• International Journal of Vascular Biomedical Engineering
• /
• 제3권1호
• /
• pp.23-29
• /
• 2005

We developed a three dimensional cardiac tissue model based on human cardiac cell and mono-domain approximation for action potential propagation. The human myocyte model proposed by ten Tusscher et al. (TNNP model) (2004) for cell electrophysiology and a mono-domain method for electric wave propagation are used to simulate the cardiac tissue propagation mechanism using a finite element method. To delineate non-homogeneity across cardiac tissue layer, we used three types of cardiac cell models. Ansiotropic effect of action potential propagation is also considered in this study. In this 3D anisotropic cardiac tissue with three cell layers, we generated a reentrant wave using S1-S2 protocol. Computational results showed that the reentrant wave was affected by the anisotropic properties of the cells. To test the reentrant wave under pathological state, we simulated a hypertopic model with non-excitable fibroblasts in stochastic manner. Compared with normal tissue, the hypertropic tissue result showed another center of reentrant wave, indicating that the wave pattern can be more easily changed from regular with a concentric focus to irregular multi-focused reentrant waves in case of patients with hypertrophy.

• 대한화장품학회지
• /
• 제33권4호
• /
• pp.245-249
• /
• 2007

노화 과정 중에 일어나는 extracellular matrix (ECM)의 변성은 피부의 주름과 탄력 감소를 유발한다. 현재까지 항노화의 주요 타겟은 metalloproteases 혹은 콜라겐이나 엘라스틴 같은 구조 단백질에 집중되어 있지만, 최근 세포와 ECM 단백질(콜라겐, 피브릴린, 파이브로넥틴) 간의 상호작용이 세포의 생존과 증식, 조직의 재건에 중요한 역할을 한다고 알려졌다. 파이브로넥틴은 다른 ECM 단백질이나 인테그린 같은 세포 표면 수용체와 결합할 수 있는 부위를 가진 부착 단백질이다. 최근 보고에 따르면 세린 프로티아제들에 의해 분해된 파이프로넥틴 조각이 골아세포에서 MMPs 발현을 증가시킨다. 그러나 파이브로넥틴 조각의 사람 피부에서의 역할은 보고된 바 없다. 본 연구에서는 노인의 피부에서 파이브로넥틴 조각이 현저히 증가되어 있으며, 섬유아세포에 파이브로넥틴 조각을 처리하였을 시, MMP-1의 발현과 MMP-2의 활성이 증가한다는 것을 입증하였다. 이 결과는 파이브로넥틴 조각이 피부 노화를 유발하는 새로운 인자일 가능성을 제시하고 있다.

• Journal of Periodontal and Implant Science
• /
• 제26권3호
• /
• pp.701-713
• /
• 1996

The purpose of this study was to evaluate the biocompatibility of the Nd:YAG lased root surface followed by root planing and/or tetracyline-HCI(T.C.-HCI) conditioning. $30,4mm{\times}4mm$ root segments were obtained from unerupted third molars and 21, periodontally involved root segments. The treatment groups were as follows : (1) healthy root cementum surface groups : 1) control(non-treated group), 2) lased only, 3) lased/root planed, and 4) lased/T.C.-HCI. (2) diseased root cementum surface groups : 1) control(root planed only), 2) lased/root planed, and 3) lased/root planed/T.C.-HCI. The specimens were treated with a Nd:YAG laser using a $320{\mu}m$ noncontact optic fiber handpiece with an energy setting of 1.5W($114.6J/cm^2$), 2.0W($152.9J/cm^2$), 5.0W($382J/cm^2$) for one minute. The fiber was held perpendicular to the petri dish(NUNC) 2cm apart in an attempt to expose the entire root segments equally. Human gingival fibroblasts were cultured from explants of normal interdental gingival tissue obtained during third morlar extraction. The attachment assay was performed with third-generation fibroblasts. The numbers of gingival fibroblasts attached to the root surface were counted on each specimen under the light microscope, and were statistically analyzed by the oneway ANOVA followed by Tukey's test in SPSS/PC+programs. The results were as follows : 1) In healthy root cementum surfaces, lased/root planed groups exhibited a significantly increased fibroblast attachment compared to controls, lased only, and lased/T.C.-HCI groups(p<0.05), 2) In diseased root cementum surfaces, laser treatment followed by root planing and/or T.C.HCl groups exhibited a increased tendency of fibroblast attachment compared to root planed only group. The results suggest that laser treatment followed by root planing and/or T.C.-HCl would appear necessary so as to render the root surface biocompatible.

• Journal of Ginseng Research
• /
• 제44권3호
• /
• pp.386-398
• /
• 2020

Tissue fibrosis is an eventual pathologic change of numerous chronic illnesses, which is characterized by resident fibroblasts differentiation into myofibroblasts during inflammation, coupled with excessive extracellular matrix deposition in tissues, ultimately leading to failure of normal organ function. Now, there are many mechanistic insights into the pathogenesis of tissue fibrosis, which facilitate the discovery of effective antifibrotic drugs. Moreover, many chronic diseases remain a significant clinical unmet need. For the past five years, many research works have undoubtedly addressed the functional dependency of ginsenosides in different types of fibrosis and the successful remission in various animal models treated with ginsenosides. Caveolin-1, interleukin, thrombospondin-1 (TSP-1), liver X receptors (LXRs), Nrf2, microRNA-27b, PPARδ-STAT3, liver kinase B1 (LKB1)-AMPK, and TGF-β1/Smads are potential therapy targeting using ginsenosides. Ginsenosides can play a targeting role and suppress chronic inflammatory response, collagen deposition, and epitheliale-mesenchymal transition (EMT), as well as myofibroblast activation to attenuate fibrosis. In this report, our aim was to focus on the therapeutic prospects of ginsenosides in fibrosis-related human diseases making use of results acquired from various animal models. These findings should provide important therapeutic clues and strategies for the exploration of new drugs for fibrosis treatment.

• Biotechnology and Bioprocess Engineering:BBE
• /
• 제6권4호
• /
• pp.231-236
• /
• 2001

How much do we know about the biology of aging from cell culture studies Most normal somatic cells have a finite potential to divide due to a process termed cellular or replicative senescence. A growing body evidence suggests that senescence evolved to protect higher eu-karyotes, particularly mammals, from developing cancer, We now know that telomere shortening due to the biochemistry of DNA replication, induces replicative senescence in human cells. How-ever in rodent cells, replicative senescence occurs despite very long telomeres. Recent findings suggest that replicative senescence is just the tip of the iceberg of a more general process termed cellular senescence. It appears that cellular senescence is a response to potentially oncogenic in-sults, including oxidative damage. In young orgainsms, growth arrest by cell senescence sup-presses tumor development, but later in life, due to the accumulation of senescent cells which se-cret factors that can disrupt tissues during aging, cellular senescence promotes tumorigenesis. Therefore, antagonistic pleiotropy may explain, if not in whole the apparently paradoxical effects of cellular senescence, though this still remains an open question.

• Bulletin of the Korean Chemical Society
• /
• 제34권11호
• /
• pp.3405-3409
• /
• 2013

The activation of heat shock factor 1 (HSF1) can be induced by the changes in environmental pH, but the mechanism of HSF1 activation by acidification is not completely understood. This paper reports that a low pH (pH~6.0) can trigger human HSF1 activation. Considering the involvement of the imidazole group of histidine residues under acid pH stress, an in vitro EMSA experiment, Trp-fluorescence spectroscopy, and protein structural analysis showed that the residue, His83, is the essential for pH-dependent human HSF1-activation. To determine the roles of His83 in the HSF1-mediated stress response affecting the cellular acid resistance, mouse embryo fibroblasts with normal wild-type or mutant mouse HSF1 expression were preconditioned by heating or pH stress. The results suggest that His83 is essential for HSF1 activation or the HSF1-mediated transcription of heat shock proteins, in protecting cells from acid pH stress.

• 한국미생물·생명공학회지
• /
• 제35권4호
• /
• pp.316-324
• /
• 2007

콩류에 다량 존재하는 제니스틴으로부터 얻을수 있는 제니스테인이 노화된 피부 섬유아세포의 활성과 피부의 주성분인 콜라겐의 합성 및 이의 주요한 분해 효소인 MMP-1의 합성에 어떤 영향을 미치는지 알아보고자 하였다. 제니스테인은 54세의 섬유아세포 증식을 유의하게 증가시켰으며, 이러한 세포증식 효과는 비타민 A와 유사하게 자연노화가 많이 진행된 세포에서 뚜렷하였다. 아울러 77세의 섬유아세포에서 제니스테인 처리에 의해 세포노화의 지표인 SA-${\beta}$-Gal 염색이 감소된 것을 확인하였다. 그리고 제니스테인은 섬유아세포에서 type I pN 콜라겐의 합성을 촉진하였고, UVA에 의해 콜라겐 합성이 매우 억제된 상황에서도 합성 증가 효과를 보였는데 이러한 현상은 자연노화가 많이 진행된 세포에서 더욱 효과적이었다. 콜라겐 매트릭스를 이용한 콜라겐 생합성 결과에서 제니스테인은 광노출부나 비노출 부위에서 얻은 모두의 세포에서 콜라겐 합성을 증가시킴을 알 수 있었으며, 이를 통해 제니스테인이 광노화 및 자연노화에 모두 효과적인 것으로 추측할 수 있다. 제니스테인은 젊은 피부의 세포에서 MMP-1의 합성에는 큰 영향을 미치지 않았으나, 노화된 피부의 세포에서 매우 증가되어 있는 MMP-1의 합성을 억제하였다. 이상의 결과에서 제니스테인은 광노화 뿐 아니라, 자연 노화에 의한 피부 주름을 예방하는데 유용한 물질이 될 것으로 사료된다.

• Journal of Nutrition and Health
• /
• 제49권6호
• /
• pp.429-436
• /
• 2016

본 연구에서는 피부의 표피와 진피에 분포하는 HaCaT 세포와 HDF 세포를 이용하여 항산화효과가 우수한 두릅순 추출물의 처리가 UVB에 의한 피부광노화를 억제할 수 있는지 알아보기 위하여 피부 염증반응과 관련한 사이토카인과 피부의 주요 구성 단백질인 collagen에 영향을 미칠 수 있는 MMP-1, type-I procollagen, TRPV-1 등의 단백질 발현에 미치는 영향을 분석하였다. HaCaT에 두릅순 추출물을 24시간 전처리한 경우 UVB ($55 mJ/cm^2$) 노출로 인해 증가한 염증매개인자인 IL-6, IL-8, $PGE_2$를 유의하게 감소시켰다. 또한, 피부 collagen의 정상적인 구조 및 양에 영향을 미치는 단백질들의 발현을 측정한 결과 HaCaT에서는 UVB 조사로 인해 증가한 TRPV-1과 MMP-1 단백질의 발현이 두릅순 에탄올 추출물의 전처리로 모두 감소하였고, HDF에서는 UVB를 조사한 대조군에 비하여 두릅순 추출물 처리가 MMP-1 단백질 발현을 감소시키는 동시에 collagen의 전구체인 type-I procollagen의 발현을 증가시키는 효과를 보였다. 이들 결과들로부터 항산화효과가 우수한 두릅순 70% 에탄올 추출물은 피부세포에서 UVB에 의한 염증반응을 억제시키는 동시에 피부 collagen의 감소를 억제시킴으로써 피부 광노화를 예방할 수 있는 천연 소재로 이용될 수 있다고 본다.

• Journal of Periodontal and Implant Science
• /
• 제36권3호
• /
• pp.613-625
• /
• 2006

Periodontal ligament(PDL) cells and human gingival fibroblasts(HGFs) play important roles in development, regeneration, normal function, and pathologic alteration. PDL cells and HGFs have the similarity related with general characteristics of fibroblast such as spindle shaped morphology, the presence of vimentin intermediate filament and the synthesis of interstitial collagens and fibronectin. There were many studies about the differences between PDL cells and HGFs, but they were not about whole gene level. In this study, we tried to explain the differences of gene expression profiles between PDL cells and HGFs, and the differences among three individuals by screening gene expression patterns of PDL cells and HGFs, using cDNA microarray. Although there were some variants among three experiments, a set of genes were consistentely and differentially expressed in one cell type. Among 3,063 genes, 49 genes were more highly expressed in PDL cells and 12 genes were more highly expressed in HGFs. The genes related with cell structure and motility were expressed more highly in PDL cells. These are cofilin 1, proteoglycan 1 secretory granule, collagen type I(${\alpha}$ 1), adducin gamma subunit, collagen type III(${\alpha}$ 1), fibronectin, lumican(keratan sulfate proteoglycan), and ${\alpha}$ -smooth muscle actin. Tissue inhibitor of metalloproteinase known as the enzyme controlling extracellular matrix with matrix metalloproteinase is more highly expressed in PDL cells, osteoprotegerin known as osteoclastogenesis inhibitory factor is more highly expressed in HGFs. We performed northern blot to verify cDNA microarray results on selected genes such as tissue inhibitor of metalloproteinase, fibronectin, osteoprogeterin. The result of northern blot analysis showed that each cell expressed the genes in similar pattern with cDNA microarray result. This result indicates that cDNA microarray is a reliable method in screening of gene expression profiles.

• BMB Reports
• /
• 제52권3호
• /
• pp.202-207
• /
• 2019

Keloids are the most common pathological form of trauma healing, with features that seriously affect appearance and body function, are difficult to treat and have a high recurrence rate. Emerging evidence suggests that miRNAs are involved in a variety of pathological processes and play an important role in the process of fibrosis. In this study, we investigated the function and regulatory network of miR-152-5p in keloids. The miRNA miR-152-5p is frequently downregulated in keloid tissue and primary cells compared to normal skin tissue and fibroblasts. In addition, the downregulation of miR-152-5p is significantly associated with the proliferation, migration and apoptosis of keloid cells. Overexpression of miR-152-5p significantly inhibits the progression of fibrosis in keloids. Smad3 is a direct target of miR-152-5p, and knockdown of Smad3 also inhibits fibrosis progression, consistent with the overexpression of miR-152-5p. The interaction between miR-152-5p and Smad3 occurs through the Erk1/2 and Akt pathways and regulates collagen3 production. In summary, our study demonstrates that miR-152-5p/Smad3 regulatory pathways involved in fibrotic progression may be a potential therapeutic target of keloids.