細胞外マトリックス分子

WordNet

(geology) amass of fine-grained rock in which fossils, crystals, or gems are embedded
mold used in the production of phonograph records, type, or other relief surface
the body substance in which tissue cells are embedded (同)intercellular substance, ground_substance
(mathematics) a rectangular array of quantities or expressions set out by rows and columns; treated as a single element and manipulated according to rules
an enclosure within which something originates or develops (from the Latin for womb)
the formative tissue at the base of a nail
(physics and chemistry) the simplest structural unit of an element or compound
located or occurring outside a cell or cells; "extracellular fluid"

PrepTutorEJDIC

（複数形 matrices, ～・es）(発生・成長の)母体 / 鋳型・模型;(レコードの)原盤;(活字の)母型,字母 / (金属・化石・宝石などの含んだ)母岩・《古》子宮・基盤; (細胞)細胞間質; (地学)基質; (印)字母; 紙型; 鋳型; (鉱)母岩; (数)行列; (コンピュータ)マトリックス (入力導線と出力導線の回路網); (言)母型文（matrix sentence）
分子《略》『mol』) / (一般に)(…の)微量《+『of』+『名』》
マトリクシング(4チャンネルに再生転換できる2チャンネルの録音方式)

UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

1. 肝線維症の病因pathogenesis of hepatic fibrosis [show details]
… but the molecule still remains a potential target for antifibrotic therapy using small molecule inhibitors that may readily access the target molecule in fibrotic liver.… which damaged regions are encapsulated by an extracellular matrix or scar.…
2. 全身性硬化症（強皮症）の病因pathogenesis of systemic sclerosis scleroderma [show details]
… into the extracellular matrix, and the number of activated endothelial cells in SSc lesions. Cytokines may directly upregulate key adhesion molecules, including intracellular adhesion molecule (ICAM)-1 …
3. 血管新生阻害剤の概要overview of angiogenesis inhibitors [show details]
… VEGF receptor small molecule kinase inhibitors or MoAbs, or soluble VEGF receptors . An alternative but indirect approach is to inhibit one or more of the molecules that stimulate VEGF… as heparan sulfates on cell surfaces and the extracellular matrix (ECM).…
4. 注入可能軟部組織充填剤：非永久性充填剤injectable soft tissue fillers temporary agents [show details]
…naturally occurring glycosaminoglycan that is an essential component of the extracellular matrix of the dermis. The molecule plays a key role in the maintenance of skin structure and function, and its …
5. 変形性関節症の病因pathogenesis of osteoarthritis [show details]
… enzymes responsible for the degradation of the extracellular matrix that results in joint tissue destruction.… that may serve as an alternative to synthetic small molecule inhibitors.…

English Journal

CCN1 enables Fas ligand-induced apoptosis in cardiomyoblast H9c2 cells by disrupting caspase inhibitor XIAP.

Su BC1, Mo FE2.Author information 1Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan; Department of Cell Biology and Anatomy, College of Medicine, National Cheng Kung University, Tainan, Taiwan.2Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan; Department of Cell Biology and Anatomy, College of Medicine, National Cheng Kung University, Tainan, Taiwan. Electronic address: femo@mail.ncku.edu.tw.AbstractCell proliferation from pre-existing cardiomyocytes is a major source of cells for normal mammalian myocardial renewal or for regeneration after myocardial injury. These proliferative cardiomyocytes may act differently from the postmitotic cardiomyocytes in a stressed heart. Extracellular matrix molecule CCN1 is produced to promote Fas ligand (FasL)-induced cardiomyocyte apoptosis in mice with stress-induced cardiac injury. We aimed to investigate the effect of CCN1 on the proliferative cardiomyocytes. We used rat embryonic cardiomyoblast H9c2 cells to study the cardiotoxicity of CCN1. We found that FasL dose-dependently increased the X-linked inhibitor of apoptosis protein (XIAP) levels to prevent the progression of apoptosis in H9c2 cells. CCN1, though it did not induce apoptosis by itself, sensitized H9c2 cells to FasL-induced apoptosis. CCN1 functions by engaging its cell-surface receptor integrin α6β1 and elevating reactive oxygen species levels, which leads to mitogen-activated protein kinase p38 activation, cytosolic Bax translocation to mitochondria, and the release of mitochondrial Smac and HtrA2 to cytosol. These elevated cytosolic Smac and HtrA2 dismantle the inhibition of XIAP, thereby facilitating the activation of caspase-3 and the apoptosis-induced by FasL. In summary, we demonstrated a novel mechanism underlying the resistance of cardiomyoblasts to FasL-induced apoptosis, and the pro-apoptotic function of CCN1 by disrupting this resistance.
Cellular signalling.Cell Signal.2014 Jun;26(6):1326-34. doi: 10.1016/j.cellsig.2014.02.019. Epub 2014 Mar 12.
Cell proliferation from pre-existing cardiomyocytes is a major source of cells for normal mammalian myocardial renewal or for regeneration after myocardial injury. These proliferative cardiomyocytes may act differently from the postmitotic cardiomyocytes in a stressed heart. Extracellular matrix mol
PMID 24631528

Resveratrol protects primary cortical neuron cultures from transient oxygen‑glucose deprivation by inhibiting MMP‑9.

Gao D, Huang T, Jiang X, Hu S, Zhang L, Fei Z.Author information Department of Neurosurgery, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi 710032, P.R. China.AbstractIt was recently shown that resveratrol exerts neuroprotective effects against cerebral ischemia in mice. The aim of the present study was to further confirm these effects in in vitro primary cortical neuron cultures with transient oxygen‑glucose deprivation (OGD), and to investigate whether these effects are due to the inhibition of matrix metalloproteinase‑9 (MMP‑9) and of cell apoptosis. Neuronal primary cultures of cerebral cortex were prepared from BALB/c mice embryos (13‑15 days). Cells from 14- to 16-day cultures were subjected to OGD for 3 h, followed by 21 h of reoxygenation to simulate transient ischemia. Different doses of resveratrol were added into the culture medium during the simulation of transient ischemia. The effect of the extracellular signal‑regulated kinase (ERK) inhibitor U0126 was studied by adding U0126 (5 µg/µl, 4 µl) into the culture medium during transient ischemia; as a control, we used treatment of cells with 50 µM of resveratrol. Cell viability was investigated using the 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) reduction assay. Cell apoptosis was assessed by flow cytometry. The effects of resveratrol on the expression of MMP‑9 were analyzed by western blotting and reverse transcription‑polymerase chain reaction (RT‑PCR), while the levels of ERK, phosphorylated (p)‑ERK, cleaved caspase‑3, Bax and Bcl‑2 were measured by western blotting. The results of the MTT assay showed that cell viability is significantly reduced by transient OGD. OGD induced cell apoptosis, the expression of Bax and the activation of caspase‑3 and ERK, inhibited the expression of Bcl‑2 and increased the expression of MMP‑9, while these effects were reversed by treatment with resveratrol. The therapeutic efficacy of resveratrol was shown to be dose‑dependent, with the most suitable dose range determined at 50‑100 µM. Treatment with U0126 inhibited MMP‑9 and Bax expression and caspase‑3 activation, while it further promoted the expression of the anti‑apoptotic molecule Bcl‑2, suggesting that resveratrol inhibits MMP‑9 expression and cell apoptosis by attenuating the activation of ERK1/2. In conclusion, OGD can induce apoptosis through canonical apoptotic signals and by regulating the expression of MMP‑9; the anti‑apoptotic activity of resveratrol and its inhibitory effect on MMP‑9 expression contribute in the reduced activation of ERK.
Molecular medicine reports.Mol Med Rep.2014 Jun;9(6):2197-204. doi: 10.3892/mmr.2014.2086. Epub 2014 Mar 28.
It was recently shown that resveratrol exerts neuroprotective effects against cerebral ischemia in mice. The aim of the present study was to further confirm these effects in in vitro primary cortical neuron cultures with transient oxygen‑glucose deprivation (OGD), and to investigate whether these
PMID 24682241

3D mouse embryonic stem cell culture for generating inner ear organoids.

Koehler KR, Hashino E.Author information 1] Medical Neuroscience Graduate Program, Indiana University School of Medicine, Indianapolis, Indiana, USA. [2] Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, Indiana, USA. [3] Department of Otolaryngology-Head and Neck Surgery, Indiana University School of Medicine, Indianapolis, Indiana, USA.AbstractThis protocol describes a culture system in which inner-ear sensory tissue is produced from mouse embryonic stem (ES) cells under chemically defined conditions. This model is amenable to basic and translational investigations into inner ear biology and regeneration. In this protocol, mouse ES cells are aggregated in 96-well plates in medium containing extracellular matrix proteins to promote epithelialization. During the first 14 d, a series of precisely timed protein and small-molecule treatments sequentially induce epithelia that represent the mouse embryonic non-neural ectoderm, preplacodal ectoderm and otic vesicle epithelia. Ultimately, these tissues develop into cysts with a pseudostratified epithelium containing inner ear hair cells and supporting cells after 16-20 d. Concurrently, sensory-like neurons generate synapse-like structures with the derived hair cells. We have designated the stem cell-derived epithelia harboring hair cells, supporting cells and sensory-like neurons as inner ear organoids. This method provides a reproducible and scalable means to generate inner ear sensory tissue in vitro.
Nature protocols.Nat Protoc.2014 Jun;9(6):1229-1244. doi: 10.1038/nprot.2014.100. Epub 2014 May 1.
This protocol describes a culture system in which inner-ear sensory tissue is produced from mouse embryonic stem (ES) cells under chemically defined conditions. This model is amenable to basic and translational investigations into inner ear biology and regeneration. In this protocol, mouse ES cells
PMID 24784820