WordNet

of or relating to the intima
a small asexual spore that develops inside the cell of some bacteria and algae
the innermost membrane of an organ (especially the inner lining of an artery or vein or lymphatic vessel)

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/01/06 22:02:09」(JST)

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The tunica intima (New Latin "inner coat"), or intima for short, is the innermost tunica (layer) of an artery or vein. It is made up of one layer of endothelial cells and is supported by an internal elastic lamina. The endothelial cells are in direct contact with the blood flow.

The tunicae of blood vessels are 3 layers: an inner layer (the tunica intima), a middle layer (the tunica media), and an outer layer (the tunica adventitia).

In dissection, the inner coat (tunica intima) can be separated from the middle (tunica media) by a little maceration, or it may be stripped off in small pieces; but, because of its friability, it cannot be separated as a complete membrane. It is a fine, transparent, colorless structure which is highly elastic, and, after death, is commonly corrugated into longitudinal wrinkles.

The inner coat consists of:

A layer of pavement endothelium, the cells of which are polygonal, oval, or fusiform, and have very distinct round or oval nuclei. This endothelium is brought into view most distinctly by staining with silver nitrate.
A subendothelial layer, consisting of delicate connective tissue with branched cells lying in the interspaces of the tissue; in arteries of less than 2 mm in diameter the subendothelial layer consists of a single stratum of stellate cells, and the connective tissue is only largely developed in vessels of a considerable size.
An elastic or fenestrated layer, which consists of a membrane containing a net-work of elastic fibers, having principally a longitudinal direction, and in which, under the microscope, small elongated apertures or perforations may be seen, giving it a fenestrated appearance. It was therefore called by Henle the fenestrated membrane. This membrane forms the chief thickness of the inner coat, and can be separated into several layers, some of which present the appearance of a network of longitudinal elastic fibers, and others a more membranous character, marked by pale lines having a longitudinal direction. In minute arteries the fenestrated membrane is a very thin layer; but in the larger arteries, and especially in the aorta, it has a considerable thickness.

Additional images

Vein
Microphotography of arterial wall with calcified (violet colour) atherosclerotic plaque (haematoxillin & eosin stain)

This article incorporates text from a public domain edition of Gray's Anatomy.

External links

Histology image: 66_02 at the University of Oklahoma Health Sciences Center - "Aorta"
Anatomy photo: Circulatory/vessels/vessels7/vessels2 - Comparative Organology at University of California, Davis - "Bird, vessels (LM, High)"
Tunica+intima at eMedicine Dictionary
Image at About.com

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English Journal

Renal involvement in antiphospholipid syndrome.

Pons-Estel GJ, Cervera R.Author information Department of Autoimmune Diseases, Hospital Clínic, Barcelona, Catalonia, Spain, gponsestel@yahoo.com.AbstractRenal involvement can be a serious problem for patients with antiphospholipid syndrome (APS). However, this complication has been poorly recognized and studied. It can be present in patients who have either primary or systemic lupus erythematosus-associated APS. Clinical and laboratory features of renal involvement in APS include hypertension, hematuria, acute renal failure, and progressive chronic renal insufficiency with mild levels of proteinuria that can progress to nephrotic-range proteinuria. The main lesions are renal artery stenosis, venous renal thrombosis, and glomerular lesions (APS nephropathy) that may be acute (thrombotic microangiopathy) and/or chronic (arteriosclerosis, arterial fibrous intimal hyperplasia, tubular thyroidization, arteriolar occlusions, and focal cortical atrophy). APS can also cause end-stage renal disease and allograft vascular thrombosis. This article reviews the range of renal abnormalities associated with APS, and their diagnosis and treatment options.
Current rheumatology reports.Curr Rheumatol Rep.2014 Feb;16(2):397. doi: 10.1007/s11926-013-0397-0.
Renal involvement can be a serious problem for patients with antiphospholipid syndrome (APS). However, this complication has been poorly recognized and studied. It can be present in patients who have either primary or systemic lupus erythematosus-associated APS. Clinical and laboratory features of r
PMID 24357443

15-LO/15-HETE mediated vascular adventitia fibrosis via p38 MAPK-dependent TGF-β.

Zhang L, Li Y, Chen M, Su X, Yi D, Lu P, Zhu D.Author information Department of Pharmacology, Harbin Medical University-Daqing, Daqing, Heilongjiang Province, People's Republic of China.Abstract15-Lipoxygenase/15-hydroxyeicosatetraenoic acid (15-LO/15-HETE) is known to modulate pulmonary vascular medial hypertrophy and intimal endothelial cells migration and angiogenesis after hypoxia. However, it is unclear whether 15-HETE affects the adventitia of the pulmonary arterial wall. We performed immunohistochemistry, adventitia fibrosis, pulmonary artery fibroblasts phenotype and extracellular matrix (ECM) deposition to determine the role of 15-HETE in hypoxia-induced pulmonary vascular adventitia remodeling. Our studies showed that O2 deprivation induced adventitia hypertrophy of pulmonary arteries with ECM accumulation in both humans with pulmonary arterial hypertension and hypoxic rats. Hypoxia induced 15-LO expression in adventitia. With the inhibitor, NDGA depressed the hypoxia induced ECM deposition and 15-LO production in hypoxic rats. Hypoxia up-regulated the expression of α-SMA, type-Ia collagen and fibronectin in cultured fibroblasts, which seemed to be due to the increased 15-LO/15-HETE. Exogenous 15-HETE mediated the ECM and phenotypic alterations of the fibroblasts as well. The 15-LO/15-HETE induced adventitia fibrosis and fibroblasts phenotypic alterations depended on signaling of the transforming growth factor-β1 (TGF-β1)/Smad2/3 pathway. P38 mitogen-activated protein kinase (p38 MAPKs) was likely to mediate 15-LO induced TGF-β1 and Smad2/3 activation after hypoxia. The results suggest that adventitia fibrosis is an important event in the hypoxia induced pulmonary arterial remodeling, which relies on 15-LO/15-HETE induced p38 MAPK-dependent TGF-β1/Smad2/3 intracellular signaling systems.
Journal of cellular physiology.J Cell Physiol.2014 Feb;229(2):245-57. doi: 10.1002/jcp.24443.
15-Lipoxygenase/15-hydroxyeicosatetraenoic acid (15-LO/15-HETE) is known to modulate pulmonary vascular medial hypertrophy and intimal endothelial cells migration and angiogenesis after hypoxia. However, it is unclear whether 15-HETE affects the adventitia of the pulmonary arterial wall. We performe
PMID 23982954

Ras-mek-erk signaling regulates nf1 heterozygous neointima formation.

Stansfield BK1, Bessler WK1, Mali R1, Mund JA1, Downing BD1, Kapur R2, Ingram DA Jr3.Author information 1Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana; Department of Pediatrics and Neonatal-Perinatal Medicine, Indiana University School of Medicine, Indianapolis, Indiana.2Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana; Department of Pediatrics and Neonatal-Perinatal Medicine, Indiana University School of Medicine, Indianapolis, Indiana; Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana.3Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana; Department of Pediatrics and Neonatal-Perinatal Medicine, Indiana University School of Medicine, Indianapolis, Indiana; Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana. Electronic address: dingram@iu.edu.AbstractNeurofibromatosis type 1 (NF1) results from mutations in the NF1 tumor-suppressor gene, which encodes neurofibromin, a negative regulator of diverse Ras signaling cascades. Arterial stenosis is a nonneoplastic manifestation of NF1 that predisposes some patients to debilitating morbidity and sudden death. Recent murine studies demonstrate that Nf1 heterozygosity (Nf1(+/-)) in monocytes/macrophages significantly enhances intimal proliferation after arterial injury. However, the downstream Ras effector pathway responsible for this phenotype is unknown. Based on in vitro assays demonstrating enhanced extracellular signal-related kinase (Erk) signaling in Nf1(+/-) macrophages and vascular smooth muscle cells and in vivo evidence of Erk amplification without alteration of phosphatidylinositol 3-kinase signaling in Nf1(+/-) neointimas, we tested the hypothesis that Ras-Erk signaling regulates intimal proliferation in a murine model of NF1 arterial stenosis. By using a well-established in vivo model of inflammatory cell migration and standard cell culture, neurofibromin-deficient macrophages demonstrate enhanced sensitivity to growth factor stimulation in vivo and in vitro, which is significantly diminished in the presence of PD0325901, a specific inhibitor of Ras-Erk signaling in phase 2 clinical trials for cancer. After carotid artery injury, Nf1(+/-) mice demonstrated increased intimal proliferation compared with wild-type mice. Daily administration of PD0325901 significantly reduced Nf1(+/-) neointima formation to levels of wild-type mice. These studies identify the Ras-Erk pathway in neurofibromin-deficient macrophages as the aberrant pathway responsible for enhanced neointima formation.
The American journal of pathology.Am J Pathol.2014 Jan;184(1):79-85. doi: 10.1016/j.ajpath.2013.09.022. Epub 2013 Nov 7.
Neurofibromatosis type 1 (NF1) results from mutations in the NF1 tumor-suppressor gene, which encodes neurofibromin, a negative regulator of diverse Ras signaling cascades. Arterial stenosis is a nonneoplastic manifestation of NF1 that predisposes some patients to debilitating morbidity and sudden d
PMID 24211110

Japanese Journal

胸部外科の指針新しい自作ステントグラフト内挿法によるStanford A型急性大動脈解離に対する全弓部置換術

木山宏,垣伸明,塩見大輔 [他]
胸部外科 65(7), 519-526, 2012-07
NAID 40019360636

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坂田則行
Anti-aging medicine 8(1), 42-48, 2012-02
NAID 40019202018

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河盛隆造
Annual review. 糖尿病・代謝・内分泌 2012(-) (-), 47-53, 2012
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「内膜」

Tunica intima
	Transverse section through a small artery and vein of the mucous membrane of the epiglottis of a child. (Tunica intima is at 'e')
Details
Latin	Tunica intima
Identifiers
Gray's	p.498
MeSH	A07.231.330.800
Code	TH H3.09.02.0.01003
TA	A12.0.00.018
FMA	FMA:55589
	Anatomical terminology