• The Korean Journal of Physiology and Pharmacology
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• 제17권2호
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• pp.149-156
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• 2013

Interstitial cells of Cajal (ICCs) are the pacemaker cells in the gastrointestinal tract, and histamine is known to regulate neuronal activity, control vascular tone, alter endothelial permeability, and modulate gastric acid secretion. However, the action mechanisms of histamine in mouse small intestinal ICCs have not been previously investigated, and thus, in the present study, we investigated the effects of histamine on mouse small intestinal ICCs, and sought to identify the receptors involved. Enzymatic digestions were used to dissociate ICCs from small intestines, and the whole-cell patch-clamp configuration was used to record potentials (in current clamp mode) from cultured ICCs. Histamine was found to depolarize resting membrane potentials concentration dependently, and whereas 2-PEA (a selective H1 receptor agonist) induced membrane depolarizations, Dimaprit (a selective H2-agonist), R-alpha-methylhistamine (R-alpha-MeHa; a selective H3-agonist), and 4-methylhistamine (4-MH; a selective H4-agonist) did not. Pretreatment with $Ca^{2+}$-free solution or thapsigargin (a $Ca^{2+}$-ATPase inhibitor in endoplasmic reticulum) abolished the generation of pacemaker potentials and suppressed histamine-induced membrane depolarization. Furthermore, treatments with U-73122 (a phospholipase C inhibitor) or 5-fluoro-2-indolyl des-chlorohalopemide (FIPI; a phospholipase D inhibitor) blocked histamine-induced membrane depolarizations in ICCs. On the other hand, KT5720 (a protein kinase A inhibitor) did not block histamine-induced membrane depolarization. These results suggest that histamine modulates pacemaker potentials through H1 receptor-mediated pathways via external $Ca^{2+}$ influx and $Ca^{2+}$ release from internal stores in a PLC and PLD dependent manner.

• Asian Pacific Journal of Cancer Prevention
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• 제14권11호
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• pp.6305-6309
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• 2013

Background: TIAM2, a Rac guanine nucleotide exchange factor, is closely associated with cell adherence and migration. Here, we aimed to investigate the role of TIAM2 in non-small cell lung cancer (NSCLC) cells. Materials and Methods: A small interference RNA (siRNA) was introduced to silence the expression of TIAM2. Invasion and motility assays were then performed to assess the invasion and motility potential of NSCLC cells. GST-pull down assays were used to detect activation of Rac1. Results: TIAM2 was highly expressed in NSCLC cells. Knockdown of TIAM2 inhibited the invasion and motility, and suppressed activation of Rac1. Further experiments demonstrated that knockdown of TIAM2 could up-regulate the expression of E-cadherin, and down-regulate the expression of MMP-3, Twist and Snail. Conclusions: Our data suggest that TIAM2 can promote invasion and motility of NSCLC cells. Activation of Rac1 and regulation of some EMT/invasion-related genes may be involved in the underlying processes.

• 한국동물학회지
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• 제38권3호
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• pp.388-394
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• 1995

동면동물인 다람쥐를 활동기와 동면기로 나누어 소장 점막 상피세포인 원주세포와 점액세포의 미세구조 변화를 투과전자현미경을 이용하여 관찰하였다. 활동기의 원주세포에서는 많은수의 미토콘드리아와 과립형질내세망을 관찰할 수 있었다. 동면기의 원주세포에서는 많은수의 리보소옴을 관찰할 수 있었다. 활동기의 점액세포에서는 크고 많은수의 점액과립과 세포소기관으로 미토콘드리아와 과립형질내세망을 관찰할 수 있었으며 현저한 분비작용을 관찰할 수 있었다. 동면기의 점액세포에서는 수와 크기에서 감소된 점액과립과 활동기보다 증가된 리보소옴을 관찰할 수 있었으며 분비작용은 활동기에 비해 감소하였다.

• 한국어류학회지
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• 제23권3호
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• pp.250-254
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• 2011

한국의 담수어류 중 짱뚱어, 큰볏말뚝말둥어, 말뚝망둥어, 미꾸리, 미꾸라지, 자가사리 등 모두 6종에서 공기로 호흡하기 위해 변형된 부속기관이 알려져 있다. 짱뚱어, 큰볏말뚝말망둥어, 말뚝망둥어, 자가사리 4종은 부족한 산소를 공기로부터 흡입하기 위해 호흡상피 (respiratory epithelium)를 갖는다. 이러한 호흡상피는 풍부한 모세혈관과 2종류의 선세포(점액세포와 곤봉세포-자가사리, 점액세포와 거대세포-짱뚱어) 또는 1종류의 선세포로 구성된 팽대세포 (말뚝망둥어와 큰볏말뚝망둥어)를 갖는다. 특히 거대세포 (swollen cell)는 상피세포의 팽대로 인해 형성된 거미줄 구조 (web-like structure)를 갖고 있다. 또한 짱뚱어의 진피성돌기 (dermal bulge)는 진피성 모세혈관이 매우 풍부하며, 지느러미 등의 부속지를 제외한 피부에 존재한다. 또한 미꾸리와 미꾸라지는 장 상피 (intestinal epithelium)에 모세혈관이 아주 풍부하게 존재한다.

• Applied Microscopy
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• 제17권1호
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• pp.177-184
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• 1987

한국산 고슴도치 유문부에 있어서 내분비세포를 전자현미경적으로 관찰하여 EC, ECL, D1 및 G형 등의 4종류의 세포를 분류하였다. EC세포는 고전자밀도의 다형태성 과립을 가지며, 과립내에는 더 높은 전자밀도의 dense body가 보였다. 과립의 크기는 $160{\sim}530nm$였다. ECL세포는 원형 또는 난원형의 과립을 가지며, 이들 과립내용물의 전자밀도는 높고, 편재하거나 공포상으로 출현하였다. 과립의 크기는 $200{\sim}560nm$였다. D1세포는 원형의 과립을 가지며, 과립의 전자밀도는 낮고, 때로 한계막과 과립내용물 사이에 좁은 halo를 나타내었다. 과립의 크기는 $130{\sim}400nm$였다. G세포는 원형 또는 난원형의 과립을 가지며, 비교적 낮은 전자밀도의 과립내용물과 한계막 사이에 좁은 halo를 보였다. 과립의 크기는 $140{\sim}370nm$였다.

• 한국동물학회지
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• 제16권2호
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• pp.119-126
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• 1973

개구리(Rana nigroamaculata)의 위장관 점막내에 출현하는 은친화성세포와 은호성세포의 발생에 따른 그 출현변화를 관찰하기 위하여 개구리 유생의 위와 소장을 발생단계별로 고정한 후 환절편을 만들어 Masson도은법 및 Bodian도온법을 사용하여 은친화성세포와 은호성세포를 관찰한 결과 다음과 같은 결론을 얻었다. 1. 위의 경우, 은친화성세포는 변태 XIII기, 은호성세포는 변태 X기에 출현하여 서서히 증가하다가 변태 XXV기가 되면서 양 세포 모두 급증하였다. 2. 소장의 경우 은친화성세포는 변태 XXV기에 출현하였고 은호성세포는 변태 XVII기에 출현하여 서서히 증가하다가 변태XXV기에서 급증하였다. 3. 본 세포들의 출현시기는 소장에서 은친화성세포를 제외한 위장관내의 은친화성세포와 은호성세포들은 근층의 발달에 따른 위장관 점막의 주름형성 이전 이었다. 4. 변태 XXV기가 되면서 은친화성세포와 은호성세포가 수적으로 급증하는 것은 양서류의 생태적 변화 및 위장과 점막분화와 관련되는 것으로 추리된다.

• Tuberculosis and Respiratory Diseases
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• 제86권4호
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• pp.304-318
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• 2023

Background: Cancer-associated fibroblasts (CAFs) are key components of the tumor microenvironment and significantly contribute to immune evasion. We investigated the effects of CAFs on the immune function of CD4+ and CD8+ T cells in non-small cell lung cancer (NSCLC). Methods: We isolated CAFs and normal fibroblasts (NFs) from tumors and normal lung tissues of NSCLC patients, respectively. CAFs were co-cultured with activated T cells to evaluate their immune regulatory function. We investigated the effect of CAF conditioned medium (CAF-CM) on the cytotoxicity of T cells. CAFs were also co-cultured with activated peripheral blood mononuclear cells and further incubated with cyclooxygenase-2 (COX2) inhibitors to investigate the potential role of COX2 in immune evasion. Results: CAFs and NFs were isolated from the lung tissues (n=8) and lymph nodes (n=3) of NSCLC patients. Immune suppressive markers, such as COX2 and programmed death-ligand 1 (PD-L1), were increased in CAFs after co-culture with activated T cells. Interestingly, CAFs promoted the expression of programmed death-1 in CD4+ and CD8+ T cells, and strongly inhibited T cell proliferation in allogenic and autologous pairs of CAFs and T cells. CAF-CM decreased the cytotoxicity of T cells. COX2 inhibitors partially restored the proliferation of CD4+ and CD8+ T cells, and downregulated the expression of COX2, prostaglandin E synthase, prostaglandin E2, and PD-L1 in CAFs. Conclusion: CAFs promote immune evasion by suppressing the function of CD4+ and CD8+ T cells via their effects on COX2 and PD-L1 in NSCLC. The immunosuppressive function of CAFs could be alleviated by COX2 inhibitors.

• Interdisciplinary Bio Central
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• 제4권4호
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• pp.13.1-13.6
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• 2012

The advanced glycation endproducts receptor (AGER) is a multiligand signal transduction receptor. One of its ligands, S100b molecules activates vascular smooth muscle cells and endothelial cells via its receptor, thus triggering activation of signaling cascades and generation of cytokines and proinflammatory molecules. Ubiquitin-conjugating enzyme Ubc9 is an E2 conjugating enzyme that transfers the activated small ubiquitin-related modifier to protein substrates, and thus it plays a critical role in SUR-Mylation-mediated cellular pathways. Previous studies have shown that both AGE-R and Ubc9 play roles in diverse cellular signaling pathways. However, until recently, little attention has been paid to interactions between AGE-R and Ubc9. In this study, sequence database searches allowed us to identify a potential interaction motif between AGE-R and Ubc9. The subsequent biochemical and molecular biological analysis suggested that there may be specificity in AGE-R and Ubc9 complex signaling in atherosclerosis and cancer cells in a cell-type specific manner. Although the determinant for specificity in AGE-R and Ubc9 complex signaling in cancer cells and atherosclerosis is yet to be determined, this study provides the basis to develop a specific therapeutic application of AGE-R, SURM (small ubiquitin-related modifier)-1, and Ubc9 complex activation pathways in atherosclerosis, diabetes, cancer and inflammatory diseases.

• Asian Pacific Journal of Cancer Prevention
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• 제13권8호
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• pp.3899-3903
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• 2012

B7-H3 is a newly discovered member of the B7/CD28 superfamily which functions as an important T-cell immune molecule. It has been reported recently that B7-H3 is highly expressed in many cancer cells, the data indicating that it may be a regulation factor contributing to tumor-resistance. In our study, we used bioinformatics to identify differentially expressed genes between colonic cancer cells and normal colonic cells, aiming to analyze mechanisms and identify sub-pathways closely related to progression, with the final aim of finding small molecule drugs which might interfere this progression. We found that ajmaline is one related factor which may enhance self-immunity in colon carcinoma therapy and B7-H3 plays important roles with regard to immunoreactions of colonic cancer cells. All the results indicate that H7-B3 is a favorable prognostic biomarker for colon carcinomas, providing novel information regarding likely targets for intervention.

• 생명과학회지
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• 제8권6호
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• pp.660-666
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• 1998

임신 7일부터 14일사이 paraquat(1,1'-dimethyl-4,4´-bipyridinium, 9m/Kg)를 모체에 경구투여하였을 때 태자와 출생후 흰쥐 위와 소장의 gastrin, somatostatin, gluca-gon, PP, CCK-8 및 serotonin면역반응세포 발생에 미치는 영향을 면역조직화학적으로 검색하였다. Paraquat 처리군의 면역반응세포는 대조군에 비해 늦은 시기의 태자부터 처음 관찰되며 출생전후 면역세포의 분포수도 차이를 보였다. 이로 보아 임신 중 모체를 통해 투여된 paraquat는 장내분비 세포의 분화를 지체시킬 뿐아니라 출생후 위장관의 성숙에도 영향을 줌을 알 수 있다.