bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of three‐dimensional culture and incubator gas concentration on phenotype and differentiation capability of human mesenchymal stem cells
Authors: Karlsen Tommy A. , Mirtaheri Peyman , Shahdadfar Aboulghassem , Fløisand Yngvar , Brinchmann Jan E. 
Published: December 2010

AbstractTo obtain sufficient numbers of cells for tissue engineering applications, human bone marrow‐derived mesenchymal stem cells (hBM‐MSC) are commonly cultured as monolayers in incubators containing room air. In this study, we investigated whether three‐dimensional (3D) culture conditions and incubator gas concentrations more similar to those observed in vivo impacted on cell expansion, differentiation capability, or phenotype of hBM‐MSC. We found that 3D culture alone increased the expression of some molecules involved in osteogenic and adipogenic differentiation. In contrast, 3D culture did not induce chondrogenic differentiation, but enhanced the response to the chondrogenic differentiation medium. Changing the oxygen concentration to 6% and the carbon dioxide concentration to 7.5% did not impact on the results of any of our assays, showing that the hyperoxia of room air is not detrimental to hBM‐MSC proliferation, differentiation, or phenotype. J. Cell. Biochem. 112: 684–693, 2011. © 2010 Wiley‐Liss, Inc.
Nonsense suppressor therapies rescue peroxisome lipid metabolism and assembly in cells from patients with specific PEX gene mutations
Authors: Dranchak Patricia K. , Di Pietro Erminia , Snowden Ann , Oesch Nathan , Braverman Nancy E. , Steinberg Steven J. , Hacia Joseph G. 
Published: December 2010

AbstractPeroxisome biogenesis disorders (PBDs) are multisystemic autosomal recessive disorders resulting from mutations in PEX genes required for normal peroxisome assembly and metabolic activities. Here, we evaluated the potential effectiveness of aminoglycoside G418 (geneticin) and PTC124 (ataluren) nonsense suppression therapies for the treatment of PBD patients with disease‐causing nonsense mutations. PBD patient skin fibroblasts producing stable PEX2 or PEX12 nonsense transcripts and Chinese hamster ovary (CHO) cells with a Pex2 nonsense allele all showed dramatic improvements in peroxisomal very long chain fatty acid catabolism and plasmalogen biosynthesis in response to G418 treatments. Cell imaging assays provided complementary confirmatory evidence of improved peroxisome assembly in G418‐treated patient fibroblasts. In contrast, we observed no appreciable rescue of peroxisome lipid metabolism or assembly for any patient fibroblast or CHO cell culture treated with various doses of PTC124. Additionally, PTC124 did not show measurable nonsense suppression in immunoblot assays that directly evaluated the read‐through of PEX7 nonsense alleles found in PBD patients with rhizomelic chondrodysplasia punctata type 1 (RCDP1). Overall, our results support the continued development of safe and effective nonsense suppressor therapies that could benefit a significant subset of individuals with PBDs. Furthermore, we suggest that the described cell culture assay systems could be useful for evaluating and screening for novel nonsense suppressor therapies. J. Cell. Biochem. 112: 1250–1258, 2011. © 2011 Wiley‐Liss, Inc.
Essential roles of the nitric oxide (no)/cGMP/protein kinase G type‐Iα (PKG‐Iα) signaling pathway and the atrial natriuretic peptide (ANP)/cGMP/PKG‐Iα autocrine loop in promoting proliferation and cell survival of OP9 bone marrow stromal cells
Authors: Wong Janica C. , Fiscus Ronald R. 
Published: December 2010

AbstractInappropriate signaling conditions within bone marrow stromal cells (BMSCs) can lead to loss of BMSC survival, contributing to the loss of a proper micro‐environmental niche for hematopoietic stem cells (HSCs), ultimately causing bone marrow failure. In the present study, we investigated the novel role of endogenous atrial natriuretic peptide (ANP) and the nitric oxide (NO)/cGMP/protein kinase G type‐Iα (PKG‐Iα) signaling pathway in regulating BMSC survival and proliferation, using the OP9 BMSC cell line commonly used for facilitating the differentiation of HSCs. Using an ANP‐receptor blocker, endogenously produced ANP was found to promote cell proliferation and prevent apoptosis. NO donor SNAP (S‐nitroso‐N‐acetylpenicillamine) at low concentrations (10 and 50 µM), which would moderately stimulate PKG activity, protected these BMSCs against spontaneous apoptosis. YC‐1, a soluble guanylyl cyclase (sGC) activator, decreased the levels of apoptosis, similar to the cytoprotective effects of low‐level NO. ODQ (1H‐[1,2,4]oxadiazolo[4,3,‐a]quinoxalin‐1‐one), which blocks endogenous NO‐induced activation of sGC and thus lowers endogenous cGMP/PKG activity, significantly elevated apoptotic levels by 2.5‐ and three‐fold. Pre‐incubation with 8‐Bromo‐cGMP or ANP, which bypass the ODQ block, almost completely prevented the ODQ‐induced apoptosis. A highly‐specific PKG inhibitor, DT‐3, at 20, and 30 µM, caused 1.5‐ and two‐fold increases in apoptosis, respectively. ODQ and DT‐3 also decreased BMSCs proliferation and colony formation. Small Interfering RNA gene knockdown of PKG‐Iα increased apoptosis and decreased proliferation in BMSCs. The data suggest that basal NO/cGMP/PKG‐Iα activity and autocrine ANP/cGMP/PKG‐Iα are necessary for preserving OP9 cell survival and promoting cell proliferation and migration. J. Cell. Biochem. 112: 829–839, 2011. © 2010 Wiley‐Liss, Inc.
Signaling networks in RUNX2‐dependent bone development
Authors: Komori Toshihisa 
Published: December 2010

AbstractRUNX2 is an essential transcription factor for osteoblast differentiation and chondrocyte maturation. SP7, another transcription factor, is required for osteoblast differentiation. Major signaling pathways, including FGF, Wnt, and IHH, also play important roles in skeletal development. RUNX2 regulates Sp7 expression at an early stage of osteoblast differentiation. FGF2 upregulates Runx2 expression and activates RUNX2, and gain‐of‐function mutations of FGFRs cause craniosynostosis and limb defect with upregulation of Runx2 expression. Wnt signaling upregulates Runx2 expression and activates RUNX2, and RUNX2 induces Tcf7 expression. IHH is required for Runx2 expression in osteoprogenitor cells during endochondral bone development, and RUNX2 directly regulates Ihh expression in chondrocytes. Thus, RUNX2 regulates osteoblast differentiation and chondrocyte maturation through the network with SP7 and with FGF, Wnt, and IHH signaling pathways during skeletal development. J. Cell. Biochem. 112: 750–755, 2011. © 2010 Wiley‐Liss, Inc.
Long‐term in vitro expansion of osteoarthritic human articular chondrocytes do not alter genetic stability: A microsatellite instability analysis
Authors: Neri Simona , Mariani Erminia , Cattini Luca , Facchini Andrea 
Published: December 2010

AbstractIn this study, we investigated genetic damage acquisition during in vitro culture of human osteoarthritic (OA) chondrocytes to evaluate their safety for use in regenerative medicine clinical applications. In particular, we have addressed the impact of long‐term in vitro culture on simple sequence repeat stability, to evaluate the involvement of the mismatch repair system (MMR) in the accumulation of genetic damage. MMR, the main post‐replicative correction pathway, has a fundamental role in maintaining genomic stability and can be monitored by assessing microsatellite instability (MSI). MMR activity has been reported to decrease with age not only in vivo, but also in vitro in relationship to culture passages. OA chondrocytes from seven donors were cultured corresponding to 13–29 population doublings. Aliquots of the cells were collected and analyzed for MSI at five DNA loci (CD4, VWA, FES, TPOX, and P53) and for MMR gene expression at each subculture. Genetic stability was confirmed throughout the culture period. MMR genes demonstrated a strong coordination at the transcriptional level among the different components; expression levels were very low, in accordance with the observed genetic stability. The reduced expression of MMR genes might underline no need for increasing DNA repair control in the culture conditions tested, in which no genetic damage was evidenced. These data argue for the safety of chondrocytes for cellular therapies and are encouraging for the potential use of in vitro expanded OA chondrocytes, supporting the extension of autologous cell therapy procedures to degenerative articular diseases. J. Cell. Physiol. 226: 2579–2585, 2011. © 2010 Wiley‐Liss, Inc.
TGFBR3, a potential negative regulator of TGF‐β signaling, protects cardiac fibroblasts from hypoxia‐induced apoptosis
Authors: Chu WenFeng , Li XiaoXue , Li Cui , Wan Lin , Shi Hui , Song XiaoHui , Liu XingYuan , Chen Xi , Zhang Chun , Shan HongLi , Lu YanJie , Yang Baofeng 
Published: December 2010

AbstractA lot of evidence indicates that cardiac fibroblasts are essential for maintaining the structure and function of heart. The present study examined whether TGFBR3 (transforming growth factor type III receptor, also known as betaglycan) could prevent hypoxia‐induced injury in neonatal mice cardiac fibroblasts, if so, its possible molecular targets. MTT, electron microscopy and TUNEL assay were used to identify cell viability and apoptosis in neonatal mice cardiac fibroblasts. Results showed that hypoxia for 24 h markedly reduce cell viability by 49.8 ± 8.9%, largely via apoptosis. However, hypoxia‐induced apoptosis in cardiac fibroblasts were almost completely prevented by overexpression of TGFBR3. In the present study, hypoxia also induced TGF‐β1, p‐Smad2/3 expression, TGFBR1–TGFBR2 complex formation and collagen production in cardiac fibroblasts, which were attenuated substantially by TGFBR3 overexpression. TGFBR3 also reversed Bax up‐regulation, Bcl‐2 down‐regulation and Caspase‐3 activation induced by hypoxia in cardiac fibroblasts. Hypoxia or TGF‐β1 itself triggered an increase of [Ca2+]i in cardiac fibroblasts, which were both inhibited by TGFBR3 overexpression. Taken together, our results indicate that TGFBR3 may act as a protective factor in apoptotic process of cardiac fibroblasts by negative regulation of TGF‐β signaling and represent a potential therapeutic target for heart remodeling after hypoxia injury. J. Cell. Physiol. 226: 2586–2594, 2011. © 2010 Wiley‐Liss, Inc.
The metabolism of human mesenchymal stem cells during proliferation and differentiation
Authors: Pattappa Girish , Heywood Hannah K. , de Bruijn Joost D. , Lee David A. 
Published: December 2010

AbstractHuman mesenchymal stem cells (MSCs) reside under hypoxic conditions in vivo, between 4% and 7% oxygen. Differentiation of MSCs under hypoxic conditions results in inhibited osteogenesis, while chondrogenesis is unaffected. The reasons for these results may be associated with the inherent metabolism of the cells. The present investigation measured the oxygen consumption, glucose consumption and lactate production of MSCs during proliferation and subsequent differentiation towards the osteogenic and chondrogenic lineages. MSCs expanded under normoxia had an oxygen consumption rate of ∼98 fmol/cell/h, 75% of which was azide‐sensitive, suggesting that these cells derive a significant proportion of ATP from oxidative phosphorylation in addition to glycolysis. By contrast, MSCs differentiated towards the chondrogenic lineage using pellet culture had significantly reduced oxygen consumption after 24 h in culture, falling to ∼12 fmol/cell/h after 21 days, indicating a shift towards a predominantly glycolytic metabolism. By comparison, MSCs retained an oxygen consumption rate of ∼98 fmol/cell/h over 21 days of osteogenic culture conditions, indicating that these cells had a more oxidative energy metabolism than the chondrogenic cultures. In conclusion, osteogenic and chondrogenic MSC cultures appear to adopt the balance of oxidative phosphorylation and glycolysis reported for the respective mature cell phenotypes. The addition of TGF‐β to chondrogenic pellet cultures significantly enhanced glycosaminoglycan accumulation, but caused no significant effect on cellular oxygen consumption. Thus, the differences between the energy metabolism of chondrogenic and osteogenic cultures may be associated with the culture conditions and not necessarily their respective differentiation. J. Cell. Physiol. 226: 2562–2570, 2011. © 2010 Wiley‐Liss, Inc.
Group X secreted phospholipase A2 specifically decreases sperm motility in mice
Authors: Escoffier Jessica , Pierre Virginie J. , Jemel Ikram , Munch Léa , Boudhraa Zied , Ray Pierre F. , De Waard Michel , Lambeau Gérard , Arnoult Christophe 
Published: December 2010

AbstractDifferent mammalian secreted phospholipases A2 (sPLA2s) are expressed in male reproductive organs and/or in sperm cells but their cellular functions are still not fully characterized. Because several reports indicate a link between cellular lipids and sperm motility, we have investigated the effect of mouse group IIA, IID, IIE, V, and X sPLA2s on sperm motility. Among these enzymes, only mouse group X sPLA2 (mGX sPLA2) acts as a potent inhibitor of sperm motility that decreases track speed (VCL) and lateral displacement of the head (ALH) of both noncapacitated and capacitated sperm. The inhibitory effect of mGX sPLA2 is dependent on its enzymatic activity because (i) both the proenzyme form of mGX sPLA2 (pro‐mGX) and the H48Q mutant of mGX sPLA2 have very weak enzymatic activity and are unable to modulate sperm motility and (ii) LY329722, a specific inhibitor of sPLA2s, blocks the inhibitory effect of mGX sPLA2. Moreover, mGX sPLA2 exerts a gradual potency on sperm subpopulations with different velocities, an effect which may be linked to the heterogeneity of lipid composition in these sperm subpopulations. Finally, we found that endogenous mGX sPLA2 released during spontaneous acrosome reaction modulates sperm motility of capacitated sperm. Together, our results suggest a new role of sPLA2 in sperm physiology where the sPLA2 selects a sperm subpopulation for fertilization based on its effect on sperm motility. J. Cell. Physiol. 226: 2601–2609, 2011. © 2010 Wiley‐Liss, Inc.
Age‐ and sex‐related differences in extra‐hepatic low‐density lipoprotein receptor
Authors: Segatto Marco , Trapani Laura , Marino Maria , Pallottini Valentina 
Published: December 2010

AbstractTo determine whether differences in LDLr behavior in extra‐hepatic tissues and whether extra‐hepatic receptors could differentially contribute to cholesterol homeostasis under physiological conditions, we evaluated the presence and regulation of LDLr from both a gender and an aging perspective. We used the brain cortex, the gastrocnemius, and the heart ventricle of 3‐ and 12‐month‐old male and female rats. We observed a protein decrease of total LDLr in 12‐month‐old female rat brains that was completely restored by 17‐β estradiol treatment. In the gastrocnemius, LDLr accumulates in the skeletal muscle in both male and female aged rats as a precursor probably due to a glycosylation impairment. In the heart, no modifications were observed in either older rats or rats of a specific gender. These data highlight a tissue‐specific dysregulation of LDLr that is age‐ and gender‐dependent. J. Cell. Physiol. 226: 2610–2616, 2011. © 2010 Wiley‐Liss, Inc.
Decorin and chondroitin‐6 sulfate inhibit B16V melanoma cell migration and invasion by cellular acidification
Authors: Stock Christian , Jungmann Oliver , Seidler Daniela G. 
Published: December 2010

AbstractIn vivo, cells are embedded in an environment generated and maintained by multiple cell–cell and cell–matrix interactions. While transiting the dermis metastasizing melanoma cells interact with the extracellular matrix (ECM) and fibroblasts. To study the roles of ECM components and fibroblasts in melanoma (B16V) cell migration and invasion, we established a co‐culture system consisting of fibroblasts, their collagen‐rich matrix and B16V cells. The crosstalk between B16V cells and fibroblasts was indicated by a clear increase in release and activity of matrix‐metallo‐protease‐2. Time‐lapse microscopy revealed that in B16V cells exposed to either decorin or chondroitin sulfates migration and invasion decreased by more than 50%. Decorin led to a reversible, chondroitin‐6‐sulfate to an irreversible, cytosolic acidification of B16V cells. Interestingly, decorin lowered NHE1 activity whereas chondroitin‐6‐sulfate did not. Furthermore, decorin and chondroitin‐6‐sulfate also acidified the pH at the cell surface which might prevent migration due to strong adhesion. In conclusion, the present co‐culture system is an appropriate tool to analyze migration, invasion, and MMP release depending on cell–matrix interactions and the crosstalk between the invasive cells and those surrounded by their self‐made matrix. We show a so far unknown function of decorin and chondroitin‐6‐sulfate: their ability to inhibit B16V cell migration by intracellular acidification. J. Cell. Physiol. 226: 2641–2650, 2011. © 2010 Wiley‐Liss, Inc.
Thyroid hormone promotes insulin‐induced glucose uptake by enhancing Akt phosphorylation and VAMP2 translocation in 3T3‐L1 adipocytes
Authors: Lin Yi , Sun Zhongjie 
Published: December 2010

AbstractThe purpose of this study was to test a hypothesis that T3 promotes glucose uptake via enhancing insulin‐induced Akt phosphorylation and VAMP2 translocation in 3T3‐L1 adipocytes. T3 significantly enhanced insulin‐induced phosphorylation of Akt, cytoplasma to cell membrane translocations of vesicle‐associated membrane protein 2 (VAMP2) and glucose transporter 4 (GLUT4), and glucose uptake in adipocytes. Akt inhibitor X abolished the promoting effects of T3, suggesting that Akt activation is essential for T3 to enhance these insulin‐induced events in adipocytes. Knockdown of VAMP2 using siRNA abrogated the effects of T3 on insulin‐induced GLUT4 translocation and glucose uptake, suggesting that VAMP2 is an important mediator of these processes. These data suggest that T3 may promote glucose uptake via enhancing insulin‐induced phosphorylation of Akt and subsequent translocations of VAMP2 and GLUT4 in 3T3‐L1 adipocytes. Akt phosphorylation is necessary for the promoting effects of T3 on insulin‐stimulated VAMP2 translocation. Further, VAMP2 is essential for T3 to increase insulin‐stimulated translocation of GLUT4 and subsequent uptake of glucose in adipocytes. J. Cell. Physiol. 226: 2625–2632, 2011. © 2010 Wiley‐Liss, Inc.
Sonographic and magnetic resonance imaging findings of pelvic abscess following uterine perforation sustained during office endometrial sampling
Authors: Abulafia Ovadia , Shah Tana , Salame Ghadir , Economos Kathrine , Serur Eli , Zinn Harry , Sokolovkski Margarita , Sherer David M. 
Published: December 2010

AbstractPipelle endometrial sampling, an outpatient, office‐based procedure, provides comparative successful endometrial sampling in comparison with other techniques including conventional dilatation and curettage. We present an unusual occurrence in which office Pipelle endometrial sampling in a perimenopausal patient was complicated 10 days later by lower abdominal pain and intermittent fever. Sonography depicted findings consistent with a large pelvic abscess overriding the uterine fundus. Sonography and magnetic resonance imaging confirmed the presence of the unusual pelvic abscess and, in addition, noted findings consistent with perforation of the uterus during endometrial sampling. © 2010 Wiley Periodicals, Inc. J Clin Ultrasound, 2011
Transrectal ultrasound guided multi‐core prostate biopsy: Pain control: Results of 106 patients
Authors: Kahriman Guven , Donmez Halil , Mavili Ertugrul , Ozcan Nevzat , Yılmaz Serpil Postgil , Kenan Bekir 
Published: December 2010

AbstractPurpose:To determine the efficacy of periprostatic nerve block (PPNB) for control of transrectal ultrasound (TRUS)‐guided multicore prostate biopsy‐related pain.Methods:A total of 106 cases with suspicion of prostate cancer underwent TRUS‐guided multicore prostate biopsy under local anesthesia using a total of 10 ml of 1% lidocaine for each patient. Lidocaine was injected around the neurovascular bundle at the base of the prostate just lateral to the seminal vesicle‐prostate junction. The pain score was assessed using visual analog pain score from 0 to 10. All patients were questioned for whether they would accept repeat biopsy or not, if necessary.Results:Pain score ranged from 0 to 5 (mean: 1.4). Thirty‐five percent (37/106) of patients reported a score of 0, whereas 17% (18/106), 32% (34/106), 8.4% (9/106), 6.7% (7/106), 0.9% (1/106) reported pain scores of 1, 2, 3, 4, and 5, respectively. There were no pain scores of 6–10. Answers for the question “would you accept repeat biopsy or not, if necessary?” was “yes” for 82% (87/106) of the patients.Conclusions:PPNB prior to multi‐core TRUS‐guided prostate biopsy is an easy, safe, and effective technique for the control of procedure‐related pain. © 2010 Wiley Periodicals, Inc. J Clin Ultrasound, 2011
Endoscopic sonography in the diagnosis and treatment of a gastric wall abscess: A case report and review of the literature
Authors: Yang Chia‐Wei , Yen, Hsu‐Heng 
Published: December 2010

AbstractWe report a case of a gastric wall abscess in a 50‐year‐old man who presented with epigastralgia and fever. Gastroscopy revealed a subepithelial lesion on the posterior wall of the gastric body into the antrum. A follow‐up abdominal CT scan showed cystic lesions around the stomach. Endoscopic sonography helped to diagnose a gastric wall abscess. The gastric wall abscess was treated endoscopically with a needle knife incision for internal drainage. The patient was treated with antibiotics for 1 week and was discharged without complication. A follow‐up endoscopy with endoscopic sonography 1 month later revealed complete resolution of the lesion. © 2010 Wiley Periodicals, Inc. J Clin Ultrasound 40:105–108, 2012
The relationship between brachial artery flow‐mediated dilatation, high sensitivity C‐reactive protein, and uterine artery doppler velocimetry in women with pre‐eclampsia
Authors: Adali Ertan , Kurdoglu Mertihan , Adali Fulya , Cim Numan , Yildizhan Recep , Kolusari Ali 
Published: December 2010

AbstractPurpose:To investigate serum high sensitivity C‐reactive protein (hs‐CRP) levels and endothelial function in pregnancies complicated by pre‐eclampsia and to clarify their relationship with uterine artery Doppler velocimetry.Methods:A cross‐sectional study was carried out in 70 pregnant women (35 patients with pre‐eclampsia and 35 age‐matched normotensive healthy pregnant women) during the third trimester of pregnancy. The maternal levels of serum hs‐CRP were determined in all cases by immunonephelometry. Uterine artery Doppler velocimetry was performed. Flow‐mediated dilatation was measured by sonography of the brachial artery for the assessment of endothelial function.Results:Serum hs‐CRP levels were higher in the pre‐eclamptic group than in the normotensive group. hs‐CRP levels were positively correlated with mean arterial pressure. Eleven patients with pre‐eclampsia had abnormal uterine artery Doppler velocimetry. hs‐CRP levels were significantly higher in pre‐eclamptic patients with than without abnormal uterine artery Doppler velocimetry. Endothelial function was inversely correlated with hs‐CRP levels and mean arterial pressure.Conclusions:These findings suggest that maternal serum hs‐CRP levels increase with the severity of pre‐eclampsia, reflecting endothelial dysfunction and constituting a potential marker of pathological utero‐placental perfusion, with a high risk for fetal growth restriction. © 2010 Wiley Periodicals, Inc. J Clin Ultrasound, 2011