• 한국수정란이식학회지
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• 제21권4호
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• pp.281-286
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• 2006

본 연구는 소 난관 상피 세포를 채취 체외 배양을 실시하고, 이에 착상과 관련이 있은 IL-4를 첨가하여 배양액내의 임신에 관련된 호르몬들(P4, E2, TGF-$\beta$)의 변화를 관찰함으로써, 소 난관 상피 세포와 착상과의 관계를 구명하고자 실시하였으며, 그에 따른 결과는 다음과 같다. 소 난관 상피 세포의 체외 배양시 IL-4 첨가에 의한 배양액내의 P4의 생산은 0.001 ng/ml의 IL-4를 첨가한 배양액의 P4의 농도는 배양 시간이 경과할수록 증가하는 경향을 보였으며, 24시간보다 120시간에서는 약 2배의 생산을 보여 유의적인 차이를 나타냈다(P<0.05). 0.01 ng/ml의 경우에도 0.001의 경우와 유사한 경향을 보였으나, 0.001 ng/ml의 경우보다는 다소 생산량이 낮았다. 0.1이나 1 ng/ml의 경우는 배양 시간에 따른 생산량은 다른 두 가지의 농도와 같이 배양시간 96시간까지는 증가하였으나, 배양 시간 120시간에서는 감소하였다. 소 난관 상피 세포의 체외 배양시 IL-4 첨가에 의한 배양액내의 E2의 생산은 0.001, 0.01 ng/ml 첨가시는 P4의 경우와 같이 배양 시간 72시간까지 배양 시간에 따라 생산량이 증가하여 유의적인 차이를 나타내었으며(P<0.05), 0.1 및 1 ng/ml의 경우는 배양 시간 96시간까지 증가하는 경향을 보였다. 그러나 배양 시간 120 시간에는 IL-4의 첨가 농도에 관계없이 배양 시간 24시간째의 생산량과 유사한 경향을 나타냈다. 소 난관 상피 세포의 체외 배양시 IL-4 첨가에 의한 배양액 내 TGF-$\beta$의 생산은 IL-4의 첨가 농도 및 배양 시간에 대하여 차이를 나타내지 않았으며, 유의성도 나타나지 않았다. 배양 초기에 비하여 배양시간 120시간에는 약간 생산이 낮아지는 것으로 나타나 IL-4에 의한 TGF-$\beta$의 생산은 배양 시간 96이후에는 활성이 저하하는 것으로 나타났다. 이상의 결과로 소 난관 상피 세포의 체외 배양시 IL-4 첨가는 P4 및 E2의 생산에 영향을 미치는 것으로 나타났으며, TGF-$\beta$의 생산에는 영향을 미치지 않는 것으로 나타나, IL-4는 소의 임신의 성립에 중요한 역할을 하며, 난관 상피 세포 이외의 자성 생식 기도 내에 있어서 IL-4와 관련된 기전에 대하여 더 많은 연구가 요구된다.

• 한국생물공학회:학술대회논문집
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• 한국생물공학회 2000년도 춘계학술발표대회
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• pp.96-97
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• 2000

• 한국동물학회:학술대회논문집
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• 한국동물학회 1995년도 한국생물과학협회 학술발표대회
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• pp.351.1-351
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• 1995

No Abstract, See Full Text

• 대한치주과학회:학술대회논문집
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• 대한치주과학회 1994년도 제34회 종합학술대회
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• pp.40-41
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• 1994

• 대한약학회:학술대회논문집
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• 대한약학회 2000년도 NEW STRATEGY FOR DRUG DEVELOPMENT IN POST-GENOMIC ERA(대한약학회)
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• pp.146.1-146.1
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• 2000

• 한국발생생물학회지:발생과생식
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• 제17권4호
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• pp.299-309
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• 2013

Transforming growth factor (TGF) family is well known to induce the chondrogenic differentiation of mesenchymal stem cells (MSC). However, the precise signal transduction pathways and underlying factors are not well known. Thus the present study aims to evaluate the possible role of C2 domain in the chondrogenic differentiation of human mesenchymal stem cells. To this end, 145 C2 domains in the adenovirus were individually transfected to hMSC, and morphological changes were examined. Among 145 C2 domains, C2 domain of protein kinase C eta ($PKC{\eta}$) was selected as a possible chondrogenic differentiation factor for hMSC. To confirm this possibility, we treated $TGF{\beta}3$, a well known chondrogenic differentiation factor of hMSC, and examined the increased-expression of glycosaminoglycan (GAG), collagen type II (COL II) as well as $PKC{\eta}$ using PT-PCR, immunocytochemistry and Western blot analysis. To further evaluation of C2 domain of $PKC{\eta}$, we examined morphological changes, expressions of GAG and COL II after transfection of $PKC{\eta}$-C2 domain in hMSC. Overexpression of $PKC{\eta}$-C2 domain induced morphological change and increased GAG and COL II expressions. The present results demonstrate that $PKC{\eta}$ involves in the TGF-${\beta}3$-induced chondrogenic differentiation of hMSC, and C2 domain of $PKC{\eta}$ has important role in this process.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2005년도 춘계 국제심포지엄 및 학술대회
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• pp.165-165
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• 2005

• The Korean Journal of Physiology and Pharmacology
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• 제13권3호
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• pp.153-159
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• 2009

We investigated whether deficiency of inducible nitric oxide synthase (iNOS) could prevent isoproterenol-induced cardiac hypertrophy in iNOS knockout (KO) mice. Isoproterenol was continuously infused subcutaneously (15 mg/kg/day) using an osmotic minipump. Isoproterenol reduced body weight and fat mass in both iNOS KO and wild-type mice compared with saline-infused wild-type mice. Isoproterenol increased the heart weight in both iNOS KO and wild-type mice but there was no difference between iNOS KO and wild-type mice. Posterior wall thickness of left ventricle showed the same tendency with heart weight. Protein level of iNOS in the left ventricle was increased in isoproterenol-infused wild-type mice. The gene expression of interleukin-6 (IL-6) and transforming growth factor-${\beta}$ (TGF-${\beta}$) in isoproterenol-infused wild-type was measured at 2, 4, 24, and 48-hour and isoproterenol increased both IL-6 (2, 4, 24, and 48-hour) and TGF-${\beta}$ (4 and 24-hour). Isoproterenol infusion for 7 days increased the mRNA level of IL-6 and TGF-${\beta}$ in iNOS KO mice, whereas the gene expression in wild-type mice was not increased. Phosphorylated form of extracellular signal-regulated kinases (pERK) was also increased by isoproterenol at 2 and 4-hour but was not increased at 7 days after infusion in wild-type mice. However, the increased pERK level in iNOS KO mice was maintained even at 7 days after isoproterenol infusion. These results suggest that deficiency of iNOS does not prevent isoproterenol-induced cardiac hypertrophy and may have potentially harmful effects on cardiac hypertrophy.

• IMMUNE NETWORK
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• 제5권4호
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• pp.215-220
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• 2005

Background: Transforming growth factor-${\beta}$ (TGF-${\beta}1$) directs class switch recombination (CSR) to IgA isotype, which is a predominant antibody in mucosal surfaces. Although IgA is preferentially committed in mucosal lymphoid tissues, it is not definitely established whether hallmarks of IgA CSR such as IgA germ-line transcripts (GLT ${\alpha}$), post-switch transcripts (PST ${\alpha}$) and circle transcripts (CT ${\alpha}$) are readily expressed in such tissues. Therefore, we compared the expression of these transcripts among mouse Peyer's patches (PP), mesenteric lymph nodes (MLN), and spleen. Methods: Levels of GLTs, PSTs and CTs were measured by RT-PCR in isolated PPs, MLNs and spleen cells. Results: GLT ${\alpha}$ and PST ${\alpha}$ were well expressed in PP and MLN cells but in spleen cells. Similar patterns were observed in the expression of GL ${\gamma}$2b and PST ${\gamma}$2b. On the other hand, these transcripts were only inducible in spleen cells upon stimulated with LPS and TGF-${\beta}1$. In addition, CT${\alpha}$ and CT${\gamma}$2b were detected in PP cells. Conclusion: PP B cells readily express IgA GLT, PST, and CT. Overall expression patterns of these transcripts were similar in MLN cells. Thus, these results suggest that microenvironment of PP and MLN influences spontaneous IgA CSR, which lacks in systemic lymphoid tissues such as spleen.

• Asian Pacific Journal of Cancer Prevention
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• 제15권20호
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• pp.8705-8708
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• 2014

Disrupted transforming growth factor-${\beta}$ (TGF-${\beta}$) signaling is involved in the development of various types of cancer and the TGF-${\beta}$ receptor II (TGFBR2) is a key mediator of TGF-${\beta}$ growth inhibitory signals. It is reported that the G-875A polymorphism in TGFBR2 is implicated in risk of various cancers. However, results for the association between this polymorphism and cancer remain conflicting. To derive a more precise estimation, a meta-analysis of 3,808 cases and 4,489 controls from nine published case-control studies was performed. Our analysis indicated that G-875A is associated with a trend of decreased cancer risk for allele A versus(vs.) allele G [odds ratio (OR) =0.64, 95% confidence intervals (CI): 0.55-0.74], as well as for both dominant model [(A/A+G/A) vs. G/G, OR=0.76, 95% CI: 0.64-0.90] and recessive model [A/A vs. (G/G+G/A), OR=0.74, 95% CI: 0.59-0.93). However, larger scale primary studies are required to further evaluate the interaction of TGFBR2 G-875A polymorphism and cancer risk in specific cancer subtypes.