• Molecules and Cells
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• 제21권2호
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• pp.206-212
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• 2006

We have established in culture a spontaneously immortalized bovine embryonic fibroblast (BEF) cell line that has lost p53 and $p16^{INK4a}$ functions. MyoD is a muscle-specific regulator capable of inducing myogenesis in a number of cell types. When the BEF cells were transduced with MyoD they differentiated efficiently to desmin-positive myofibers in the presence of 2% horse serum and 1.7 nM insulin. The myogenic differentiation of this cell line was more rapid and obvious than that of C2C12 cells, as judged by morphological changes and expression of various muscle regulatory factors. To confirm that lack of the p53 and $p16^{INK4a}$ pathway does not prevent MyoD-mediated myogenesis, we established a cell line transformed with SV40LT (BEFV) and introduced MyoD into it. In the presence of 2% horse serum and 1.7 nM insulin, the MyoD-transduced BEFV cells differentiated like the MyoD-transduced BEFS cells, and displayed a similar pattern of expression of muscle regulatory proteins. Taken together, our results indicate that MyoD overexpression overcomes the defect in muscle differentiation associated with immortalization and cell transformation caused by the loss of p53 and Rb functions.

• 한국수산과학회지
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• 제55권6호
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• pp.960-966
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• 2022

We aimed to determine the dietary myo-inositol (MI) requirements of Pacific white shrimp Litopenaeus vannamei. A basal diet was formulated without myo-inositol (M0) and a negative control diet (M0-) was prepared by adding tetracycline hydrochloride to the basal diet to prevent intestinal inositol synthesis. Five MI diets were prepared by adding MI at 300, 600, 900, 1,200 and 1,500 mg/kg to the basal diet (designated as, M300, M600, M900, M1200 and M1500, respectively). Triplicate groups of shrimp (initial body weight, 0.55±0.01 g) were fed one of the experimental diets for 42 days. The growth performance of shrimp in M0- group was significantly lower when compared to that of shrimp in M0, M1200 and M1500 groups. Feed efficiency was significantly improved in M1200 and M1500 groups when compared to the M0 and M0- groups. GPx activity was significantly higher in M1200 and M1500 groups compared to that in M0 and M0- groups. Therefore, a practical diet (over 240 mg/kg) meets the minimum MI requirements of Pacific white shrimp. However, the optimum dietary MI level would be potentially above 1,200 mg/kg for better feed utilization efficiency and antioxidant capacity of Pacific white shrimp.

• Mass Spectrometry Letters
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• 제7권1호
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• pp.12-15
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• 2016

Results of free and bound myo-inositol in infant formula (IF) are presented. Inositol was analyzed by HILIC ultra-performance liquid chromatography coupled with mass spectrometer. The levels of free myo-inositol in 27 Australian and 4 EU originated IF samples were 300-600 mg/kg of powder or 1.6-3.1 mg/100 kJ. The amount of bound inositol in lipid fraction of IF was, on average, 10% of free myo-inositol.

• 한국환경보건학회지
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• 제22권3호
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• pp.8-16
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• 1996

Effects of water extract of aloe vera on lead-induced neurotoxicity were investigated in sciatic nerve isolated from rat. The mechanism on toxicity reduction by measuring activities of axonal enzymes, metabolism of myo-inositol in nerve, lead concentration in several organs and so on were further examimed. In the lead-treated rats, the transport rate of axonal enzyme, such as acetyl cholinesterase and choline acetyltransferase, was reduced by from 50% to 30% respectively. Reduction in myo-inositol concentration and $Na^+/K^+$ ATPase activity were also observed in sciatic nerve from lead-treated rat. However, the aloe extract administration significantly eliminated the impairment and maintained myo-inositol concentration to about 85% of normal level. Also aloe extract promoted the excretion rate of lead which is accumulated in blood, sciatic nerve and kidney. These results suggest that lead-induced neurotoxicity was significantly reduced by administration of aloe extract and the mechanism might be partly increase in kidney excretion rate of lead and parity normalization of $Na^+/K^+$ ATPase activity which is critical factor in order to keep nerve maintaining normal myo-inositol level.

• 대한화학회지
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• 제50권2호
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• pp.129-136
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• 2006

마이오 이노시톨을 이용한 새로운 고분자 리간드를 합성하였다. 형태적으로 안정한 이노시톨 고분자를 얻기 위해 고리화 고분자반응을 시도하였으며, 고리화의 메커니즘 및 고리 구조가 입증되었다. 또한, 분광학적 비교 방법을 이용해 합성된 고분자들의 형태가 밝혀졌다. 마이오 이노시톨 카보네이트를 이용해 형태적으로 고정된 고분자 리간드를 성공적으로 합성하였다.

• Bulletin of the Korean Chemical Society
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• 제27권3호
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• pp.359-360
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• 2006

• 한국수정란이식학회지
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• 제25권1호
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• pp.1-7
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• 2010

The objective of this study was to examine the effect of vitamin B (pantothenic acid, folic acid, and myo-inositol) that was supplemented to embryo culture medium on in vitro development of parthenogenetically activated (PA) pig embryos. Cumulus-oocyte complexes derived from slaughtered ovaries were matured in TCM-199 supplemented with porcine follicular fluid, cysteine, pyruvate, EGF, insulin, and hormones (hCG and eCG) for the first 22 h and then further cultured in hormone-free medium for an additional 22 h. After maturation culture, metaphase II oocytes that extruded 1st polar body were electrically activated and treated with $5.0\;{\mu}g/ml$ cytochalasin B for 4 h. Then, PA embryos were cultured for 7 days in a modified NCSU-23 that was supplemented with pantothenic acid, myo-inositol, or folic acid at different concentrations ($3{\sim}300\;{\mu}M$) according to the experimental design. Myo-inositol added to culture medium did not show any beneficial or inhibitory effects on embryo cleavage and blastocyst formation. However, $300\;{\mu}M$ pantothenic acid significantly inhibited blastocyst formation compared to control (no addition) (24% vs. 36%, p<0.05). Folic acid ($300\;{\mu}M$) significantly (p<0.05) increased blastocyst formation (56%) compared to control (41%). Our results demonstrated that in vitro development of PA embryos was significantly influenced by vitamin B and addition of $300\;{\mu}M$ folic acid to culture medium improved in vitro development of pig PA embryos.

• Applied Biological Chemistry
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• 제13권3호
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• pp.197-205
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• 1970

1. myo-inositol (aeeeee) 에서 scyllo- (eeeeee), epi-(aeaeee) 및 muco-inositol (aaaeee)에 도달(到達)시킬 수 있었다. 2. inositol의 과산화수소(過酸化水素) 산화(酸化)는 ax. 수산기(水酸基)가 산화(酸化)되어 microbial oxidation, 접촉산화(接觸酸化)에서와 대등(對等)한 inosose를 얻고, 이것은 산성(酸性)에서 $NaBH_4$로 환원(還元)하면 eq.-alcohol이 되며, 한편 접촉산원(接觸還元)하면 az. alcohol 이 된다. 3. inositol의 p-HBA ester인 사종(四種) 신화합물(新化合物) [III], [XII], [XVI], [XXI]을 합성(合成)하였다. 4. 이들 ester는 모두 항균작용(抗菌作用)이 있고 pH의 저하(低下)로 증대(增大)되는 경향(領向)이 있으며 muco-inositol ester는 가장 강력(强力)하고, 이는 입체구조(立體構造)와 관련(關聯)되는 것 같다.

• BMB Reports
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• 제40권6호
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• pp.921-927
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• 2007

UCP2 and UCP3 are members of the uncoupling protein family, which may play roles in energy homeostasis. In order to determine the regulation of the predominant expression of UCP3 in skeletal muscle, the effects of differentiation and myogenic regulatory factors on the promoter activities of the mouse UCP2 and UCP3 genes were studied. Reporter plasmids, containing approximately 3 kb of the 5'-upstream region of the mouse UCP2 and UCP3 genes, were transfected into C2C12 myoblasts, which were then induced to differentiate. Differentiation positively induced the reporter expression about 20-fold via the UCP3 promoter, but by only 2-fold via the UCP2 promoter. C2C12 myoblasts were cotransfected with expression vectors for myogenin and/or MyoD as well as reporter constructs. The simultaneous expression of myogenin and MyoD caused an additional 20-fold increase in the reporter expression via the UCP3 promoter, but only a weak effect via the UCP2 promoter. In L6 myoblasts, only MyoD activated the UCP3 promoter, but in 3T3-L1 cells neither factor activated the UCP3 promoter, indicating that additional cofactors are required, which are present only in C2C12 myoblasts. The expression of UCP2 and UCP3 is differentially regulated during muscle differentiation due to the different responsiveness of their promoter regions to myogenin and MyoD.

• 대한한방내과학회지
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• 제29권1호
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• pp.243-257
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• 2008

Myostatin, a negative regulator of myogenesis, is shown to function by controlling the proliferation of myoblasts. In this study we show that myostatin is an inhibitor of myoblast differentiation and that this inhibition is mediated through Smad 3. To determine MyoD expression by Dodamtang treatment, we compared the expression pattern of $C_{2}C_{12}$ mouse myoblasts that constitutively express myostatin with control cells. In vitro, increasing concentrations of Dodamtang reversibly prevented the myogenic blockage of myoblasts by myostatin expression. ELISA assay, Western and confocal analysis indicated that treatment of Dodamtang to the low serum culture media increased the levels of MyoD leading to the inhibition of myogenic differentiation by myostatin. The stable transfection of $C_{2}C_{12}$ myoblasts with myostatin expressing constructs did rescue MyoD-induced myogenic differentiation. Consistent with this, the treatment of Dodamtang rescued the expression of a MyoD in $C_{2}C_{12}$ myoblasts treated with myostatin. Taken together, these results suggest that induction of MyoD by Dodamtang inhibits myostatin activity and expression via SMAD3 resulting in the rescue of the myoblasts to differentiate into myotubes. Thus we propose that myostatin action by Dodamtang plays a critical role in myogenic differentiation and that the muscular hyperplasia and hypertrophy seen in animals that blockage of functional myostatin is because of deregulated proliferation and differentiation of myoblasts.