NSTL
    • Wiley

    PIK3CB promotes oesophageal cancer proliferation through the PI3K/AKT/mTOR signalling axis

    Wei XuZhiqiang WangZhi ZhangJian Xu...
    10页
    查看更多>>摘要：Abstract PIK3CB is abnormally expressed in various carcinomas and affects the proliferation, invasion?and drug resistance of cancer cells. However, its role in oesophageal squamous cell carcinoma (ESCC) is still unclear. In this study, PIK3CB was found to be highly expressed in ESCC tissues and cells and positively correlated with the poor prognosis of ESCC. Silencing PIK3CB inhibited the proliferation of ESCC cells, arrested the cell cycle, and promoted apoptosis. Mechanistic studies showed that the tumour‐promoting effect of PIK3CB was achieved through PI3K/AKT/mTOR signalling pathway activation. Moreover, the high PIK3CB expression level in ESCC may be closely associated with the hypomethylation status of the gene promoter. In conclusion, PIK3CB promotes ESCC by activating the PI3K/AKT/mTOR signalling axis. PIK3CB may be a potential target in ESCC.
      原文链接:
    • NSTL
    • Wiley

    LMCD1 facilitates the induction of pluripotency via cell proliferation, metabolism, and epithelial‐mesenchymal transition

    Zhikai YeGe ChenCuicui HouZhenlong Jiang...
    14页
    查看更多>>摘要：Abstract Somatic cell reprogramming was achieved by lentivirus mediated overexpression of four transcription factors called OSKM: OCT3/4, SOX2, KLF4, and c‐MYC but it was not very efficient. Here, we reported that the transcription factor, LMCD1 (LIM and cysteine rich domains 1) together with OSKM can induce reprogramming of human dermal fibroblasts into induced pluripotent stem cells (iPSCs) more efficiently than OSKM alone. At the same time, the number of iPSCs clones were reduced when we knocked down LMCD1. Further study showed that LMCD1 can enhance the cell proliferation, the glycolytic capability, the epithelial‐mesenchymal transition (EMT), and reduce the epigenetic barrier by upregulating epigenetic factors (EZH2, WDR5, BMI1, and KDM2B) in the early stage of reprogramming, making the cells more accessible to gain pluripotency. Additional research suggested that LMCD1 can not only inhibit the developmental gene GATA6, but also promote multiple signaling pathways, such as AKT and glycolysis, which are closely related to reprogramming efficiency. Therefore, we identified the novel function of the transcription factor LMCD1, which reduces the barriers of the reprogramming from somatic to pluripotent cells in several ways in the early stage of reprogramming.
      原文链接:
    • NSTL
    • Wiley

    CoCl2‐simulated hypoxia potentiates the osteogenic differentiation of fibroblasts derived from?tympanosclerosis by upregulating the expression of BMP‐2

    Chen ZhangYang‐Wenyi LiuMin ChenShiyao Min...
    10页
    查看更多>>摘要：Abstract Tympanosclerosis (TS) is a result of long‐standing middle ear inflammation characterized by fibroblasts ossification. Fibrosis is the last revertible stage in the progress of middle ear inflammation to TS. It was hypothesized that chronic hypoxia could be modulating fibrosis, which in turn additionally further aggravated hypoxia via decreasing oxygen diffusion. However, the effects of hypoxia on osteoinductive activity of fibroblasts have not been explored. Herein, we purposed to explore the role of hypoxia in osteogenic differentiation of fibroblasts derived from TS. The expression of bone morphogenetic protein‐2 (BMP‐2), hypoxia‐inducible factor‐1α (HIF‐1α), and Vimentin in the human surgical specimens of tympansclerosis was investigated by immunofluorescent staining. Furthermore, cultured fibroblasts were stratified into the following study groups: control, 25, 50, and 100?μM cobaltous chloride (CoCl2) group. BMP‐2, as well as HIF‐1α levels of expression were detected via western blotting and immunofluorescence analysis. We found that the expression of BMP‐2 and HIF‐1α was significantly upregulated in TS tissues and these fibroblasts, which was vimentin positive surrounding sclerotic plaques, were also expressing HIF‐1α positive. The results also demonstrated that CoCl2 treatment increased nuclear HIF‐1α protein level in the fibroblast. Furthermore, treatment with CoCl2 significantly increased BMP‐2 expression and remarkably elevated alkaline phosphatse activity and the mineralized nodules area. These data illustrate that hypoxia may play an osteogenic role in TS fibroblasts via the elevated expression of a possible osteogenic factor, BMP‐2.
      原文链接:
    • NSTL
    • Wiley