bluuebunny/crossref_metadata_2025_split huggingface dataset:
Circulating osteogenic cells: Implications for injury, repair, and regeneration
Authors: Pignolo Robert J , Kassem Moustapha 
Published: May 2011

Abstract
The aim of this review is to provide a critical reading of recent literature pertaining to the presence of circulating, fluid-phase osteoblastic cells and their possible contribution to bone formation. We have termed this group of cells collectively as circulating osteogenic precursor (COP) cells. We present evidence for their existence, methods used for their isolation and identification, possible physiological and pathophysiological roles, cellular origins, and possible mechanisms for their migration to target tissues. © 2011 American Society for Bone and Mineral Research
Caspase‐2 deficiency protects mice from diabetes‐induced marrow adiposity
Authors: Coe Lindsay M. , Lippner Dennean , Perez Gloria I. , McCabe Laura R. 
Published: May 2011

AbstractType I (T1) diabetes is an autoimmune and metabolic disease associated with bone loss. Bone formation and density are decreased in T1‐diabetic mice. Correspondingly, the number of TUNEL positive, dying osteoblasts increases in bones of T1‐diabetic mice. Moreover, two known mediators of osteoblast death, TNFα and ROS, are increased in T1‐diabetic bone. TNFα and oxidative stress are known to activate caspase‐2, a factor involved in the extrinsic apoptotic pathway. Therefore, we investigated the requirement of caspase‐2 for diabetes‐induced osteoblast death and bone loss. Diabetes was induced in 16‐week old C57BL/6 caspase‐2 deficient mice and their wild type littermates and markers of osteoblast death, bone formation and resorption, and marrow adiposity were examined. Despite its involvement in extrinsic cell death, deficiency of caspase‐2 did not prevent or reduce diabetes‐induced osteoblast death as evidenced by a twofold increase in TUNEL positive osteoblasts in both mouse genotypes. Similarly, deficiency of caspase‐2 did not prevent T1‐diabetes induced bone loss in trabecular bone (BV/TV decreased by 30 and 50%, respectively) and cortical bone (decreased cortical thickness and area with increased marrow area). Interestingly, at this age, differences in bone parameters were not seen between genotypes. However, caspase‐2 deficiency attenuated diabetes‐induced bone marrow adiposity and adipocyte gene expression. Taken together, our data suggest that caspase‐2 deficiency may play a role in promoting marrow adiposity under stress or disease conditions, but it is not required for T1‐diabetes induced bone loss. J. Cell. Biochem. 112: 2403–2411, 2011. © 2011 Wiley‐Liss, Inc.
Apoptotic osteocytes regulate osteoclast precursor recruitment and differentiation in vitro
Authors: Al‐Dujaili Saja A. , Lau Esther , Al‐Dujaili Hashem , Tsang Kyle , Guenther Axel , You Lidan 
Published: May 2011

AbstractFatigue loading causes a spatial distribution of osteocyte apoptosis co‐localized with bone resorption spaces peaking around microdamage sites. Since osteocytes have been shown to regulate osteoclast formation and activity, we hypothesize that osteocyte apoptosis regulates osteoclastogenesis. In this study, we used serum‐starvation to mimic reduced nutrient transport in microdamaged bone and induce apoptosis in MLO‐Y4 osteocyte‐like cells; conditioned medium was used to apply soluble factors released by apoptotic osteocytes (aOCY) to healthy non‐apoptotic MLO‐Y4 cells. Osteoclast precursor (RAW264.7 monocyte) migration and differentiation were assessed in the presence of conditioned media (CM) from: (A) aOCY, (B) osteocytes treated with apoptosis conditioned medium (i.e., healthy osteocytes in the presence of apoptosis cues; apoptosis CM‐treated osteocytes (atOCY)), and (C) osteocytes treated with non‐apoptosis conditioned medium (i.e., healthy osteocytes in the absence of apoptosis cues; non‐apoptosis CM‐treated osteocytes (natOCY)). Receptor activator for nuclear factor‐κB ligand (RANKL), macrophage colony stimulating factor (M‐CSF), vascular endothelial growth factor (VEGF) and osteoprotegerin (OPG) mRNA, and protein expression were measured. Our findings indicate that soluble factors released by aOCY and atOCY promoted osteoclast precursor migration (up to 64% and 24% increase, respectively) and osteoclast formation (up to 450% and 265% increase, respectively). Osteoclast size increased up to 233% in the presence of aOCY and atOCY CM. Recruitment, formation and size were unaltered by natOCY. RANKL mRNA and protein expression were upregulated only in aOCY, while M‐CSF and VEGF increased in atOCY. Addition of RANKL‐blocking antibody abolished aOCY‐induced osteoclast precursor migration and osteoclast formation. VEGF and M‐CSF blocking antibodies abolished atOCY‐induced osteoclastogenesis. These findings suggest that aOCY directly and indirectly (through atOCY) initiate targeted bone resorption by regulating osteoclast precursor recruitment and differentiation. J. Cell. Biochem. 112: 2412–2423, 2011. © 2011 Wiley‐Liss, Inc.
Analgesic‐antitumor peptide inhibits proliferation and migration of SHG‐44 human malignant glioma cells
Authors: Zhao Youlong , Cai Xueting , Ye Tingmei , Huo Jiege , Liu Chao , Zhang Shuangquan , Cao Peng 
Published: May 2011

AbstractMalignant gliomas, the most common subtype of primary brain tumors, are characterized by high proliferation, great invasion, and neurological destruction and considered to be the deadliest of human cancers. Analgesic‐antitumor peptide (AGAP), one of scorpion toxic polypeptides, has been shown to have antitumor activity. Here, we show that recombinant AGAP (rAGAP) not only inhibits the proliferation of gliomas cell SHG‐44 and rat glioma cell C6, but also suppresses the migration of SHG‐44 cells during wound healing. To explain these phenomena, we find that rAGAP leads to cell cycle of SHG‐44 arrested in G1 phase accompanied by suppressing G1 cell cycle regulatory proteins CDK2, CDK6, and p‐RB by means of the down‐regulated protein expression of p‐AKT. Meanwhile, rAGAP significantly decreases the production of NF‐κB, BCL‐2, p‐p38, p‐c‐Jun, and p‐Erk1/2 and further suppresses the activation of VEGF and MMP‐9 in SHG‐44 cells. These findings suggest rAGAP inhibit proliferation and migration of SHG‐44 cells by arresting cell cycle and interfering p‐AKT, NF‐κB, BCL‐2, and MAPK signaling pathways. J. Cell. Biochem. 112: 2424–2434, 2011. © 2011 Wiley‐Liss, Inc.
Matrix metalloproteinase‐1 induces cleavage of exogenous alphab‐crystallin transduced by a cell‐penetrating peptide
Authors: Yang Seung Won , Lee Seung‐Min , Choi Eun Young , Lee Kyung Hye , Kim Soo Hyuk , Shin Min‐Jeong , Han Ye Sun , Kang Seok‐Min , Chung Ji Hyung 
Published: May 2011

AbstractCell‐penetrating peptides (CPPs), including TAT‐CPP, have been used to deliver exogenous proteins into living cells. Although a number of proteins fused to TAT‐CPP can be delivered into various cells, little is known about the proteolytic cleavage of TAT‐fusion proteins in cells. In this study, we demonstrate that a small heat shock protein (sHSP), alphaB‐crystallin (αB‐crystallin), delivered by TAT‐CPP is susceptible to proteolytic cleavage by matrix metalloproteinase‐1 (MMP‐1) in cardiac myoblast H9c2 cells. Recombinant TAT‐αB‐crystallin was efficiently transduced into H9c2 cells. For a few hours following protein transduction, generation of a 14‐kDa fragment, a cleavage band of TAT‐αB‐crystallin, increased in a time‐dependent manner. This fragment was observed only in detergent‐insoluble fractions. Interestingly, treatment with MMP inhibitors blocked the cleavage of TAT‐αB‐crystallin. In test tubes, recombinant MMP‐1 processed TAT‐αB‐crystallin to generate the major cleavage fragment 14‐kDa, as observed in the cells treated with TAT‐αB‐crystallin. The N‐terminal sequences of the 14‐kDa fragment were identified as Leu‐Arg‐Ala‐Pro‐Ser‐Trp‐Phe, indicating that this fragment is generated by cleavage at Phe54‐Leu55 of αB‐crystallin. The MMP‐1‐selective inhibitor abolished the production of 14‐kDa fragments in cells. In addition, the cleaved fragment of TAT‐αB‐crystallin was significantly reduced in cells transfected with MMP‐1 siRNA. Moreover, the enzymatic activity of MMP‐1 was markedly increased in TAT‐αB‐crystallin‐treated cells. TAT‐αB‐crystallin has a cytoprotective effect on H9c2 cells under hypoxic insult, moreover, MMP‐1‐selective inhibitor treatment led to even increased cell viability. These results suggest that MMP‐1 is responsible for proteolytic cleavage of TAT‐αB‐crystallin during its intracellular transduction in H9c2 cells. J. Cell. Biochem. 112: 2454–2462, 2011. © 2011 Wiley‐Liss, Inc.
Evidence that the kinase‐truncated c‐Src regulates NF‐κB signaling by targeting NEMO
Authors: Dai S. , Abu‐Amer W. , Karuppaiah K. , Abu‐Amer Y. 
Published: May 2011

AbstractThe tyrosine kinase c‐Src and transcription factor NF‐κB are considered crucial components required for normal osteoclastogenesis. Genetic ablation of either pathway leads to detrimental osteopetrotic phenotypes in mice. Similarly, obstruction of either pathway halts osteoclastogenesis and lessens various forms of bone loss. It has been shown previously that mice expressing a kinase domain‐truncated c‐Src, termed Src251, develop severe osteopetrosis owing to increased osteoclast apoptosis. It was further suggested that this phenomenon is associated with reduced Akt kinase activity. However, the precise mechanism underlying the osteoclast inhibitory effect of Src251 remains obscure. C‐Src associates with TRAF6‐p62 interacting with receptor activator of NF‐κB (RANK) distal region and the complex facilitate activation of RANK down stream signal transduction cascades including NF‐κB. Given this proximity between c‐Src and NF‐κB signaling in osteoclasts, we surmised that inhibition of osteoclastogenesis by Src251 may be achieved through inhibition of NF‐κB signaling. We have demonstrated recently that NEMO, the regulatory subunit of the IKK complex, is crucial for osteoclastogenesis and interacts with c‐Src in osteoclast progenitors. Transfection studies, in which we employed various forms of c‐Src and NEMO, revealed that the dominant negative form of c‐Src, namely Src251, mediates degradation of NEMO thus halting NF‐κB signaling. Furthermore, degradation of NEMO requires its intact zinc finger domain which is located at the ubiquitination domain. This process also requires appropriate cellular localization of Src251, since deletion of its myristoylation domain ablates its degradation capacity. Buttressing these findings, the expression of NEMO and NF‐κB signaling were significantly reduced in monocytes collected from Src251 transgenic mice. J. Cell. Biochem. 112: 2463–2470, 2011. © 2011 Wiley‐Liss, Inc.
Induction of autophagy by dimethyl cardamonin is associated with proliferative arrest in human colorectal carcinoma HCT116 and LOVO cells
Authors: Ko Hyeonseok , Kim Young‐Joo , Amor Evangeline C. , Lee Jong Wha , Kim Han‐Cheon , Kim Hee Ju , Yang Hyun Ok 
Published: May 2011

AbstractDimethyl cardamonin (2′,4′‐dihydroxy‐6′‐methoxy‐3′,5′‐dimethylchalcone; DMC) is a naturally occurring chalcone, and it is the major compound isolated from the leaves of Syzygium samarangense (Blume) Merr. & L.M. Perry (Myrtaceae). Experiments were conducted to determine the effects of DMC on cell proliferation, cell‐cycle distribution, and programmed cell death in cultures of human colorectal carcinoma HCT116 and LOVO cells. Results showed that DMC inhibited HCT116 and LOVO cell proliferation and induced G2/M cell cycle arrest, which was associated with the conversion of microtubule associated protein light chain 3 (LC3)‐I–LC3‐II, an autophagosome marker, and the incorporation of monodansylcadaverine (MDC), a marker for the acidic compartment of autolysosomes or acidic vesicular organelles. The treatment of HCT116 and LOVO cells using a combination of DMC with an autophagy inhibitor, such as 3‐methyladenine (3‐MA), beclin 1 siRNA, or atg5 siRNA, suppressed the effect of DMC‐mediated anti‐proliferation. These results imply that DMC can suppress colorectal carcinoma HCT116 and LOVO cell proliferation through a G2/M phase cell‐cycle delay, and can induce autophagy, the hallmark of Type II programmed cell death (PCD). Taken together, our results suggest that DMC may be an effective chemotherapeutic agent for HCT116 and LOVO colorectal carcinoma cells. J. Cell. Biochem. 112: 2471–2479, 2011. © 2011 Wiley‐Liss, Inc.
The effects of dilution rate and glucose concentration on continuous acetone–butanol–ethanol fermentation by Clostridium acetobutylicum immobilized on bricks
Authors: Yen Hong‐Wei , Li Ruei‐Jei 
Published: May 2011

AbstractBACKGROUND: Owing to the rapid depletion of petroleum fuel, the production of butanol through biological routes has attracted increasing attention. However, low butanol productivity severely impedes its potential industrial production. It is known that the immobilization of whole cells can enhance productivity in the acetone‐butanol‐ethanol (ABE) continuous fermentation process. Therefore, the objective of this study was to develop a low‐cost continuous operation for butanol production.RESULTS: Bricks were chosen as cell support because of their low cost and ease of use for immobilization. The solvent productivity for the bricks with immobilized cells was 0.7 g L−1 h−1, 1.89 times that of free cells (0.37 g L−1 h−1) at a dilution rate of 0.054 h−1. The productivity improvement can contribute to greater retention of biomass inside the reactor due to immobilization. The increase in glucose feed concentration raised total solvent production. However, it resulted in a decrease in yield (grams of solvents produced per gram of glucose introduced). Continuous operation with immobilized cells at a dilution rate of 0.107 h−1 resulted in a solvent productivity of 1.21 g L−1 h−1, 2.1 times that of the operation at 0.027 h−1. However, the yield (butanol produced per glucose consumed) was decreased to 0.19 from 0.29 under the same glucose feeding condition of 60 g L−1.CONCLUSION: The increase in dilution rate and feed glucose concentration enhanced productivity, but decreased the utilization of substrates and the final solvent concentration. Therefore, a balance between productivity and glucose utilization is required to ensure continuous process operation. Copyright © 2011 Society of Chemical Industry
Sonographic appearance of a schwannoma mimicking an axillary lymphadenopathy
Authors: Sohn Yu‐Mee , Kim Sue Yon , Kim Eun‐Kyung 
Published: May 2011

AbstractSchwannomas are benign nerve sheath tumors derived from Schwann cells and are the most common type of peripheral nerve tumor. Schwannomas occur mainly in the extremities, trunk, and head and are rarely manifested in the axilla. Although various solid tumors can develop in the axilla, only a few cases of schwannoma in the axillary cavity have been reported. Herein, we describe the sonographic appearance of a schwannoma arising from the brachial plexus in the axilla. © 2011 Wiley Periodicals, Inc. J Clin Ultrasound, 2011
First‐trimester septated cystic hygroma and cavum velum interpositum cyst
Authors: Sherer David M. , Dalloul Mudar , Miller Michelle J. , Kheyman Mila , Zinn Harry L. , Abulafia Ovadia 
Published: May 2011

AbstractFirst‐trimester septated cystic hygroma, frequently noted during general obstetric first‐trimester screening, is strongly associated with fetal aneuploidy and structural anomalies and is considered an ominous finding. We present the case of a fetus with a first‐trimester septated cystic hygroma and cavum velum interpositum cyst. © 2011 Wiley Periodicals, Inc. J Clin Ultrasound, 2011
Altered oxidative stress profile in the cortex of mice fed an enriched branched‐chain amino acids diet: Possible link with amyotrophic lateral sclerosis?
Authors: Piscopo P. , Crestini A. , Adduci A. , Ferrante A. , Massari M. , Popoli P. , Vanacore N. , Confaloni A. 
Published: May 2011

AbstractBranched‐chain amino acids (BCAAs), valine, isoleucine, and leucine, are widely used among athletes as dietary integrators. Although the occurrence of untoward effects of BCCA supplementation, with particular regard to neurological disturbances, cannot be excluded, no specific studies have been performed so far. The aim of this work was to evaluate the effects of a diet enriched in BCAAs on the expression of oxidative stress pathway genes in the brain of C57Bl/6J mice. Animals were fed a standard or a BCAA diet for 95 days starting from postnatal day 21 until sacrifice. BCAA treatment, at doses comparable to human usage, significantly down‐regulated the expression of some antioxidant genes, while up‐regulating the expression of some oxygen transporters. In conclusion, it appears that BCAAs administered by diet could alter some specific oxidative stress pathways in the brain. Caution should thus be exercised in the widespread use of BCAAs as dietary integrators in sports practice. © 2011 Wiley‐Liss, Inc.
Tin protoporphyrin provides protection following cerebral hypoxia‐ischemia: Involvement of alternative pathways
Authors: Sutherland Brad A. , Shaw Odette M. , Clarkson Andrew N. , Winburn Ian C. , Errington Adam C. , Dixon Christine L. , Lees George , Sammut Ivan A. , Appleton Ian 
Published: May 2011

AbstractThe contribution of heme oxygenase (HO)‐linked pathways to neurodegeneration following cerebral hypoxia‐ischemia (HI) remains unclear. We investigated whether HO modulators affected HI‐induced brain damage and explored potential mechanisms involved. HI was induced in 26‐day‐old male Wistar rats by left common carotid artery ligation, followed by exposure to a humidified atmosphere of 8% oxygen for 1 hr. Tin protoporphyrin (SnPP; an HO inhibitor), ferriprotoporphyrin (FePP; an HO inducer), or saline was administered intraperitoneally once daily from 1 day prior to HI until sacrifice at 3 days post‐HI. SnPP reduced (P < 0.05) infarct volume compared with saline‐treated animals, but FePP had no effect on brain injury. SnPP did not significantly inhibit HO activity at 3 days post‐HI, but SnPP increased (P < 0.001) total nitric oxide synthase (NOS) activity compared with HI + saline. Both inducible NOS and cyclooxygenase activities were attenuated (P < 0.05) by SnPP, whereas mitochondrial complex I and V activities were augmented (P < 0.05) by SnPP. SnPP had no effect on NMDA receptor currents. Overall, like other HO inhibitors, SnPP produced many nonselective effects, such as attenuation of inflammatory enzymes and increased mitochondrial respiratory function, which were associated with a protective response 3 days post‐HI. © 2011 Wiley‐Liss, Inc.
Reduced gap junctional communication among astrocytes in experimental diabetes: Contributions of altered connexin protein levels and oxidative–nitrosative modifications
Authors: Ball Kelly K. , Harik Lamia , Gandhi Gautam K. , Cruz Nancy F. , Dienel Gerald A. 
Published: May 2011

AbstractExperimental diabetes increases production of reactive oxygen–nitrogen species and inhibits astrocytic gap junctional communication in tissue culture and brain slices from streptozotocin (STZ)‐diabetic rats by unidentified mechanisms. Relative connexin (Cx) protein levels were assessed by Western blotting using extracts from cultured astrocytes grown in high (25 mmol/liter) or low (5.5 mmol/liter) glucose for 2–3 weeks and STZ‐diabetic rat brain. Chemiluminescent signals for diabetic samples were normalized to those of controls on the same blot and same protein load. Growth in high glucose did not alter relative Cx26 level, whereas Cx30 and glyceraldehyde‐3‐phosphate dehydrogenase (GAPDH) were reduced by ∼30%, and Cx43 increased ∼1.9‐fold. In the inferior colliculus of STZ‐diabetic rats, Cx30 and Cx43 levels in three of four rats were half those of controls, whereas GAPDH and actin were unaffected. Diabetes did not affect levels of Cx30, Cx43, or GAPDH in cerebral cortex, but actin level rose 24%. Cx43 was predominantly phosphorylated in control and diabetic samples, so the reduced dye transfer is not due to overall dephosphorylation of Cx43. Astrocytic growth in high glucose reduced the dye‐labeled area by 75%, but 10 min of treatment with dithiothreitol restored normal dye transfer. In contrast, nitric oxide donors inhibited dye transfer among astrocytes grown in low glucose by 50–65% within 1 hr. Thus, modifications arising from oxidative–nitrosative stress, not altered connexin levels, may underlie the reduced dye transfer among severely hyperglycemic cultured astrocytes, whereas both oxidative–nitrosative stress and regionally selective down‐regulation of connexin protein content may affect gap junctional communication in the brains of STZ‐diabetic rats. © 2011 Wiley‐Liss, Inc.
Overuse of training increases mechanoreceptors in supraspinatus tendon of rats SHR
Authors: de Castro Pochini Alberto , Ejnisman Benno , de Seixas Alves Maria Teresa , Uyeda Luiz Fernando , Nouailhetas Viviane Louise Andree , Han Sang W. , Cohen Moises , Albertoni Walter Manna 
Published: May 2011

AbstractThe presence of mechanoreceptors in tendon after overuse activities can be a further step to learn about tendinopathy and overuse. Studies of tendons mechanoreceptors in rats are rare. We studied 12 isogenic spontaneous hypertensive rats (SHR), which underwent an overuse protocol consisting of an hour per daily session of treadmill running at a speed of 17 m/min, 5 times/week for 4 months. Supraspinatus tendons were evaluated with immunohistochemistry using S100 protein antibodies and histological protocol. Supraspinatus tendons at the end of 4 months of overuse protocol had a high number of media mechanoreceptors (4.3) than controls (0.6). The overexpression of S100 protein antibody in overuse activities maybe could represent a adaptative effort to tendon before the tear. © 2011 Orthopaedic Research Society Published by Wiley Periodicals, Inc. J Orthop Res 29:1771–1774, 2011
Ionic interactions and salinity affect monoterpene and phenolic diterpene composition in rosemary (Rosmarinus officinalis)
Authors: Tounekti Taïeb , Vadel Ahmedou Mohammed , Ennajeh Mustapha , Khemira Habib , Munné‐Bosch Sergi 
Published: May 2011

AbstractIn this study, we evaluated how increased cation supply can alleviate the toxic effects of NaCl on plants and how it affects essential oils (EOs) and phenolic diterpene composition in leaves of rosemary (Rosmarinus officinalisL.) plants grown in pots. Two concentrations of the chloride salts KCl, CaCl2, MgCl2, and FeCl3were used together with 100 mM NaCl to study the effects of these nutrients on plant mineral nutrition and leaf monoterpene, phenolic diterpene, and EO composition. The addition of 100 mM NaCl, which decreased K+, Ca2+, and Mg2+concentrations with increasing Na+in leaves, significantly altered secondary metabolite accumulation. Addition of MgCl2and FeCl3altered leaf EO composition in 100 mM NaCl–treated rosemary plants while KCl and CaCl2did not. Furthermore, addition of CaCl2promoted the accumulation of the major phenolic diterpene, carnosic acid, in the leaves. The carnosol concentration was reduced by the addition of KCl to salt‐stressed plants. It is concluded that different salt applications in combination with NaCl treatment may have a pronounced effect on phenolic diterpene and EO composition in rosemary leaves thus indicating that ionic interactions may be carefully considered in the cultivation of these species to achieve the desired concentrations of these secondary metabolites.