What Is the Adventitia?

The outer membrane, also known as the fibrous membrane, is the connective tissue membrane that is wrapped around the animal's internal organs. It starts from the digestive tract of molluscs and contains nerves, blood vessels, lymphatic vessels, smooth muscle fibers, and fat cells. Thickness, density, and components vary with the site. The outer membrane of the tube wall is usually composed of loose connective tissue, which is rich in elastic fibers and can sometimes migrate with the surrounding connective tissue. The outer membrane of the parenchymal organs is composed of dense connective tissue containing a large amount of elastic fibers, and some are very rich in smooth muscle, such as the fibrous membrane of the spleen. It has the function of protecting, connecting and fixing organs. If the surface of the adventitia is covered with mesothelium, it is called serosa, which has the function of keeping the surface smooth and reducing friction during movement between organs.

The outer membrane, also known as the fibrous membrane, is the connective tissue membrane that is wrapped around the animal's internal organs. It starts from the digestive tract of molluscs and contains nerves, blood vessels, lymphatic vessels, smooth muscle fibers, and fat cells. Thickness, density, and components vary from site to site. The outer membrane of the tube wall is usually composed of loose connective tissue, which is rich in elastic fibers and can sometimes migrate with the surrounding connective tissue. The outer membrane of the parenchymal organs is composed of dense connective tissue containing a large amount of elastic fibers, and some are very rich in smooth muscle, such as the fibrous membrane of the spleen. It has the function of protecting, connecting and fixing organs. If the surface of the adventitia is covered with mesothelium, it is called serosa, which has the function of keeping the surface smooth and reducing friction during movement between organs.

Chinese name

Outer membrane

Foreign name

outer membrane

Nature

Unit membrane structure

Location

Surrounded by mitochondria

Surface

Smooth

Also known as

Outer wall

Marker enzyme

Monoamine oxidase

Outer membrane morphological characteristics

A unit of membrane structure surrounding the mitochondria. It is 6nm thick, flat and smooth, and has a large porin on it, which allows molecules with a relative molecular mass of about 5kDa to pass. There are also some enzymes that synthesize lipids on the outer membrane and enzymes that convert lipids to further metabolism in the matrix. The outer membrane marker enzyme is monoamine oxidase.

Outer membrane study

Studies have found that the adventitia of blood vessels are involved in the development of AS, but the specific mechanism is still unclear. In response to this, we established an animal model of adventitial injury using collagenase digestion + mechanical separation. HE staining was used to observe the morphological changes of the adventitious vessels. Real-time quantitative PCR was used to detect the oxidase NADPH subunits in the vascular tissues after adventitia The mRNA expressions of p22phox, antioxidant enzyme HO-1, ROS sensitive genes MCP-1 and PDGF were detected by fluorescent probes to detect ROS production in vascular tissues after adventitial injury. The results showed that adventitia injury can cause intimal hyperplasia, p22phox / HO-1, MCP-1, and PDGF mRNA expression were significantly increased after operation; ROS production increased, which was basically consistent with the change of p22phox / HO-1. After treatment with Tongxinluo and atorvastatin, vascular lesions were significantly reduced, and p22phox mRNA expression was reduced. Based on the above experimental results, the following conclusions can be drawn: 1.The outer membrane of blood vessels participates in the pathological process of intimal lesion formation; oxidative stress caused by increased NADPH oxidase activity may be one of the mechanisms of intimal lesions caused by outer membrane injury Inhibition of NADPH oxidase-dependent oxidative stress may be the mechanism of Tongxinluo and atorvastatin against AS.

Adventitia

1.Recognition of the role of adventitia in maintaining vascular homeostasis

The adventitia of the blood vessel is a component structure located in the outermost layer of the blood vessel. It mainly includes the outer elastic layer, nourishing blood vessels, nerve endings and surrounding loose connective tissue (including fibroblasts and tissue macrophages). Some parts have special receptors such as the neck. The arterial body, the sympathetic and parasympathetic nerve fibers that govern vasoconstriction enter the blood vessels from the adventitia, and the nourishing blood vessels also enter from the adventitia to provide nutrients for the adventitia. The adventitia of the blood vessel is not only a layer of supporting structure of the blood vessel wall, but also can play a role through complex interaction effects with other components of the blood vessel wall [1]. The outer membrane of blood vessels secretes active factors, participates in cell phenotypic transformation, proliferation, apoptosis, migration, intimal hyperplasia, and collagen synthesis and secretion, thereby regulating blood vessel growth, function regulation, maintaining vascular homeostasis, and vascular remodeling, calcification and fibrosis It plays an important role in other processes. In vascular remodeling diseases such as hypertension, atherosclerosis, and vascular restenosis, the adventitia of the blood vessel is the starting site of vascular disease and is an "active participant" in the occurrence and progression of the disease. The order of disease occurrence should be "outside to inside."

2.The mechanism and way of affecting the homeostasis of blood vessels through the adventitia pathway

(1) Vessel adventitia and inflammation:

"Adventitia inflammation" refers to the infiltration of more inflammatory cells in the adventitia of blood vessels, forming the "three-stage lymphoid organs of adventitia of blood vessels" (ATLO). In addition to the most characteristic exudative changes in inflammation, the adventitia Obvious macrophage, fibroblast proliferation, migration and phenotypic transformation [2]. Atherosclerosis (AS) is an inflammatory response of the blood vessel wall, and "outer membrane inflammation" is the initiating link of AS, and is the portal of AS caused by inflammatory cells invading the vessel wall [3].

(2) Adventitia and oxidative stress:

The maintenance of vascular homeostasis is closely related to the reactive oxygen species (ROS) and reactive nitrogen species (RNS) produced by the vascular wall. When oxygen free radicals are generated and eliminated, imbalances or excessive ingestion of exogenous oxidants cause ROS and RNS in the body or Excessive accumulation in cells results in cell damage, known as oxidative stress (OS).

(3) Outer membrane and vasoactive peptide:

Vasoactive peptides have the characteristics of small molecular weight, wide variety, wide distribution, flexible regulation, and complex biological effects. They are endocrine and paracrine / autocrine, through G protein-coupled receptors on the surface of their target cells, localized in the blood vessels. It exerts its complex biological role in regulating vasomotor contraction, cell proliferation, migration and secretion, and performs complex regulation of circulatory system functions to maintain cardiovascular homeostasis [6].

(4) Vessel outer membrane and gas small molecules:

Small gas molecules can act as signal molecules and play a role in the homeostasis and remodeling of blood vessels. They can be produced endogenously under enzyme catalysis, do not depend on the corresponding plasma membrane receptors to freely pass through the cell membrane, the regulation of metabolic pathways within the receptors, and have specific functions at physiological concentrations. Their cytological effects can be dependent or not. Relying on the second messenger mediation, it has specific cellular and molecular targets, and has the characteristics of continuous generation, rapid spread and rapid diffusion.

3. Outer membrane homeostasis and cardiovascular disease

(1) Hypertension:

In a comparative test between spontaneously hypertensive rats (SHR) and ordinary rats, SHR vascular adventitial fibroblasts proliferated, responded to a variety of growth factors, and participated in vascular remodeling by synthesizing type I and III collagen [7]. Foreign scholars have found that infiltration of adventitia macrophages in hypertensive animal models is consistent with vascular wall hypertrophy, and mechanical stress can stimulate vascular smooth muscle cells to increase MCP-1 expression. CC family chemokine receptor-2 gene-deficient hypertensive mice had significantly reduced infiltration of outer membrane macrophages and significantly reduced vascular thickening. The adventitia of the blood vessels play a role in maintaining vascular homeostasis. In the hypertension model of renal artery stenosis, hypertension not only induces the thickening of the media and adventitia, but also has a significant effect on the adventitia of the nourishing vessels. Lesions precede the intima and media. [8]. It is suggested that the adventitial membrane secretes active factors to induce the aggregation of inflammatory cells and interact with the medial and intimal membranes, which leads to the remodeling of hypertension blood vessels. In this process, nourishing blood vessels also play a certain role.

(2) AS:

The essence of AS is the inflammatory response of the blood vessel wall, and the outer membrane is the starting point of AS. During the inflammation of the outer membrane, fibroblasts are activated, transformed into myofibroblasts, and the ability to secrete and migrate is increased. The expressed cytokines undergo cross-talking. Up-regulation of the expression of chemokines and adhesion molecules has a cascade amplification effect, which further stimulates the expression of inflammatory factors, which is closely related to the occurrence and progression of AS.

(3) Restenosis after vascular injury:

The neutrophil can be detected in the adventitia after 0.5h of blood vessel strain, and the adherent neutrophils can be detected in the elastic membrane of the intima / media membrane after 2h to 3 days of strain. There are more neutrophils in the membrane than intima and media, and macrophages are also added to the outer membrane. In the form of secretion of vasoactive substances and chemotaxis. Vascular endothelial growth factor (VEGF) was significantly expressed in the adventitia at the early stage of the strain, and was expressed in the neointima, the intima and the adventitia in the late stage. When the VEGF receptor anti-Flt-1 was injected into the vascular adventitial membrane, VEGF expression was down-regulated, infiltration of adventitial macrophages was reduced, and neointimal formation was reduced.