scholarly journals PlGF Reduction Compromises Angiogenesis in Diabetic Foot Disease Through Macrophages

2021 ◽  
Vol 12 ◽  
Author(s):  
Lingyan Zhu ◽  
Jieqi Qian ◽  
Yinan Jiang ◽  
Tianlun Yang ◽  
Qiong Duan ◽  
...  
Keyword(s):  
Growth Factor ◽  
Diabetic Foot ◽  
Cell Types ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Adeno Associated Virus ◽  
Diabetic Foot Disease ◽  
Foot Disease ◽  
Endothelial Growth Factor

Diabetic foot disease (DFD) is a common and serious complication for diabetes and is characterized with impaired angiogenesis. In addition to the well-defined role of vascular endothelial growth factor (VEGF) -A and its defect in the pathogenesis of DFD, another VEGF family member, placental growth factor (PlGF), was also recently found to alter expression pattern in the DFD patients with undetermined mechanisms. This question was thus addressed in the current study. We detected attenuated PlGF upregulation in a mouse DFD model. In addition, the major cell types at the wound to express the unique PlGF receptor, VEGF receptor 1 (VEGFR1), were macrophages and endothelial cells. To assess how PlGF regulates DFD-associated angiogenesis, we injected recombinant PlGF and depleted VEGF1R specifically in macrophages by local injection of an adeno-associated virus (AAV) carrying siRNA for VEGFR1 under a macrophage-specific CD68 promoter. We found that the angiogenesis and recovery of the DFD were both improved by PlGF injection. The PlGF-induced improvement in angiogenesis and the recovery of skin injury were largely attenuated by macrophage-specific depletion of VEGF1R, likely resulting from reduced macrophage number and reduced M2 polarization. Together, our data suggest that reduced PlGF compromises angiogenesis in DFD at least partially through macrophages.

A STUDY ON THE ROLE OF EPIDERMAL GROWTH FACTOR IN DIABETIC ULCER MANAGEMENT

2021 ◽  
pp. 62-63
Author(s):  
R. Rani Suganya ◽  
M. Annapoorani ◽  
C. Naveen Kumar
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Diabetic Foot ◽  
Diabetic Ulcer ◽  
Epidermal Growth Factor Treatment ◽  
Epidermal Growth ◽  
Diabetic Foot Disease ◽  
Foot Disease

Diabetes mellitus is a disease of large magnitude with 25 million people affected by the disease in India. One of the common complications of this disease is Diabetic foot disease characterised by non-healing ulcers over the foot predominantly. This study is aimed at evaluating the efcacy and tolerability of Recombinant Epidermal Growth Factor treatment in increasing the rate of healing of ulcers and decreasing the duration of ulcer healing among patients with diabetic foot disease thereby improving the quality of life, preventing further morbidity and mortality and shortening hospital stay.

scholarly journals Peran reseptor vascular endothelial growth factor (VEGF) pada konka hipertrofi disebabkan oleh rinitis alergi

2016 ◽  
Vol 46 (2) ◽  
pp. 129
Author(s):  
Indra Zachreini ◽  
Muhammad Nadjib Dahlan Lubis ◽  
Adi Koesoema Aman ◽  
Suprihati Suprihati
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Allergic Rhinitis ◽  
Growth Factor ◽  
Odds Ratio ◽  
Protective Factor ◽  
Case Control ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

Latar belakang: Konka hipertrofi walaupun tidak mengancam jiwa, namun dapat menyebabkan gangguan kualitas hidup akibat sumbatan hidung. Patogenesis terjadinya konka hipertrofi adalah akibat airway remodelling terutama pada konka nasal inferior. Vascular endothelial growth factor (VEGF) merupakan salah satu faktor angiogenik yang berperan dalam proses neovaskularisasi. Bagaimana peran angiogenik reseptor VEGF pada konka hipertrofi yang terjadi pada rinitis alergi, sampai saat ini belum jelas dan belum banyak diteliti. Tujuan: Mengetahui peran VEGF sebagai faktor angiogenesis pada konka hipertrofi yang terjadi pada rinitis alergi. Metode: Penelitian ini bersifat observasional analitik dengan rancangan case control pada sampel penelitian yang memenuhi kriteria inklusi. Reseptor VEGF diperiksa secara imunohistokimia, di mana nilainya terdiri dari nilai negatif dan positif. Hasil: Pada penelitian ini, didapati nilai odds ratio 0,11 dan 95% CI 0,013-0,982. Hal tersebut menunjukkan bahwa reseptor VEGF berperan sebagai faktor protektif pada konka hipertrofi yang terjadi pada rinitis alergi. Kesimpulan: Reseptor VEGF dianggap berperan sebagai faktor protektif terjadinya konka hipertrofi yang terjadi pada rinitis alergi.Kata kunci: Reseptor vascular endothelial growth factor, konka nasal hipertrofi, rinitis alergi, imunohistokimia ABSTRACT Background: Although hypertrophic turbinate is not life threatening, this condition often decreases quality of life, resulted from nasal obstruction. Pathogenesis of hypertrophic turbinate resulted from airway remodeling especially in inferior turbinate. Vascular endothelial growth factor (VEGF) is one of angiogenic factors which has a role in neovascularitation process. However, it is still unclear what is the role of VEGF receptor in angiogenic of allergic rhinitis, and until now there were very few studies about this matter. Purpose: To identify the role of VEGF as an angiogenic factor in hypertrophic turbinate caused by allergic rhinitis. Methods: This study was an analytical observation by case control method. VEGF receptors were examined by immunohistochemistry with negative and positive result. Result: This study found odds ratio 0.11 and 95% CI 0.013-0.982, which means that VEGF receptor was a protective factor in hypertrophic turbinate caused by allergic rhinitis. Conclusion: VEGF receptor was considered as a protective factor for the occurrence hypertrophic turbinate caused by allergic rhinitis.Keywords: Vascular endothelial growth factor receptor, hypertrophic turbinate, allergic rhinitis, immunohistochemistry

scholarly journals Vascular Endothelial Growth Factor Induces Abnormal Microvasculature in the Endoglin Heterozygous Mouse Brain

2004 ◽  
Vol 24 (2) ◽  
pp. 237-244 ◽  
Author(s):  
Bin Xu ◽  
Yong Qin Wu ◽  
Madeleine Huey ◽  
Helen M. Arthur ◽  
Douglas A. Marchuk ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Mouse Brain ◽  
Disease Model ◽  
Cell Types ◽  
Saline Group ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Loss Of Function ◽  
Endothelial Growth Factor

Hereditary hemorrhagic telangiectasia (HHT), associated with brain arteriovenous malformations, is caused by a loss of function mutation in either the endoglin (HHT1) or activin receptor-like kinase 1 gene (ALK-1, HHT2). Endoglin heterozygous ( Eng+/−)mice have been proposed as a disease model. To better understand the role of endoglin in vascular malformation development, we examined the effect of vascular endothelial growth factor (VEGF) hyperstimulation on microvessels in adult endoglin heterozygous ( Eng+/−) mice using an adenoviral vector to deliver recombinant human VEGF165 cDNA (Ad hVEGF) into basal ganglia. VEGF expression was increased in Ad hVEGF mice compared with the Ad lacZ and saline group ( P < 0.05) and localized to multiple cell types (neurons, astrocytes, endothelial cells, and smooth muscle cells) by double-labeled immunostaining. VEGF overexpression increased microvessel count for up to 4 weeks in both the Eng+/+ and Eng+/+ groups ( Eng+/+ 185 ± 14 vs. Eng+/− 201 ± 10 microvessels/mm2). Confocal microscopic examination revealed grossly abnormal microvessels in eight of nine Eng+/− mouse brains compared with zero of nine in Eng+/+ mice ( P < 0.05). Abnormal microvessels featured enlargement, clustering, twist, or spirals. VEGF receptor Flk-1 and TGF-β receptor 1 (TβR1) expression were reduced in the Eng+/− mouse brain compared with control. Excessive VEGF stimulation may play a pivotal role in the initiation and development of brain vessel malformations in states of relative endoglin insufficiency in adulthood. These observations are relevant to our general understanding of the maintenance of vascular integrity.

PlGF and sVEGFR-1 in chronic subdural hematoma: implications for hematoma development

2013 ◽  
Vol 118 (2) ◽  
pp. 353-357 ◽  
Author(s):  
Theodosis Kalamatianos ◽  
Lampis C. Stavrinou ◽  
Christos Koutsarnakis ◽  
Christina Psachoulia ◽  
Damianos E. Sakas ◽  
...  
Keyword(s):  
Growth Factor ◽  
Subdural Hematoma ◽  
Chronic Subdural Hematoma ◽  
Serum Levels ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Pathological Angiogenesis ◽  
Enhanced Expression ◽  
Endothelial Growth Factor

Object A considerable body of evidence indicates that inflammation and angiogenesis play a significant role in the development and progression of chronic subdural hematoma (CSDH). While various experimental and clinical studies have implicated placental growth factor (PlGF) in the processes that underpin pathological angiogenesis, no study has thus far investigated its expression in CSDH. The actions of PlGF and its related proangiogenic vascular endothelial growth factor (VEGF) are antagonized by a high-affinity soluble receptor, namely soluble VEGF receptor–1 (sVEGFR-1), and thus the ratio between sVEGFR-1 and angiogenic factors provides an index of angiogenic capacity. Methods In the present study, using an automated electrochemiluminescence assay, levels of PlGF and sVEGFR-1 were quantified in serum and hematoma fluid obtained in 16 patients with CSDH. Results Levels of PlGF and sVEGFR-1 were significantly higher in hematoma fluid than in serum (p < 0.0001). In serum, levels of sVEGFR-1 were higher than those of PlGF (p < 0.0001), whereas in hematoma fluid this difference was not apparent. Furthermore, the ratio of sVEGFR-1 to PlGF was significantly lower in hematoma fluid than in serum (p < 0.0001). Conclusions Given previous evidence indicating a role for PlGF in promoting angiogenesis, inflammatory cell chemotaxis, and stimulation, as well as its ability to amplify VEGF-driven signaling under conditions favoring pathological angiogenesis, enhanced expression of PlGF in hematoma fluid suggests the involvement of this factor in the mechanisms of inflammation and angiogenesis in CSDH. Furthermore, a reduced ratio of sVEGFR-1 to PlGF in hematoma fluid is consistent with the proangiogenic capacity of CSDH. Future studies are warranted to clarify the precise role of PlGF and sVEGFR-1 in CSDH.

scholarly journals VEGF involvement in psoriasis

2015 ◽  
Vol 88 (3) ◽  
pp. 247-252 ◽  
Author(s):  
Mihaela Elena Marina ◽  
Iulia Ioana Roman ◽  
Anne-Marie Constantin ◽  
Carmen Mihaela Mihu ◽  
Alexandru Dumitru Tătaru
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Vascular Endothelial Cells ◽  
Cell Types ◽  
Vascular Endothelial ◽  
Hematopoietic Stem ◽  
Promising Target ◽  
Vegf Pathway ◽  
Endothelial Growth Factor

Vascular endothelial growth factor (VEGF) is a key growth factor, regulating the neovascularization, during embryogenesis, skeletal growth, reproductive functions and pathological processes. The VEGF receptors (VEGFR) are present in endothelial cells and other cell types, such as vascular smooth muscle cells, hematopoietic stem cells, monocytes, neurons, macrophages, and platelets.Angiogenesis is initiated by the activation of vascular endothelial cells through several factors. The excess dermal vascularity and VEGF production are markers of psoriasis.The pathological role of VEGF/VEGFR signaling during the psoriasis onset and evolution makes it a promising target for the treatment of psoriasis. Antibodies and other types of molecules targeting the VEGF pathway are currently evaluated in arresting the evolution of psoriasis.

Signal transduction by vascular endothelial growth factor receptors

2003 ◽  
Vol 31 (1) ◽  
pp. 20-24 ◽  
Author(s):  
L. Claesson-Welsh
Keyword(s):  
Signal Transduction ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Cell Types ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Lymphatic Endothelial Cells ◽  
Vascular Permeability Factor ◽  
Wide Range ◽  
Endothelial Growth Factor

Vascular endothelial growth factor (VEGF)/vascular permeability factor is the prototype for a growing family of dimeric growth factors, which exert their effects on vascular and lymphatic endothelial cells, as well as on a wide range of other cell types. Gene targeting shows that most, if not all, of the factors and receptors in this family serve critical functions during vascular development or in adult physiological and pathological angiogenesis. Growing tumours produce VEGF, and many different strategies for inhibiting tumour growth by inhibiting VEGF production are being tested in clinical trials at present. This review focuses on the signal transduction properties of VEGF receptor-1 and VEGF receptor-2.

Role of the Vascular Endothelial Growth Factor Pathway in Tumor Growth and Angiogenesis

2005 ◽  
Vol 23 (5) ◽  
pp. 1011-1027 ◽  
Author(s):  
Daniel J. Hicklin ◽  
Lee M. Ellis
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Tumor Growth ◽  
Tumor Angiogenesis ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Anti Vegf ◽  
Vegf Pathway ◽  
Endothelial Growth Factor

New blood vessel formation (angiogenesis) is a fundamental event in the process of tumor growth and metastatic dissemination. Hence, the molecular basis of tumor angiogenesis has been of keen interest in the field of cancer research. The vascular endothelial growth factor (VEGF) pathway is well established as one of the key regulators of this process. The VEGF/VEGF-receptor axis is composed of multiple ligands and receptors with overlapping and distinct ligand-receptor binding specificities, cell-type expression, and function. Activation of the VEGF-receptor pathway triggers a network of signaling processes that promote endothelial cell growth, migration, and survival from pre-existing vasculature. In addition, VEGF mediates vessel permeability, and has been associated with malignant effusions. More recently, an important role for VEGF has emerged in mobilization of endothelial progenitor cells from the bone marrow to distant sites of neovascularization. The well-established role of VEGF in promoting tumor angiogenesis and the pathogenesis of human cancers has led to the rational design and development of agents that selectively target this pathway. Studies with various anti-VEGF/VEGF-receptor therapies have shown that these agents can potently inhibit angiogenesis and tumor growth in preclinical models. Recently, an anti-VEGF antibody (bevacizumab), when used in combination with chemotherapy, was shown to significantly improve survival and response rates in patients with metastatic colorectal cancer and thus, validate VEGF pathway inhibitors as an important new treatment modality in cancer therapy.

scholarly journals New insights on the role of vascular endothelial growth factor in biliary pathophysiology

JHEP Reports ◽  
2021 ◽  
Vol 3 (3) ◽  
pp. 100251
Author(s):  
Valeria Mariotti ◽  
Romina Fiorotto ◽  
Massimiliano Cadamuro ◽  
Luca Fabris ◽  
Mario Strazzabosco
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

scholarly journals Role of Vascular Endothelial Growth Factor (VEGF) in Human Embryo Implantation: Clinical Implications

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 253
Author(s):  
Xi Guo ◽  
Hong Yi ◽  
Tin Chiu Li ◽  
Yu Wang ◽  
Huilin Wang ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Recurrent Miscarriage ◽  
Embryo Implantation ◽  
Critical Role ◽  
Angiogenic Factor ◽  
Vascular Endothelial ◽  
Underlying Mechanisms ◽  
Endothelial Growth Factor

Vascular endothelial growth factor (VEGF) is a well-known angiogenic factor that plays a critical role in various physiological and pathological processes. VEGF also contributes to the process of embryo implantation by enhancing embryo development, improving endometrial receptivity, and facilitating the interactions between the developing embryo and the endometrium. There is a correlation between the alteration of VEGF expression and reproductive failure, including recurrent implantation failure (RIF) and recurrent miscarriage (RM). In order to clarify the role of VEGF in embryo implantation, we reviewed recent literature concerning the expression and function of VEGF in the reproductive system around the time of embryo implantation and we provide a summary of the findings reported so far. We also explored the effects and the possible underlying mechanisms of action of VEGF in embryo implantation.

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