bluuebunny/crossref_metadata_2025_split huggingface dataset:
Lactoferricin mediates anabolic and anti‐catabolic effects in the intervertebral disc
Authors: Kim Jae‐Sung , Ellman Michael B. , An Howard S. , Yan Dongyao , van Wijnen Andre J. , Murphy Gillian , Hoskin David W. , Im Hee‐Jeong 
Published: June 2011

AbstractLactoferricin (LfcinB) antagonizes biological effects mediated by angiogenic and catabolic growth factors, in addition to pro‐inflammatory cytokines and chemokines in human endothelial cells and tumor cells. However, the effect of LfcinB on intervertebral disc (IVD) cell metabolism has not yet been investigated. Using bovine nucleus pulposus (NP) cells, we analyzed the effect of LfcinB on proteoglycan (PG) accumulation, PG synthesis, and anabolic gene expression. We assessed expression of genes for matrix‐degrading enzymes such as matrix metalloproteases (MMPs) and a disintegrin‐like and metalloprotease with thrombospondin motifs (ADAMTS family), as well as their endogenous inhibitors, tissue inhibitor of metalloproteases (TIMPs). In order to understand the specific molecular mechanisms by which LfcinB exerts its biological effects, we investigated intracellular signaling pathways in NP cells. LfcinB increased PG accumulation mainly via PG synthesis in a dose‐dependent manner. Simultaneously, LfcinB dose‐dependently downregulated catabolic enzymes. LfcinB's anti‐catabolic effects were further demonstrated by a dose‐dependent increase in multiple TIMP family members. Our results demonstrate that ERK and/or p38 mitogen‐activated protein kinase pathways are the key signaling cascades that exert the biological effects of LfcinB in NP cells, regulating transcription of aggrecan, SOX‐9, TIMP‐1, TIMP‐2, TIMP‐3, and iNOS. Our results suggest that LfcinB has anabolic and potent anti‐catabolic biological effects on bovine IVD cells that may have considerable promise in the treatment of disc degeneration in the future. J. Cell. Physiol. 227: 1512–1520, 2012. © 2011 Wiley Periodicals, Inc.
Reduction of ribosome biogenesis with activation of the mTOR pathway in denervated atrophic muscle
Authors: Machida Masanao , Takeda Kohei , Yokono Hiroyuki , Ikemune Sachiko , Taniguchi Yuka , Kiyosawa Hidenori , Takemasa Tohru 
Published: June 2011

AbstractMammalian target of rapamycin (mTOR) pathway positively regulates the cell growth through ribosome biogenesis in many cell type. In general, myostatin is understood to repress skeletal muscle hypertrophy through inhibition of mTOR pathway and myogenesis. However, these relationships have not been clarified in skeletal muscle undergoing atrophy. Here, we observed a significant decrease of skeletal muscle mass at 2 weeks after denervation. Unexpectedly, however, mTOR pathway and the expression of genes related to myogenesis were markedly increased, and that of myostatin was decreased. However, de novo ribosomal RNA synthesis and the levels of ribosomal RNAs were dramatically decreased in denervated muscle. These results indicate that ribosome biogenesis is strongly controlled by factors other than the mTOR pathway in denervated atrophic muscle. Finally, we assessed rRNA transcription factors expression and observed that TAFIa was the only factor decreased. TAFIa might be a one of the limiting factor for rRNA synthesis in denervated muscle. J. Cell. Physiol. 227: 1569–1576, 2012. © 2011 Wiley Periodicals, Inc.
Human peripheral blood CD34‐positive cells enhance therapeutic regeneration of chronically injured liver in nude rats
Authors: Nakamura Toru , Tsutsumi Victor , Torimura Takuji , Naitou Masako , Iwamoto Hideki , Masuda Hiroshi , Hashimoto Osamu , Koga Hironori , Abe Mitsuhiko , Ii Masaaki , Kawamoto Atsuhiko , Asahara Takayuki , Ueno Takato , Sata Michio 
Published: June 2011

AbstractWe investigated whether transplantation of purified human peripheral blood CD34+ cells could reduce established liver fibrosis and up‐regulate therapeutic regeneration. Human peripheral blood CD34+ cells were isolated from total mononuclear cells of healthy volunteers by magnetic cell sorting. Recipient nude rats were injected intraperitoneally with carbon tetrachloride (CCl4) twice weekly for 3 weeks before single administration of CD34+ cells. CCl4 was then re‐administered twice weekly for 3 more weeks, and the nude rats were sacrificed. Saline (control group), 1 × 105 (low‐dose group), 5 × 105 (middle‐dose group), or 2 × 106 (high‐dose group) CD34+ cells/kg body weight were intrasplenically transplanted after CCl4 treatment for 3 weeks. Reverse transcriptase‐polymerase chain reaction analysis of the freshly isolated CD34+ cells revealed the expression of CD31, keratin19, α‐smooth muscle actin (α‐SMA), and epithelial growth factor, but not other liver related markers. The transplanted cells differentiated into vascular and sinusoidal endothelial cells, and vascular smooth muscle cells. CD34+ cell transplantation reduced liver fibrosis in a dose‐dependent fashion, with decreased collagen type‐I and α‐SMA‐positive cells after 6 weeks of CCl4 treatment by Mallory's Azan and immunohistochemical staining. Gelatin zymography showed that the expression levels of active matrix metalloproteinase‐2 and ‐9 in CD34+ cell transplanted livers were significantly stronger than those in saline‐infused livers. In recipients of high‐doses of CD34+ cells, the number of PCNA‐positive hepatocyte increased 6 weeks after CCl4 treatment compared with saline‐infused livers. We conclude that human peripheral blood CD34+ cell transplantation halts established liver fibrosis and promotes hepatic regeneration in CCl4‐induced chronic liver injury. J. Cell. Physiol. 227: 1538–1552, 2012. © 2011 Wiley Periodicals, Inc.
Interplay between membrane lipid peroxidation, transglutaminase activity, and Cyclooxygenase 2 expression in the tissue adjoining to breast cancer
Authors: Balestrieri Maria Luisa , Dicitore Alessandra , Benevento Raffaella , Di Maio Massimo , Santoriello Antonio , Canonico Silvestro , Giordano Antonio , Stiuso Paola 
Published: June 2011

AbstractBreast cancer, a leading cause of cancer related deaths worldwide, is one of the most common neoplasms in women. The increased generation of reactive oxygen species (ROS) in breast lesion is critically involved in the mutagenic processes that drive to breast carcinoma initiation and progression. To date, the molecular events occurring in the tissue adjoin the cancer lesion have not been elucidated. Here, we investigated the role of excess ROS generation during human breast carcinogenesis by evaluating oxidative stress biomarkers, tissue transglutaminase (t‐TGase) activity, and expression levels of ubiquitin and cyclooxygenase‐2 (COX‐2) in the normal tissue adjoin to fibroadenoma (nFA), atypical ductal hyperplasia (nADH), and invasive ductal carcinoma (nIDC) from 45 breast cancer patients. We found that lipid peroxidation and nitric oxide production significantly increased in nIDC respect to nFA and nADH (P < 0.005) whereas the 4‐hydroxy‐2‐nonenal (HNE) protein‐adducts increased only in nADH (P < 0.005). The increased lipid damage observed in nIDC correlates with estrogen receptor exposure in IDC (R2 = 0.89). Moreover, nIDC and invasive ductal carcinoma (IDC) showed a 10‐fold higher t‐TGase activity compared to nFA and nADH. Contrary, COX‐2 expression levels significantly decreased nIDC and IDC respect to the nFA and nADH (P < 0.001). The analysis of the free ubiquitin expression revealed equal levels in nADH and nIDC samples whereas high molecular weight‐ubiquitin conjugate increased about fivefold only in nIDC (P < 0.01 vs. nADH). These novel findings reveal an interplay between membrane lipid peroxidation, t‐TGase activity, and COX‐2 expression levels in the tissue adjoining to neoplastic lesion during breast cancer progression. J. Cell. Physiol. 227: 1577–1582, 2012. © 2011 Wiley Periodicals, Inc.
Transactivation of EGFR/PI3K/Akt involved in ATP‐induced inflammatory protein expression and cell motility
Authors: Lin Chih‐Chung , Lin Wei‐Ning , Cheng Shin‐Ei , Tung Wei‐Hsuan , Wang Hui‐Hsin , Yang Chuen‐Mao 
Published: June 2011

AbstractPhenotype transition of vascular smooth muscle cells (VSMCs) is important in vascular diseases, such as atherosclerosis and restenosis. Once released, ATP may promote activation of VSMCs by stimulating cyclooxygenase‐2 (COX‐2), cytosolic phospholipase A2 (cPLA2) expression and prostaglandin (PG)E2 synthesis via activation of MAPKs and NF‐κB. However, whether alternative signaling pathways participated in regulating COX‐2 and cPLA2 expression associated with cell migration were investigated in rat VSMCs. Western blot analysis, RT‐PCR, promoter assay and PGE2 ELISA were used to determine expression of COX‐2, cPLA2 and PGE2. Specific inhibitors and siRNAs against various protein kinases or transcription factors were used to investigate the related signaling components in inflammatory protein induction by ATPγS. We found that ATPγS‐induced COX‐2 and cPLA2 expression and PGE2 release was attenuated by the pharmacological inhibitors or transfection with siRNA against PKCδ, c‐Src, EGFR, PI3‐K, Akt, p44/p42 MAPK or Elk‐1. Moreover, ATPγS‐stimulated phosphorylation of PKCδ, c‐Src, EGFR, Akt, p42/p44 MAPK and Elk‐1, suggesting the participation of PKCδ/c‐Src/EGFR/PI3‐K/Akt/p42/p44 MAPK cascade in mediating Elk‐1 activities in VSMCs. In addition, migration assay revealed that ATPγS promoted cell mobility through up‐regulation of COX‐2 and cPLA2 expression and PGE2 release, which was attenuated by pretreatment with PGE2 receptor antagonists. Taken together, these data showed that ATPγS up‐regulated the expression of COX‐2 and cPLA2 through transactivation of PKCδ/c‐Src/EGFR/PI3K/Akt/Elk‐1 pathway. Newly synthesized PGE2 acted on its receptors to promote cell motility of ATPγS‐stimulated VSMCs. J. Cell. Physiol. 227: 1628–1638, 2012. © 2011 Wiley Periodicals, Inc.
Angiogenin inhibits nuclear translocation of apoptosis inducing factor in a Bcl‐2‐dependent manner
Authors: Li Shuping , Yu Wenhao , Hu Guo‐Fu 
Published: June 2011

AbstractLoss‐of‐function mutations in angiogenin (ANG) gene were discovered in amyotrophic lateral sclerosis (ALS) patients and ANG has been shown to prevent neuronal death both in vitro and in vivo. The neuro‐protective activity of ANG was brought about partially by inhibiting stress‐induced apoptosis. ANG attenuates both the extrinsic and the intrinsic apoptotic signals by activating Nf‐κb‐mediated cell survival pathway and Bcl‐2‐mediated anti‐apoptotic pathway. Here we report that ANG inhibits nuclear translocation of apoptosis inducing factor (AIF), an important cell death‐executing molecule known to play a dominant role in neurodegenerative diseases. ANG inhibits serum withdrawal‐induced apoptosis by attenuating a series of Bcl‐2‐dependent events including caspase‐3 activation, poly ADP‐ribose polymerase‐1 (PARP‐1) cleavage, and AIF nuclear translocation. J. Cell. Physiol. 227: 1639–1644, 2012. © 2011 Wiley Periodicals, Inc.
Identification of RUNX3 as a component of the MST/Hpo signaling pathway
Authors: Min Boram , Kim Min‐Kyu , Zhang Joo‐Won , Kim Jiyeon , Chung Kwang‐Chul , Oh Byung‐Chul , Stein Gary S. , Lee Yong‐Hee , van Wijnen Andre J. , Bae Suk‐Chul 
Published: June 2011

AbstractRecent genetic screens of fly mutants and molecular analysis have revealed that the Hippo (Hpo) pathway controls both cell proliferation and cell death. Deregulation of its human counterpart (the MST pathway) has been implicated in human cancers. However, how this pathway is linked with the known tumor suppressor network remains to be established. RUNX3 functions as a tumor suppressor of gastric cancer, lung cancer, bladder cancer, and colon cancer. Here, we show that RUNX3 is a principal and evolutionarily conserved component of the MST pathway. SAV1/WW45 facilitates the close association between MST2 and RUNX3. MST2, in turn, stimulates the SAV1–RUNX3 interaction. In addition, we show that siRNA‐mediated RUNX3 knockdown abolishes MST/Hpo‐mediated cell death. By establishing that RUNX3 is an endpoint effector of the MST pathway and that RUNX3 is capable of inducing cell death in cooperation with MST and SAV1, we define an evolutionarily conserved novel regulatory mechanism loop for tumor suppression in human cancers. J. Cell. Physiol. 227: 839–849, 2012. © 2011 Wiley Periodicals, Inc.
PML expression in soft tissue sarcoma: Prognostic and predictive value in alkylating agents/antracycline‐based first line therapy
Authors: Vincenzi Bruno , Santini Daniele , Schiavon Gaia , Frezza Anna Maria , Silletta Marianna , Crucitti Pierfilippo , Casali Paolo , Tos Angelo P. Dei , Rossi Sabrina , Rizzo Sergio , Badalamenti Giuseppe , Tomasino Rosa Maria , Russo Antonio , Butrynski James E. , Tonini Giuseppe 
Published: June 2011

AbstractSoft tissue sarcomas are aggressive tumors representing <1% of all adult neoplasms. Aim of our study was to evaluate promyelocytic leukemia gene expression value as prognostic factor and as a factor predicting response to alkylating agents/antracycline‐based first line therapy. One hundred eleven patients affected by locally advanced and metastatic soft tissue sarcoma were selected. PML expression was evaluated by immunohistochemical analysis in pathological samples and in the corresponding normal tissue from each case. PML immunohistochemical results were correlated with prognosis and with radiological response to alkylating agents/antracycline‐based first line therapy. PML expression was significantly reduced in synovial sarcomas (P < 0.0001), in myofibroblastic sarcomas (P < 0.0001), angiosarcomas (P < 0.0001), in leiomyosarcomas (P = 0.003), in mixoid liposarcomas (P < 0.0001), and in dedifferentiated liposarcomas (P < 0.0001). No significant difference was found for pleomorphic sarcoma [31.8 (95% CI: 16.7–41.0); P = 0.21]. and pleomorphic liposarcomas (P = 0.51). Loss of PML expression was found to be statistically correlated with TTP (P < 0.0001), median duration of response (P = 0.007), and OS (P = 0.02). No correlation was observed between PML expression and treatment efficacy. PML IHC expression is down‐regulated in synovial sarcomas, myofibroblastic sarcomas, angiosarcomas, liposarcoma, and leiomyosarcomas and its expression correlated with prognosis. J. Cell. Physiol. 227: 1657–1662, 2012. © 2011 Wiley Periodicals, Inc.
The phenotype and functional alterations of macrophages in mice with hyperglycemia for long term
Authors: Sun Chenming , Sun Lina , Ma Haixia , Peng Jianxia , Zhen Yu , Duan Kaizhong , Liu Guangwei , Ding Wenjun , Zhao Yong 
Published: June 2011

AbstractAbnormal immunity and its related complications are the major causes of mortality and morbidity in diabetes patients. Macrophages, as one of the important innate cells, play pivotal roles in controlling immune homeostasis, immunity, and tolerance. The effects of hyperglycemia on the function of macrophages in hosts remain to be determined. Here we used mice with streptozotocin (STZ)‐induced diabetes for long term to study the changes of macrophages. We found that F4/80+ peritoneal exudate macrophages (PEMs) from mice with diabetes for 4 months displayed significantly reduced CD86 and CD54 expression and tumor necrosis factor (TNF)‐α and IL‐6 production but enhanced nitric oxide (NO) secretion compared with control mice when treated with interferon (IFN)‐γ and lipopolysaccharide (LPS), while the activity of arginase in PEMs from diabetic mice was significantly higher than control mice when stimulating with IL‐4. These dysfunctions of macrophages could be efficiently reversed by insulin treatment. Importantly, in vitro bone marrow‐derived macrophages showed similar functional changes, indicating the epigenetic alteration of macrophage precursors in these mice. In an in vitro culture system, high glucose and insulin significantly altered TNF‐α, IL‐6, and NO production and arginase activity of macrophages, which was reversed by the treatment with AKT and ERK inhibitors. Therefore, hyperglycemia and insulin deficiency can modify macrophage function through AKT‐mTOR and ERK pathways and through epigenetic effects on macrophage precursors. To further identify different components of diabetes on the dysfunction of macrophages is important for efficient prevention of diabetic complications. J. Cell. Physiol. 227: 1670–1679, 2012. © 2011 Wiley Periodicals, Inc.
Human mesenchymal stem cell differentiation to the osteogenic or adipogenic lineage is regulated by AMP‐activated protein kinase
Authors: Kim Eung‐Kyun , Lim Seyoung , Park Ji‐Man , Seo Jeong Kon , Kim Jae Ho , Kim Kyong Tai , Ryu Sung Ho , Suh Pann‐Ghill 
Published: June 2011

AbstractAMP‐activated protein kinase (AMPK) is an energy‐sensing kinase that has recently been shown to regulate the differentiation of preadipocytes and osteoblasts. However, the role of AMPK in stem cell differentiation is largely unknown. Using in vitro culture models, the present study demonstrates that AMPK is a critical regulatory factor for osteogenic differentiation. We observed that expression and phosphorylation of AMPK were increased during osteogenesis in human adipose tissue‐derived mesenchymal stem cells (hAMSC). To elucidate the role of AMPK in osteogenic differentiation, we investigated the effect of AMPK inhibition or knockdown on mineralization of hAMSC. Compound C, an AMPK inhibitor, reduced mineralized matrix deposition and suppressed the expression of osteoblast‐specific genes, including alkaline phosphatase (ALP), runt‐related transcription factor 2 (RUNX2), and osteocalcin (OCN). Knockdown of AMPK by shRNA‐lentivirus infection also reduced osteogenesis. In addition, inhibition or knockdown of AMPK during osteogenesis inhibited ERK phosphorylation, which is required for osteogenesis. Interestingly, inhibition of AMPK induced adipogenic differentiation of hAMSC, even in osteogenic induction medium (OIM). These results provide a potential mechanism involving AMPK activation in osteogenic differentiation of hAMSC and suggest that commitment of hAMSC to osteogenic or adipogenic lineage is governed by activation or inhibition of AMPK, respectively. J. Cell. Physiol. 227: 1680–1687, 2012. © 2011 Wiley Periodicals, Inc.
A viable technology to generate third‐generation biofuel
Authors: Singh Anoop , Olsen Stig Irving , Nigam Poonam Singh 
Published: June 2011

AbstractFirst generation biofuels are widely available because the production technologies are well developed. However, growth of the raw materials conflicts with food security, so that first‐ generation biofuels are not so promising. The second generation of biofuels will not compete directly with food but requires several energy intensive processes to produce them, and also increases land‐use change, which reduces its environmental and economic feasibility. The production of third‐generation biofuels avoids the issues met with first‐ and second‐ generation biofuels, namely food–fuel competition, land‐use change, etc., and is thus considered a viable alternative energy resource. On all dimensions of sustainability (environmental, social and economical), a life cycle assessment approach is most relevant to avoid issues in problem shifting. The utilization of organic waste and carbon dioxide in flue gases for the production of biomass further increases the sustainability of third generation biofuels, as it minimizes greenhouse gas emissions and disposal problems. Copyright © 2011 Society of Chemical Industry
Effect of pre‐treatments based on UV photocatalysis and photo‐oxidation on toluene biofiltration performance
Authors: Palau Jordi , Penya‐Roja Josep M. , Gabaldón Carmen , Álvarez‐Hornos Francisco Javier , Martínez‐Soria Vicente 
Published: June 2011

AbstractBACKGROUND: The integration of UV photocatalysis and biofiltration seems to be a promising combination of technologies for the removal of hydrophobic and poorly biodegradable air pollutants. The influence of pre‐treatments based on UV254 nm photocatalysis and photo‐oxidation on the biofiltration of toluene as a target compound was evaluated in a controlled long‐term experimental study using different system configurations: a standalone biofilter, a combined UV photocatalytic reactor‐biofilter, and a combined UV photo‐oxidation reactor (without catalyst)‐biofilter.RESULTS: Under the operational conditions used (residence time of 2.7 s and toluene concentrations 600–1200 mg C m−3), relatively low removal efficiencies (6–3%) were reached in the photocatalytic reactor and no degradation of toluene was found when the photo‐oxidation reactor was operated without catalyst. A noticeable improvement in the performance of the biofilter combined with a photocatalytic reactor was observed, and the elimination capacity of the biological process increased by more than 12 g C h−1 m−3 at the inlet loads studied of 50–100 g C h−1 m−3. No positive effect on toluene removal was observed for the combination of UV photoreactor and biofilter.CONCLUSIONS: Biofilter pre‐treatment based on UV254 nm photocatalysis showed promising results for the removal of hydrophobic and recalcitrant air pollutants, providing synergistic improvement in the removal of toluene. Copyright © 2011 Society of Chemical Industry
MRT letter: Nanoscopy of protein colocalization in living cells by STED and GSDIM
Authors: Lalkens Birka , Testa Ilaria , Willig Katrin I. , Hell Stefan W. 
Published: June 2011

AbstractWe report the use of superresolution fluorescence microscopy for studying the nanoscale distribution of protein colocalization in living mammalian cells. Nanoscale imaging is attained both by a targeted and a stochastic fluorescence on‐off switching superresolution method, namely by stimulated emission depletion (STED) and ground state depletion microscopy followed by individual molecular return (GSDIM), respectively. Analysis of protein colocalization is performed by bimolecular fluorescence complementation (BiFC). Specifically, a nonfluorescent fragment of the yellow fluorescent protein Citrine is fused to tubulin while a counterpart nonfluorescent fragment is fused to the microtubulin‐associated protein MAP2 such that fluorescence is reconstituted on contact of the fragment‐carrying proteins. Images with resolution down to 65 nm prove a powerful new way for studying protein colocalization in living cells at the nanoscale. Microsc. Res. Tech., 2012. © 2011 Wiley Periodicals, Inc.
Transmission electron microscopy as a tool to image bioinorganic nanohybrids: The case of phage‐gold nanocomposites
Authors: Cao Binrui , Xu Hong , Mao Chuanbin 
Published: June 2011

AbstractIn recent years, bioinorganic nanohybrids composed of biological macromolecules and functional inorganic nanomaterials have revealed many unique properties that show promise for the future. Transmission electron microscopy (TEM) is a popular and relatively simple tool that can offer a direct visualization of the nanomaterials with high resolutions. When TEM is applied to visualize bioinorganic nanohybrids, a treatment of negative staining is necessary due to the presence of biological molecules in the nanohybrids except for those with densely packed inorganic materials. However, the conventional negative‐staining procedure for regular biological samples cannot be directly applied to such bioinorganic nanohybrids. To image a specific bioinorganic nanohybrid, negative‐staining factors such as negative stain type, working pH, staining time, and drying method, should be identified. Currently, no detailed studies have been done to investigate how to adjust negative‐staining factors based on specific bioinorganic nanohybrids. In this study, bacteriophage‐gold nanoparticle hybrids were chosen as a model to systematically study the effects of each factor on the negative staining of the nanohybrids. The best staining conditions for gold nanoparticle‐phage nanohybrids were obtained and the effects of each factor on the negative staining of general nanohybrids were discussed. This work indicates that with proper staining it is possible to use TEM to visualize directly both biological and inorganic components without introducing any artifact. Microsc. Res. Tech. 2011. © 2011 Wiley‐Liss, Inc.