Vascular Endothelial Growth Factor: An Essential Component of Angiogenesis and Fracture Healing
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Fractures require adequate stability and blood supply to heal. The vascular supply to long bones is compromised in a fracture, and the ability to heal hinges on the ability of new blood vessels to proliferate from surrounding vessels in a process known as angiogenesis. This process is largely driven by the growth factor, vascular endothelial growth factor (VEGF), whose levels are increased locally and systemically during fracture healing. VEGF is involved in many steps throughout the fracture healing cascade, from initially being concentrated in fracture hematoma, to the promotion of bone turnover during the final remodeling phase. This article reviews the current literature surrounding the role of VEGF and other growth factors in reestablishing vascular supply to fractured bone, as well as medications and surgical techniques that may inhibit this process.Keywords:
Blood supply
Bone remodeling
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Abstract Background The fracture of mandible remains one of the most facial fractures and its healing is a complex process, involving nerve and growth factors. Currently, nerve growth factor not only benefits maintenance of sympathetic neurite growth, but also takes part in intricate regulatory network to stimulate other growth factors such as bone growth protein and vascular endothelial growth factor, which promote together essential osteogenesis and angiogenesis to physiological bone formation, growth and fracture healing. Therefore, it is necessary to analysis the combination of nerve growth factor, bone growth protein-9 and vascular endothelial growth factor to accelerate healing rate of mandible fracture. Methods The models of mandible fracture with local nerve injury established in forty-eight rabbits were randomly divided into nerve growth factor group (NGF group), gelatin sponge group (GS group), blank group and intact group with 12 rabbits in each group. The fracture healing was observed with visual and X-ray after the operation, then callus tissue in mandibular fracture area were collected for HE staining observation, and quantitative RT-PCR was used to detect the expression of BMP-9 and VEGF in callus at different stages. Results The combined results of macroscopic observation, X-ray examination and histological section showed that a large number of osteoblasts and some vascular endothelial cells were found around the trabecular bone in NGF group and the amount of callus formation and reconstruction were better than GS group at 2th weeks after the operation. Quantitative RT-PCR result indicated that the expression levels of BMP-9 mRNA and VEGF mRNA in the four groups reached the highest value at the second week, and then decreased with time. At the same time, the content of BMP-9 and VEGF in callus tissue in mandibular fracture area increased significantly in NGF group than GS group. Conclusion The exogenous NGF could improve the expressions of BMP-9 and VEGF in the early stage of mandibular fracture to accelerate healing of mandible fracture. This work provides a new foundation and theoretical basis to make clear mechanism of fracture healing, thereby promoting patients’ fracture healing and reducing their disability rate.
Mandible (arthropod mouthpart)
Mandibular fracture
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Εισαγωγή-Σκοπός: Η αγγειογένεση είναι απαραίτητη διαδικασία στην καρκινογένεση και ο αυξητικός παράγοντας αγγειακού ενδοθηλίου (vascularendothelial growth factor/VEGF) είναι ο σηµαντικότερος αγγειογενετικός παράγοντας. Ο VEGF έχει βρεθεί αυξηµένος σε µεγάλο αριθµό όγκων, µεταξύ των οποίων σε καρκίνο µαστού και σε καρκίνο παχέος εντέρου-ορθού.Σκοπός µας ήταν η συγκριτική προοπτική µελέτη της περιεγχειρητικής διακύµανσης του VEGF σε δύο διαφορετικές οµάδες ασθενών: µία οµάδα ασθενών µε καρκίνο µαστού και µία οµάδα ασθενών µε καρκίνο παχέος εντέρου, οι οποίοι υποβλήθηκαν σε ογκολογικές επεµβάσεις διαφορετικής διάρκειας και βαρύτητας/έκτασης τραύµατος. Ασθενείς-Μέθοδος: Μετρήθηκαν οι τιµές του VEGF στον ορό του περιφερικού φλεβικού αίµατος (µε τη µέθοδο ELISA) σε τριάντα ασθενείς µε καρκίνο µαστού και τριάντα ασθενείς µε καρκίνο παχέος εντέρου-ορθού, προεγχειρητικά, την 1η µετεγχειρητική ηµέρα και την 7η µετεγχειρητική ηµέρα. Ακολούθησε συγκριτική στατιστική ανάλυση των αποτελεσµάτων. Αποτελέσµατα: ∆ιαπιστώθηκε στατιστικώς σηµαντική διαφορά (αύξηση)των µετεγχειρητικών (της 7ης µετεγχειρητικής ηµέρας) τιµών του VEGF στον ορό σε σχέση µε τις προεγχειρητικές και στις δύο οµάδες των ασθενών και στατιστικώς σηµαντικά µεγαλύτερη στην οµάδα των ασθενών µε καρκίνο του παχέος εντέρου σε σχέση µε την οµάδα των ασθενών µε καρκίνο του µαστού.Την 1η µετεγχειρητική ηµέρα οι τιµές του VEGF παρουσίασαν µικρή µείωση,σε σχέση µε τις προεγχειρητικές, και στις δύο οµάδες ασθενών. Συµπεράσµατα: Η αύξηση των τιµών του VEGF την 7η µετεγχειρητική ηµέρα θεωρούµε ότι οφείλεται στην έκταση του χειρουργικού τραύµατος και για το λόγο αυτό εµφανίζεται στατιστικώς σηµαντικά µεγαλύτερη στην οµάδα των ασθενών µε καρκίνο του παχέος εντέρου. Οι αυξηµένες µετεγχειρητικές τιµές του VEGF θα µπορούσαν να αποτελέσουν αντικείµενο περαιτέρω µελέτης, προκειµένου να αξιολογηθεί η πιθανότητα χρησιµοποίησής τους ως βιολογικού δείκτη για εφαρµογή εξατοµικευµένης συµπληρωµατικής (αντι-αγγειογενετικής) θεραπείας.
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血管内皮細胞は，様々な病的状況下においては，活発に増殖して新しい血管ネットワークを形成する．この血管新生という現象の過程の中心をなすものは，血管内皮増殖性因子（vascular endothelial growth factor:VEGF）を介する血管内皮細胞の発生・増殖・分化とプログラム化された細胞死である．喘息気道においても，VEGFとVEGF受容体の過剰発現が観察され，血管新生の進展への密接な関与が推察される．さらに近年，VEGFの作用を調節する因子としてangiopoietin（Ang）ファミリーの生理作用が注目されており，VEGFとAngの相互作用による血管新生の精巧なメカニズムが明らかにされた．しかしながら，これまで血管内皮細胞に特異的に作用するとされてきたVEGFが，上皮下基底膜肥厚の形成・進展の過程に深く関与することを示唆する多数の知見が集積されつつある．そこで，本稿では喘息気道における血管リモデリングを引き金とする気道リモデリングの成立・進展に関するメカニズムを概説した．
Angiopoietin 2
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pfu。每个组的三只忍受 osteosarcoma 老鼠在第 11 点被牺牲，第 14，在 MG63 房间的培植以后的第 17 白天。在植入的肿瘤和血浆液的 VEGF 的表示被 ELISA 方法检测。然后，左老鼠都在实验(第 19 天) 的结束被牺牲。在植入的肿瘤的 VEGF 的表示被 RT-PCR 检测，在植入的肿瘤和血浆液的有免疫力的组织化学方法，和那被 ELISA 方法检测。在老鼠的结果(1 ) 肿瘤能从 MG63 房间的培植在第 5 白天被看见。(2 ) VEGF 的表达式能被 RT-PCR 和有免疫力的组织化学在所有组检测，它在比二个控制组收到 AD-VEGF-siRNA 治疗的组是低得多的(P < 0.05 ) 。(3 ) 在忍受 osteosarcoma 老鼠的血浆液的 VEGF 的表示比由 ELISA 的三只健康老鼠的高得多(P < 0.05 ) 。(4 ) 在血浆液的 VEGF 和在 AD-VEGF-siRNA 组的瘤的表达式在二个控制组是比那低得多的(P < 0.05 ) 。结论 AD-VEGF-siRNA 能有效地禁止的 VEGF 表示在活体内。这种技术将在骨肉瘤为我们 antiangiogenesis 的治疗带给一些好参考书。
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症例は58歳女性,下肢脱力と全身倦怠感を主訴に受診し,多発性神経炎,肝脾腫・甲状腺機能低下症, Mタンパク,皮膚硬化を認めPOEMS症候群と診断した.肺高血圧症の合併も認めた.ステロイドパルス療法を行い症状改善,治療前vascular endothelial growth factor (VEGF)の異常高値を認めたが治療後減少した. POEMS症候群は稀な疾患であるが, VEGFの推移を追跡し疾患活動性の指標として有用であったので報告する.
POEMS syndrome
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연구 목적 : 자간전증의 중요한 중간 원인은 혈관 내피세포의 기능 이상으로 알려져 있다. 따라서 자간전증 임신부의 혈액에서 높은 농도로 존재하는 것으로 알려진 VEGF가 혈관 내피세포의 기능 이상을 초래하여 자간전증을 유발하는 지를 알아보기 위해, 실험실에서 제대 정맥의 혈관 내피세포에 대한 VEGF의 영향을 알아보고자 하였다.
연구 방법 : 자간전증 임신부와 정상 임신부의 혈청에서 효소 면역 분석법을 이용하여 VEGF의 농도를 측정하였다. 제대정맥에서 혈관 내피세포를 분리하여 배양한 후, 제대정맥 혈관 내피세포를 VEGF, 자간전증 임신부 및 정상 임신부의 혈청으로 24시간 동안 자극시킨 후에 생성된 prostacyclin의 농도를 측정하였다.
연구 결과 : 자간전증 임신부가 정상 임신부에 비해 혈청 VEGF 농도가 유의하게 높게 나타났다. VEGF 농도가 증가함에 따라 prostacyclin 생성도 증가하였으며, 제대정맥 내피세포를 자간전증 임신부의 혈청으로 자극시켰을 때 postacyclin의 생성이 증가하였고 혈청 VEGF 농도와 prostatytlin 생성 사이에는 상당한 연관성이 있었다.
결론 : VEGF는 혈관 내피세포의 기능 이상을 초래할 수 있는 인자 중의 하나이며, 자간전증 임신부에서 나타나는 VEGF의 높은 혈청 농도가 자간전증의 병리학적 기전에 중요한 작용을 할 것으로 생각된다.
Pathogenesis
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The role of angiogenesis in the pathogenesis of systemic sclerosis (SSc) is well known. The imbalance between vascular endothelial growth factor (VEGF) and their anti-angiogenic soluble receptors (sVEGFR-1 and VEGFR-2) has been proposed as a possible cause of microangiopathy. To determine the levels of VEGF, sVEGFR-1 and sVEGFR-2 and the VEGF/sVEGFR1 and VEGF/sVEGFR2 ratios in SSc patients and to study their relation with clinical manifestations and capillaroscopy findings. The study included 44 SSc patients and 44 controls. The sclerosis severity was assessed by the modified Rodnan skin score (mRss) and capillaroscopy performed in patients. Serum VEGF, sVEGFR-1 and sVEGFR-2 were measured in patients and control. SSc patients had a mean age of 40.7 ± 12.8 years, M:F (1:9) and disease duration was 56.2 ± 60.6 months. 27 patients (61.4%) had diffuse-SSc and 17 (38.6%) limited. The mean VEGF was significantly higher (363.4 ± 133.9 pg/ml) and sVEGFR-2 lower (2039.6 ± 109 pg/ml) in patients compared to control (93.9 ± 25.2 pg/ml and 2366 ± 116.5 pg/ml; p = 0.05 and p = 0.04, respectively). Serum levels of sVEGFR-2 in patients with early, active and nonspecific scleroderma pattern of capillaroscopy was higher in comparison to patients with late scleroderma pattern (p = 0.05). There were no significant differences in the studied parameters between those patients with and without digital ulcerations and interstitial pulmonary fibrosis. A significant correlation was found between mRss and VEGF (p = 0.04). An overproduction of VEGF, a potent angiogenic molecule or down regulated production of its natural inhibitors (sVEGFR-2) might be involved in the development of vasculopathy in SSc patients.
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1. A long delay in bone fracture healing can be produced by reducing the blood supply to the affected bone. This technic is suggested for the study of therapeutic measures to promote the healing of delayed union of bone in the aged. 2. Glucose-1-phosphate, when administered by subcutaneous injection, had no favorable effect on the healing of bone fractures.
Blood supply
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