インタールイウキン-8は,血管新生のマクロファージ由来媒介体として作用する

A E Koch¹, P J Polverini, S L Kunkel

¹Department of Medicine, Northwestern University Medical School, Chicago, IL 60611.

Science (New York, N.Y.)

|December 11, 1992

まとめ

サイトカインであるインタールユーキン-8 (IL-8) は,血管新生を促進し,新しい血管の形成を促します. この発見は,IL-8が炎症性疾患と腫瘍の成長に役割を果たすことを示唆しています.

科学分野:

免疫学免疫学とは
細胞生物学細胞生物学
血管生物学血管生物学

背景:

モノサイトマクロファージは,慢性炎症疾患において重要な血管新生因子を産生する.
持続的な血管新生は,リウマチ性関節炎のような疾患の特徴です.

研究の目的:

既知のサイトカインであるインターリューキン-8 (IL-8) も血管新生性を持つかどうかを調査する.
血管新生に依存する疾患におけるIL-8の役割を調査する.

主な方法:

人間の再結合IL-8をネズミの角膜に埋め込みました.
内皮細胞の増殖と化学作用の評価.
IL-8と腫瘍死滅因子-alphaに対する抗体を用いて血管新生活動を阻害する.
IL-8アンチセンセスのオリゴヌクレオチドを用いて,単細胞誘発の血管新生を抑制する.

主要な成果:

人間の再結合IL-8は,ネズミの角膜モデルで強力な血管新生活性を示した.
IL-8はヒトの静脈内皮細胞の増殖と化学作用を誘発した.
IL-8またはTNF-αに対する抗体は,マクロファージおよびモノサイト培養における血管新生活性を中和した.
IL-8アンチセンスのオリゴヌクレオチドは,単細胞由来血管新生活性を特異的に抑制しました.

結論:

マクロファージ由来のIL-8は,血管新生因子として機能する.
IL-8は,リウマチ性関節炎,腫瘍の成長,傷の修復など,血管新生に依存した疾患の病原化に関与しています.

さらに関連する動画

13:05

Micropatterning and Assembly of 3D Microvessels

Published on: September 9, 2016

09:46

Generation of Human Blood Vessel Organoids from Pluripotent Stem Cells

Published on: January 20, 2023

関連する概念動画

01:10

Mechanism of Angiogenesis

Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...

01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits. Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...

01:24

Overview of Cell-Matrix Interactions

The extracellular matrix or ECM holds cells together to form a tissue and allows the cells within the tissue to communicate. ECM comprises proteins such as fibronectin, collagen, laminin, etc. The most abundant protein in this space is collagen. Collagen fibers are interwoven with carbohydrate-containing protein molecules called proteoglycans. ECM allows cell migration and provides a structural scaffold at cell adhesion that anchors the cell when the extracellular matrix proteins interact with...

01:16

Vascular Spasm

The vascular phase, also known as vasospasm, is the initial stage of hemostasis, crucial for preventing excessive bleeding when a blood vessel is injured. After a vessel is cut, nerves in the damaged area trigger pain and other sensory impulses. Simultaneously, the smooth muscles in the vessel wall contract, resulting in a vascular spasm. This contraction reduces the vessel's diameter at the injury site, slowing or stopping blood loss through the vessel wall. Vascular spasms typically last for...

01:20

Extrinsic and Intrinsic Pathways of Hemostasis

Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which forms a...

01:16

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.

関連する実験動画