- 関
- capillary endothelial cell
WordNet
- small room in which a monk or nun lives (同)cubicle
- a device that delivers an electric current as the result of a chemical reaction (同)electric cell
- a room where a prisoner is kept (同)jail cell, prison cell
- (biology) the basic structural and functional unit of all organisms; they may exist as independent units of life (as in monads) or may form colonies or tissues as in higher plants and animals
- any small compartment; "the cells of a honeycomb"
- a small unit serving as part of or as the nucleus of a larger political movement (同)cadre
- of or relating to or located in the endothelium
PrepTutorEJDIC
- (刑務所の)『独房』;(修道院の)小さい独居室 / (ミツバチの)みつ房,巣穴 / 小さい部屋 / 『細胞』 / 電池 / 花粉室 / (共産党などの)細胞
UpToDate Contents
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English Journal
- Bradykinin regulates the expression of claudin-5 in brain microvascular endothelial cells via calcium-induced calcium release.
- Zhou L1, Yang B, Wang Y, Zhang HL, Chen RW, Wang YB.Author information 1Department of Neurosurgery, First Affiliated Hospital of China Medical University, Shenyang, People's Republic of China.AbstractTo investigate the mechanism underlying the regulation of claudin-5, a tight junction protein that participates primarily in the constitution of the blood-brain barrier by bradykinin (BK), we established a primary culture of rat brain microvascular endothelial cells (BMECs). BMECs were treated with 10(-5) M BK, and changes in the intracellular Ca(2+) levels were measured by using the sensitive fluorescent dye fluo-3; the expression and distribution of claudin-5 were investigated by immunocytochemistry and Western blot analyses. We did not detect any expression of bradykinin B2 receptors in the BMECs or freshly isolated rat brain microvessels. We found that 10(-5) M BK triggered Ca(2+) transients in BMECs, and further investigations revealed that inositol 1,4,5-trisphosphate receptors (IP3 Rs) and ryanodine receptors (RyRs) on the endoplasmic reticulum (ER) were responsible for the Ca(2+) fluctuation. Consequently, these intracellular Ca(2+) changes that occur in response to BK application were identified as Ca(2+) -induced Ca(2+) release (CICR). Immunocytochemistry and Western blot results demonstrated that 10(-5) M BK could cause the internalization and a decrease in the expression of claudin-5; agonists of IP3 Rs and RyRs, such as IP3 and caffeine, enhanced the BK-induced downregulation of claudin-5, whereas antagonists of IP3 Rs and RyRs, such as 2-APB and ryanodine, abrogated BK's effect on claudin-5. In conclusion, the BK-induced CICR in primary culture BMECs might be the mechanism by which BK modulates claudin-5. © 2014 Wiley Periodicals, Inc.
- Journal of neuroscience research.J Neurosci Res.2014 May;92(5):597-606. doi: 10.1002/jnr.23350. Epub 2014 Jan 27.
- To investigate the mechanism underlying the regulation of claudin-5, a tight junction protein that participates primarily in the constitution of the blood-brain barrier by bradykinin (BK), we established a primary culture of rat brain microvascular endothelial cells (BMECs). BMECs were treated with
- PMID 24464430
- Apelin-13 stimulates angiogenesis by promoting cross‑talk between AMP-activated protein kinase and Akt signaling in myocardial microvascular endothelial cells.
- Yang X, Zhu W, Zhang P, Chen K, Zhao L, Li J, Wei M, Liu M.Author information Division of Cardiology, Shanghai 6th People's Hospital, Shanghai Jiao Tong University School of Medicine, State Key Discipline Division, Shanghai 200233, P.R. China.AbstractCurrently, there is major interest in the functions of apelin-13, an endogenous ligand for the orphan G-protein coupled receptor APJ, a receptor that closely resembles the angiotensin receptor AT1. In the present study, the role of apelin-13 in angiogenesis and its mechanism as a novel angiogenic factor in myocardial microvascular endothelial cells (MMVECs) was investigated. It was revealed that apelin-13 can promote proliferation, migration and tube formation in MMVECs. In addition, apelin-13 dose dependently stimulated the phosphorylation of AMP-activated protein kinase (AMPK) and endothelial nitric oxide synthase (eNOS) at Thr-172 and Ser-1179, respectively. The treatment with the AMPK (compound C) and protein kinase Akt/protein kinase B (Akt; LY294002) inhibitor significantly suppressed the apelin‑13-induced AMPK, Akt and eNOS phosphorylation. They also inhibited the apelin13‑stimulated endothelial cell migration and tube formation. Therefore, we hypothesize that apelin-13 promotes angiogenesis through the modulation of AMPK and Akt signaling in MMVECs.
- Molecular medicine reports.Mol Med Rep.2014 May;9(5):1590-6. doi: 10.3892/mmr.2014.1984. Epub 2014 Feb 25.
- Currently, there is major interest in the functions of apelin-13, an endogenous ligand for the orphan G-protein coupled receptor APJ, a receptor that closely resembles the angiotensin receptor AT1. In the present study, the role of apelin-13 in angiogenesis and its mechanism as a novel angiogenic fa
- PMID 24573187
- VEGFA Activates Erythropoietin Receptor and Enhances VEGFR2-Mediated Pathological Angiogenesis.
- Yang Z1, Wang H1, Jiang Y1, Hartnett ME2.Author information 1The John Moran Eye Center, The University of Utah, Salt Lake City, Utah.2The John Moran Eye Center, The University of Utah, Salt Lake City, Utah. Electronic address: me.hartnett@hsc.utah.edu.AbstractClinical and animal studies implicate erythropoietin (EPO) and EPO receptor (EPOR) signaling in angiogenesis. In the eye, EPO is involved in both physiological and pathological angiogenesis in the retina. We hypothesized that EPOR signaling is important in pathological angiogenesis and tested this hypothesis using a rat model of oxygen-induced retinopathy that is representative of human retinopathy of prematurity. We first determined that EPOR expression and activation were increased and that activated EPOR was localized to retinal vascular endothelial cells (ECs) in retinas at postnatal day 18 (p18), when pathological angiogenesis in the form of intravitreal neovascularization occurred. In human retinal microvascular ECs, EPOR was up-regulated and activated by VEGF. Lentiviral-delivered shRNAs that knocked down Müller cell-expressed VEGF in the retinopathy of prematurity model also reduced phosphorylated EPOR (p-EPOR) and VEGFR2 (p-VEGFR2) in retinal ECs. In human retinal microvascular ECs, VEGFR2-activated EPOR caused an interaction between p-EPOR and p-VEGFR2; knockdown of EPOR by siRNA transfection reduced VEGF-induced EC proliferation in association with reduced p-VEGFR2 and p-STAT3; however, inhibition of VEGFR2 activation by siRNA transfection or semaxanib (SU5416) abolished VEGFA-induced proliferation of ECs and phosphorylation of VEGFR2, EPOR, and STAT3. Our results show that VEGFA-induced p-VEGFR2 activates EPOR and causes an interaction between p-EPOR and p-VEGFR2 to enhance VEGFA-induced EC proliferation by exacerbating STAT3 activation, leading to pathological angiogenesis.
- The American journal of pathology.Am J Pathol.2014 Apr;184(4):1230-9. doi: 10.1016/j.ajpath.2013.12.023. Epub 2014 Mar 12.
- Clinical and animal studies implicate erythropoietin (EPO) and EPO receptor (EPOR) signaling in angiogenesis. In the eye, EPO is involved in both physiological and pathological angiogenesis in the retina. We hypothesized that EPOR signaling is important in pathological angiogenesis and tested this h
- PMID 24630601
Japanese Journal
- Hepatocyte growth factor enhances the barrier function in primary cultures of rat brain microvascular endothelial cells
- Yamada Narumi,Nakagawa Shinsuke,Horai Shoji,Tanaka Kunihiko,Deli Maria A.,Yatsuhashi Hiroshi,Niwa Masami
- Microvascular
- … The effects of hepatocyte growth factor (HGF) on barrier functions were investigated by a blood-brain barrier (BBB) in vitro model comprising a primary culture of rat brain capillary endothelial cells (RBEC). … In order to examine the response of the peripheral endothelial cells to HGF, human umbilical vascular endothelial cells (HUVEC) and human dermal microvascular endothelial cells (HMVEC) were also treated with HGF. …
- NAID 120005460337
- 血液神経関門と糖尿病性ニューロパチー : 糖尿病性ニューロパチーでは血液神経関門が破綻する(ミニ・レビュー : 中村賞受賞者)
- 清水 文崇
- 山口医学 63(1), 17-24, 2014-02-01
- … われわれが最近明らかとした｢BNBが生理的条件下でどのように制御され,病的状況下でどのように破綻するか｣という命題について概説する.It is important to understand the cellular properties of endoneurial microvascular endothelial cells and pericytes which constitute blood-nerve barrier(BNB),since this barrier structure in the peripheral nervous system(PNS)may play pivotal pathophysiological roles in various PNS disorders including inflammatory neuropathy and diabetic …
- NAID 120005435142
- 血液神経関門と糖尿病性ニューロパチー －糖尿病性ニューロパチーでは血液神経関門が破綻する－
- 清水 文崇
- 山口医学 63(1), 17-24, 2014
- 血液神経関門（blood-nerve barrier：BNB）は末梢神経神経内膜内微小血管内皮細胞とペリサイトの２者のみから構成され，BNBの破綻はギランバレー症候群などの免疫性ニューロパチーや糖尿病性ニューロパチーの発症・増悪に大いに関わる．これらの難治性ニューロパチーにおけるBNB破綻の分子メカニズムを解明するために，われわれはヒト坐骨神経よりBNB由来の血管内皮細胞とペリサイトの不死化細胞株 …
- NAID 130004476033
Related Links
- 正常ヒト微小血管内皮細胞と低血清増殖用培地 正常ヒト微小血管内皮細胞および専用培地;増殖用低血清培地をご用意 クラボウと細胞製造元Lifeline Cell Technology社の厳しい品質管理基準を設定 各細胞ロットの細胞増殖データあり、必要 ...
- Endothelial Cells (Microvascular) The walls of capillaries are composed of a single layer of microvascular endothelial cells. This layer is so thin that molecules such as oxygen, water, and lipids can pass through it by diffusion and ...
★リンクテーブル★
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- 関
- endothelial cell、lymphatic endothelial cell、microvascular endothelial cell、vascular endothelial cell
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- 英
- capillary endothelial cell、microvascular endothelial cell
- 関
- 内皮細胞、血管内皮細胞、リンパ管内皮細胞、微小血管内皮細胞
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- 英
- microvascular endothelial cell、capillary endothelial cell
- 関
- 毛細血管内皮細胞
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- 関
- DMVEC
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- 関
- endodermis、endothelia、endothelium
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- 関
- endodermis、endothelial、endothelium
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- 関
- microvessel
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細胞