[show abstract][hide abstract] ABSTRACT: Rotenone is an inhibitor of mitochondrial complex I-induced neurotoxicity in PC12 cells and has been widely studied to elucidate the pathogenesis of Parkinson's disease. We investigated the neuroprotective effects of betaine on rotenone-induced neurotoxicity in PC12 cells. Betaine inhibited rotenone-induced apoptosis in a dose-dependent manner, with cell viability increasing from 50 % with rotenone treatment alone to 71 % with rotenone plus 100-μM betaine treatment. Flow cytometric analysis demonstrated cell death in the rotenone-treated cells to be over 50 %; the number of live cells increased with betaine pretreatment. Betaine pretreatment of PC12 cells attenuated rotenone-mediated mitochondrial dysfunction, including nuclear fragmentation, ATP depletion, mitochondrial membrane depolarization, caspase-3/7 activation, and reactive oxygen species production. Western blots demonstrated activation of caspase-3 and caspase-9, and their increased expression levels in rotenone-treated cells; betaine decreased caspase-3 and caspase-9 expression levels and suppressed their activation. Together, these results suggest that betaine may serve as a neuroprotective agent in the treatment of neurodegenerative diseases.
Cellular and Molecular Neurobiology 04/2013; · 2.29 Impact Factor
[show abstract][hide abstract] ABSTRACT: Antimycin A (AMA) damages the mitochondria through inhibition of mitochondrial electron
transport. In this study, exposure of L6 rat skeletal muscle cells to AMA induced a decrease in
ATP content, followed by a decrease in mitochondrial membrane potential, leading to apoptosis.
We evaluated the protective effects of water and ethanol extracts of Nelumbo nucifera
seeds on L6 cells with AMA-induced oxidative stress. We found that the extracts reduced cellular
apoptosis; preserved the mitochondrial membrane potential; protected mitochondrial
ATP production; inhibited p53, Bax, and caspase 3 activities; and induced Bcl-2 production.
Our results suggested that AMA induced apoptosis in L6 cells via impairment of mitochon-
drial function. N. nucifera extracts protected the cells from this mitochondria-mediated cell
Environmental Toxicology and Pharmacology 03/2013; 36(1):19-29. · 2.01 Impact Factor
[show abstract][hide abstract] ABSTRACT: The aim of this systematic review is to analyse the trial data on the efficacy of herbal medicines for acute otitis media.
The following 11 databases will be searched from their inception: MEDLINE, the Cumulative Index to Nursing and Allied Health Literature (CINAHL), EMBASE, Allied and Complementary Medicine Database (AMED), the Cochrane Central Register of Controlled Trials (CENTRAL), China Network Knowledge Infrastructure (CNKI) and five Korean databases (Oriental Medicine Advanced Searching Integrated System (OASIS), DBPIA, KoreaMed, Research Information Service System (RISS) and the Korean Studies Information Service System (KISS)). The selection of the studies, the data abstraction and the validations will be performed independently by two researchers.
The systematic review will be published in a peer-reviewed journal. The review will also be disseminated electronically and in print. Updates of the review will be conducted to inform and guide the healthcare practice and policy.
BMJ Open 01/2013; 3(11):e003728. · 1.58 Impact Factor
[show abstract][hide abstract] ABSTRACT: The inhibitory effect of propofol on platelet aggregation remains unclear, and studies on the subject disagree. Furthermore, although propofol infusions are widely used for general anesthesia and as sedatives for patients in intensive care units, little information is available on its concentration- and time-related effects on platelet aggregation. Here, the authors investigated the in vitro effect of propofol, at concentrations required for sedation and general anesthesia, on platelet aggregation after 1, 2, or 3 h. Blood from healthy volunteers (n = 9) was incubated at propofol plasma concentrations of 0, 2, 4, and 10 μg/mL in a water bath at 37°C. Platelet aggregation was measured using a platelet function analyzer (PFA-100) after 1, 2, or 3 h of incubation. Times to occlude collagen/epinephrine (CEPI) or collagen/adenosine 5'-diphosphate (CADP)-coated membranes (closure times, CTs) were measured. The CEPI and CADP CTs of non-incubated blood were 125.6 ± 19.5 s and 93.0 ± 12.2 s, respectively, and no significant difference in CEPI CTs was observed at propofol plasma concentrations of 0, 2, 4, and 10 μg/mL after incubation for 1, 2, or 3 h. CADP CTs were comparable at propofol concentrations of 0, 2, 4, and 10 μg/mL at each incubation time. These findings suggest that propofol at concentrations required for sedation and general anesthesia has no inhibitory effect on platelet aggregation after 3 h of incubation.
[show abstract][hide abstract] ABSTRACT: Multiple surface markers have been utilized for the enrichment of bone marrow mesenchymal stromal cells (MSCs) and to define primitive stem cells. We classified human bone marrow-derived MSC populations according to tissue nonspecific alkaline phosphatase (TNAP) activity. TNAP expression varied among unexpanded primary MSCs, and its level was not related to colony-forming activity or putative surface markers, such as CD105 and CD29, donor age, or gender. TNAP levels were increased in larger cells, and a colony-forming unit-fibroblast assay revealed that the colony size was decreased during in vitro expansion. TNAP-positive (TNAP+) MSCs showed limited multipotential capacity, whereas TNAP-negative (TNAP-) MSCs retained the differentiation potential into 3 lineages (osteogenic-, adipogenic-, and chondrogenic differentiation). High degree of calcium mineralization and high level of osteogenic-related gene expression (osteopontin, dlx5, and cbfa1) were found in TNAP+ cells. In contrast, during chondrogenic differentiation, type II collagen was successfully induced in TNAP- cells, but not in TNAP+ cells. TNAP+ cells showed high levels of the hypertrophic markers, type X collagen and cbfa1. Mesenchymal stem cell antigen-1 (MSCA-1) is identical to TNAP. Therefore, TNAP+ cells were sorted by using antibody targeting MSCA-1. MSCA-1-positive cells sorted for TNAP+ cells exhibited low proliferation rates. Expression of cell cycle-related genes (cyclin A2, CDK2, and CDK4) and pluripotency marker genes (rex1 and nanog) were higher in TNAP- MSC than in TNAP+ MSC. Therefore, TNAP- cells can be described as more primitive bone marrow-derived cells and TNAP levels in MSCs can be used to predict chondrocyte hypertrophy or osteogenic capacity.
Stem cells and development 06/2012; 21(16):2958-68. · 4.15 Impact Factor
[show abstract][hide abstract] ABSTRACT: This in vitro study investigated time-related effects of propofol at the plasma concentrations required for sedation and general anaesthesia, on RBC aggregation, deformability, and morphology. Blood containing propofol at plasma concentrations of 0, 2 and 4 μg ml-1 was incubated in a water bath at 37°C for 1, 2, or 4 hours. RBC elongation indices (EIs) and aggregation indices (AIs), which represent RBC deformability and aggregation, respectively, were measured. Also, RBC morphological indices (MIs), which represent RBC morphology, were calculated. EIs and AIs were similar at propofol concentrations of 0, 2, or 4 μg ml-1 after 1, 2, or 4 hours of incubation. MIs at propofol plasma concentrations 0 or 2 μg ml-1 were similar after 1, 2, and 4 hours of incubation, however, MI at a propofol concentration of 4 μg ml-1 after 4 hours of incubation was higher than its value after 1 or 2 hours of incubation. No significant difference was observed between MIs at propofol plasma concentrations 0, 2, or 4 μg ml-1 after 1, 2, and 4 hours of incubation. At clinical doses, propofol has no direct effects on RBC deformability, aggregation, or morphology over a 4 hours incubation period.
Clinical hemorheology and microcirculation 03/2012; 51(4):287-92. · 3.40 Impact Factor
[show abstract][hide abstract] ABSTRACT: Antimycin A (AMA) damages mitochondria by inhibiting mitochondrial electron transport and can produce reactive oxygen species (ROS). ROS formation, aging, and reduction of mitochondrial biogenesis contribute to mitochondrial dysfunction. The present study sought to investigate extracts of Scutellaria baicalensis and its flavonoids (baicalin, baicalein, and wogonin), whether they could protect mitochondria against oxidative damage. The viability of L6 cells treated with AMA increased in the presence of flavonoids and extracts of S. baicalensis. ATP production decreased in the AMA treated group, but increased by 50% in cells treated with flavonoids (except wogonin) and extracts of S. baicalensis compared to AMA-treated group. AMA treatment caused a significant reduction (depolarized) in mitochondrial membrane potential (MMP), whereas flavonoid treatment induced a significant increase in MMP. Mitochondrial superoxide levels increased in AMA treated cells, whereas its levels decreased when cells were treated with flavonoids or extracts of S. baicalensis. L6 cells treated with flavonoids and extracts of S. baicalensis increased their levels of protein expression compared with AMA-treated cells, especially water extracts performed the highest levels of protein expression. These results suggest that the S. baicalensis extracts and flavonoids protect against AMA-induced mitochondrial dysfunction by increasing ATP production, upregulating MMP, and enhancing mitochondrial function.
Evidence-based Complementary and Alternative Medicine 01/2012; 2012:517965. · 1.72 Impact Factor
[show abstract][hide abstract] ABSTRACT: Microtia reconstructive surgery is usually a multi-stage repair procedure that involves the use of cartilage and skin grafts. Complications can arise at both ear reconstruction sites and cartilage donor sites. In particular, pneumothorax, atelectasis, chest scars, and chest deformities are known to be associated with the harvesting of costal cartilage. However, delayed pleural effusion can also develop. Our patient complained of a cough and chest pain at 5 days postoperatively, and pleural effusion was detected by chest radiography. However, thoracentesis was not performed and the effusion resolved spontaneously and completely.
Korean journal of anesthesiology 08/2011; 61(2):166-8.
[show abstract][hide abstract] ABSTRACT: Adipogenesis is largely dependent on the signal transducers and activators of transcription (STAT) pathway. However, the molecular mechanism of the STAT pathway in the adipogenesis of human bone marrow-derived stromal cells (hBMSCs) remains not well understood. The purpose of this research was to characterize the transcriptional regulation involved in expression of STAT5A and STAT5B during adipogenesis in hBMSCs and 3T3-L1 cells. The expression of STAT5A and STAT5B increases with the onset of adipogenesis in hBMSCs and 3T3-L1 cells. The PPAR response elements regulatory element of STAT5A exists at a promoter region ranging from -346 to -101, and the CCAAT/enhancer-binding protein (C/EBP) regulatory element is located at -196 to -118 of the STAT5B promoter. C/EBPβ and C/EBPα bound to the STAT5B promoter region, whereas peroxisome proliferator-activated receptor γ (PPARγ) bound to STAT5A. RNA interference of STAT5A completely blocked differentiation, whereas the inhibition of STAT5B only partially blocked differentiation. We propose that C/EBPα, C/EBPβ, and PPARγ control adipogenesis by regulating STAT5B and STAT5A and that STAT5A is necessary, whereas STAT5B plays a supplementary role during adipogenesis. Further, the regulation of PPARγ-STAT5 by C/EBPβ signaling seems to be the crucial adipogenesis pathway-initiating cascade of the various adipogenic genes.
Stem cells and development 06/2011; 21(3):465-75. · 4.15 Impact Factor
[show abstract][hide abstract] ABSTRACT: Imbalances between osteogenic and adipogenic differentiation leads to diseases such as osteoporosis. The aim of our study was to demonstrate the differences in extracellular signal-regulated kinase (ERK) phosphorylation during both adipogenesis and osteogenesis of human bone marrow-derived stem cells (BMSCs).
Using troglitazone, GW9662 and U0126, we investigated their role in hBMSC differentiation to adipogenic and osteogenic fates.
ERK1/2 inhibition by U0126 suppressed proliferator-activated receptor (PPAR)γ expression and lipid accumulation, while it decreased the mRNA expression of adipogenic genes (lipoprotein lipase, PPARγ, and adipocyte protein) and osteogenic genes (type I collagen and osteopontin). ERK phosphorylation was transient and decreased during adipogenesis, whereas it occurred steadily during osteogenesis. Troglitazone, a PPARγ agonist, induced adipogenesis by inhibiting ERK phosphorylation even in an osteogenic medium, suggesting that ERK signaling needs to be shut off in order to proceed with adipose cell commitment. Cell proliferation was greatly increased in osteogenesis but was not changed during adipogenesis, indicating that ERK might play different roles in cellular proliferation and differentiation between the two committed cell types.
The duration and magnitude of ERK activation might be a crucial factor for the balance between adipogenesis and osteogenesis in human bone marrow-derived stem cells.
Yonsei medical journal 01/2011; 52(1):165-72. · 0.77 Impact Factor
[show abstract][hide abstract] ABSTRACT: Mutations in TP53, a tumor suppressor gene, are associated with prognosis of many cancers. However, the prognostic values of TP53 mutation sites are not known for patients with hepatocellular carcinoma (HCC) because of heterogeneity in their geographic and etiologic backgrounds.
TP53 mutations were investigated in a total of 409 HCC patients, including Chinese (n = 336) and white (n = 73) patients, using the direct sequencing method.
A total of 125 TP53 mutations were found in Chinese patients with HCC (37.2%). HCC patients with TP53 mutations had a shorter overall survival time compared with patients with wild-type TP53 (hazard ratio [HR], 1.86; 95% confidence interval [CI]: 1.37-2.52; P < .001). The hot spot mutations R249S and V157F were significantly associated with worse prognosis in univariate (HR, 2.11; 95% CI: 1.51-2.94; P < .001) and multivariate analyses (HR, 1.79; 95% CI: 1.29-2.51; P < .001). Gene expression analysis revealed the existence of stem cell-like traits in tumors with TP53 mutations. These findings were validated in breast and lung tumor samples with TP53 mutations.
TP53 mutations, particularly the hot spot mutations R249S and V157F, are associated with poor prognosis for patients with HCC. The acquisition of stem cell-like gene expression traits might contribute to the aggressive behavior of tumors with TP53 mutation.
[show abstract][hide abstract] ABSTRACT: Neuronal precursor cells (NPCs) are temporally regulated and have the ability to proliferate and differentiate into mature neurons, oligodendrocytes, and astrocytes in the presence of growth factors (GFs). In the present study, the role of the Jak pathway in brain development was investigated in NPCs derived from neurosphere cultures using Jak2 and Jak3 small interfering RNAs and specific inhibitors. Jak2 inhibition profoundly decreased NPC proliferation, preventing further differentiation into neurons and glial cells. However, Jak3 inhibition induced neuronal differentiation accompanied by neurite growth. This phenomenon was due to the Jak3 inhibition-mediated induction of neurogenin (Ngn)2 and NeuroD in NPCs. Jak3 inhibition induced NPCs to differentiate into scattered neurons and increased the expression of Tuj1, microtubule associated protein 2 (MAP2), Olig2, and neuroglial protein (NG)2, but decreased glial fibrillary acidic protein (GFAP) expression, with predominant neurogenesis/polydendrogenesis compared with astrogliogenesis. Therefore, Jak2 may be important for NPC proliferation and maintenance, whereas knocking-down of Jak3 signaling is essential for NPC differentiation into neurons and oligodendrocytes but does not lead to astrocyte differentiation. These results suggest that NPC proliferation and differentiation are differentially regulated by the Jak pathway.
[show abstract][hide abstract] ABSTRACT: Cyclooxygenase-2 (COX-2) inhibitors suppress bone repair and bone formation by suppressing angiogenesis as well as potentially interfering with osteoblast and osteoclast functions. In spite of these reports, there is a controversy over the exact effects of COX-2 inhibitors on bone formation processes itself. This work was designed to investigate the effect of COX-2 inhibitor on osteogenesis of human bone marrow-derived mesenchymal stem cells (MSC). MSCs in osteogenesis were treated with COX-2 inhibitor (celecoxib and naproxen) in the absence or presence of interleukin-1β (IL-1β), which was used to induce inflammation. Following differentiation, alkaline phosphatase (ALP) and calcium contents of IL-1β-treated MSC were significantly reduced by high doses of COX-2 inhibitors compared with the low-dose group. However, in non-inflammatory-conditioned MSCs, ALP and calcium contents were not reduced by COX-2 inhibitors. The mRNA expression of Runx2/Cbf alpha 1, Dlx5, and osteocalcin was also decreased by COX-2 inhibitors in inflammatory-conditioned MSCs and showed a significant decrease for the high dose while they remained constant in the non-inflammatory-conditioned MSCs. These data indicate that the osteogenic potential of MSC is inhibited/delayed by the treatment of high-dose NSAIDs under inflammatory conditions.
Stem cells and development 10/2010; 19(10):1523-33. · 4.15 Impact Factor
[show abstract][hide abstract] ABSTRACT: The role of individual supplements necessary for the long-term self-renewal of embryonic stem (ES) cells is poorly characterized in feeder/serum-free culture systems. This study sought to characterize the relationship between the effects of glucose on ES cell proliferation and fibronectin (FN) synthesis, and to assess the mechanisms responsible for these cellular effects of glucose. Treatment of the two ES cells (ES-E14TG2a and ES-R1) with 25 mM glucose (high glucose) increased the expression levels of FN mRNA and protein. In addition, high glucose and ANG II synergistically increased FN expression level, which coincident with data showing that high glucose increased the mRNA expression of angiotensin II (ANG II) type 1 receptor (AT(1)R), angiotensinogen, and FN, but not ANG II type 2 receptor. High glucose also increased the intracellular calcium (Ca(2+)) concentration and pan-protein kinase C (PKC) phosphorylation. Inhibition of the Ca(2+)/PKC pathway blocked high glucose-induced FN expression. High glucose or ANG II also synergistically increased transforming growth factor-beta1 (TGF-beta(1)) expression, while pretreatment with losartan abolished the high glucose-induced increase in TGF-beta(1) production. Moreover, TGF-beta(1)-specific small interfering RNA inhibited high glucose-induced FN expression and c-Jun N-terminal kinase (JNK) activation. The JNK inhibitor SP600125 blocked high glucose-induced FN expression and inhibited cell cycle regulatory protein expression induced by high glucose or TGF-beta(1). In this study, inhibition of AT(1)R, Ca(2+)/PKC, TGF-beta(1), JNK, FN receptor blocked the high glucose-induced DNA synthesis, increased the cell population in S phase, and the number of cells. It is concluded that high glucose increases FN synthesis through the ANG II or TGF-beta1 pathways, which in part mediates proliferation of mouse ES cells.
Journal of Cellular Physiology 05/2010; 223(2):397-407. · 4.22 Impact Factor
[show abstract][hide abstract] ABSTRACT: To provide estimates of maternal age-specific rates of fetal chromosomal abnormalities at 16-20 weeks' gestation for Korean women >or=35 years of age.
Using the logistic regression method, we analyzed the amniocentesis data of 2,032 gravidas who had fetal karyotyping for the sole indication of advanced maternal age. Also, we compared the prevalence of trisomy 21 among countries using previously published datasets.
The incidence of aneuploidies increased exponentially with maternal age (p < 0.001). The expected rate of trisomy 21 was 3.7 per 1,000 gravidas at 35 years of age. Comparison with other countries showed that Japan has a significantly lower rate of trisomy 21 than North America (p = 0.041; 95% CI 0.522-0.986) and the UK (p = 0.011; 95% CI 0.474-0.909).
These age-related risk figures are the first data for Korean women. Advanced maternal age was in this study ascertained to be a strong risk factor for chromosomal abnormalities; however, the age-specific risk can be influenced by racial factors.
Fetal Diagnosis and Therapy 01/2010; 27(4):214-21. · 1.90 Impact Factor
[show abstract][hide abstract] ABSTRACT: Abstract It is unknown why the influenza B virus causes less severe clinical signs than the influenza A virus in humans. Here we show that influenza B virus induces a lower levels of inflammatory cytokines in the lungs of infected ferrets, and causes less pathological damage to their lung tissues than does influenza A virus. The copy numbers of inflammatory cytokine genes, such as TNF-alpha and IFN-alpha, was significantly lower in the lungs of ferrets infected with influenza B virus than in those infected with influenza A virus. There were also significantly lower viral titers in the lungs of ferrets infected with the influenza B virus than with the influenza A virus. In addition, the duration of viral presence was shorter in the lungs of ferrets infected with influenza B virus than with influenza A virus. Taken together, our results suggest that the lower induction of inflammatory cytokines and lower viral titers in the lungs may be responsible for the milder clinical signs seen in ferrets or humans infected with influenza B virus.
[show abstract][hide abstract] ABSTRACT: The purpose of this study was to evaluate the mechanism of crosstalk between the type II collagen and TGF-beta1 signaling pathways in chondrocytic cells. Articular chondrocytes, isolated from porcine knee cartilage, and the SW1353 cell line were cultured on either type II collagen-coated or -uncoated plates in the presence or absence of TGF-beta1. Expression of pSMAD 2, pSMAD 3, pFAK(Y397) and pFAK(Y925) in articular chondrocytes and the SW1353 cell line was analyzed by immunoblotting. Cell proliferation rates and glycosaminoglycan (GAG) content was determined after treatment with type II collagen or/and TGF-beta1. For inhibition study, human FAK-specific RNA small interference (siFAK) in SW1353 cell line was performed. In this study, expression of pSMAD 2, pSMAD 3, pFAK(Y397) and pFAK(Y925) were synergistically increased by co-treatment with type II collagen and TGF-beta1 in articular chondrocytes. The proliferation of porcine articular chondrocytes and GAG secretion in SW1353 cells were synergistically increased by co-stimulation with type II collagen and TGF-beta1. Synergistically increased expression and nuclear translocation of pSMAD 2 and pSMAD 3 and GAG secretion of SW1353 cells were significantly inhibited by siFAK transfection. Therefore, we suggest that FAK-SMAD 2/3 mediates signal crosstalk between type II collagen and TGF-beta1 and regulates GAG secretion in chondrocytic cells.
Matrix biology: journal of the International Society for Matrix Biology 10/2009; 29(2):135-42. · 3.56 Impact Factor
[show abstract][hide abstract] ABSTRACT: Reactive oxygen species (ROS) generated by a variety of endogenous factors and roles in embryonic stem (ES) cells has yet to be identified. Thus, we examined role of arachidonic acid (AA) in H(2)O(2)-induced proliferation of mouse ES cells and its related signaling molecules. AA release was maximally increased in response to 10(-4) M H(2)O(2) for 1 h. In addition, H(2)O(2) increased intracellular Ca(2+) concentration ([Ca(2+)](i)) and the phosphorylation of protein kinase C (PKC), p44/42, p38 mitogen-activated protein kinase (MAPK), and JNK/SAPK. Moreover, H(2)O(2) induced an increase in the phosphorylation of epidermal growth factor receptor (EGFR), which was blocked by the inhibition of p44/42 or p38 MAPKs. The inhibition of each signal molecule with specific inhibitors blocked H(2)O(2)-induced cytosolic phospholipase A(2) (cPLA(2)) activation and AA release. H(2)O(2) increased NF-kappaB phosphorylation to induce an increase in the levels of cyclooxygenase (COX)-2 proteins. Subsequently, H(2)O(2) stimulated PGE(2) synthesis, which was reduced by the inhibition of NF-kappaB activation. Moreover, each H(2)O(2) or PGE(2) increased DNA synthesis and the number of cells. However, H(2)O(2)-induced increase in DNA synthesis was inhibited by the suppression of cPLA(2) pathway. In conclusion, H(2)O(2) increased AA release and PGE(2) production by the upregulation of cPLA(2) and COX-2 via Ca(2+)/PKC/MAPKs and EGFR transactivation, subsequently proliferation of mouse ES cells.
Journal of Cellular Biochemistry 03/2009; 106(5):787-97. · 3.06 Impact Factor
[show abstract][hide abstract] ABSTRACT: This study investigated the effect of linoleic acid (LA) on cell proliferation and the related signaling cascade in mouse embryonic stem (ES) cells.
To examine effects of LA, mouse ES cells (ES-E14TG2a) were used. Moreover, DNA synthesis, glucose production, protein and mRNA expressions were measured.
LA increased DNA synthesis in a concentration- (> or = 10(-9) M) and time- (> or = 24 h) dependent manner, as determined by [3H] thymidine incorporation and increased cell number. LA increased intracellular Ca2+ levels via regulation of phospholipase C (PLC) and activated protein kinase C (PKC). LA activated phosphatidylinositol 3-kinase (PI3K)/Akt and p44/42 mitogen-activated protein kinases (MAPKs). U73122 (PLC inhibitor), staurosporine (PKC inhibitor), LY294002 (PI3K inhibitor), and Akt inhibitor blocked the phosphorylation of p44/42 MAPKs. In addition, LA stimulated gluconeogenesis through increase expression of glucose-6-phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (PEPCK). LA-induced increases in the cell cycle regulatory proteins, cyclin D1, cyclin E, cyclin-dependent kinase (CDK) 2, and CDK 4, were blocked by U73122, staurosporine, LY294002, Akt inhibitor, PD98059, and metformin (gluconeogenesis inhibitor).
LA stimulated cell proliferation via Ca2+, PLC/PKC, PI3K/Akt, and p44/42 MAPKs signaling pathways in mouse ES cells.
Cellular Physiology and Biochemistry 02/2009; 23(1-3):53-64. · 3.42 Impact Factor