VEGF (Vascular Endothelial Growth Factor) and Fibrotic Lung Disease

Barratt, Shaney; Flower, Victoria; Pauling, John D; Millar, Ann

doi:10.3390/ijms19051269

Cited by 81 publications

(63 citation statements)

References 144 publications

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Section: Vascular Endothelial Growth Factormentioning

confidence: 99%

“…The VEGF family comprises a series of structurally and functionally related proteins, namely VEGF-A, VEGF-B, VEGF-C, VEGF-D, VEGF-E, and placental growth factor (PlGF) [30,32,34]. VEGF-A is the most studied member of the VEGF superfamily, as it is the key angiogenesis regulator and the most potent inducer of angiogenesis [31,34]. VEGF-A is selectively spliced to produce seven proangiogenic and five anti-angiogenic isoforms, e.g., VEGF-A 121 , VEGF-A 145 , VEGF-A 165 , VEGF-A 189 , and VEGF-A 206 (indicating the number of amino acid residues in each polypeptide) [30][31][32].…”

Section: Vascular Endothelial Growth Factormentioning

confidence: 99%

“…VEGF-A is selectively spliced to produce seven proangiogenic and five anti-angiogenic isoforms, e.g., VEGF-A 121 , VEGF-A 145 , VEGF-A 165 , VEGF-A 189 , and VEGF-A 206 (indicating the number of amino acid residues in each polypeptide) [30][31][32]. VEGF-B is abundantly found in the cardiac and skeletal muscle, contributing to the pulmonary vascular remodeling after exposure to chronic hypoxia, VEGF-C and VEGF-D are key lymphangiogenesis regulators, and VEGF-E is an Orf virus-encoded VEGF homolog, which is not present in the human genome [34][35][36][37]. Most abundantly found in the placenta, thyroid, and lungs, the exact role of PlGF is unclear, with studies showing that it can act as an endogenous competitive inhibitor [34].…”

Section: Vascular Endothelial Growth Factormentioning

confidence: 99%

“…VEGF-B is abundantly found in the cardiac and skeletal muscle, contributing to the pulmonary vascular remodeling after exposure to chronic hypoxia, VEGF-C and VEGF-D are key lymphangiogenesis regulators, and VEGF-E is an Orf virus-encoded VEGF homolog, which is not present in the human genome [34][35][36][37]. Most abundantly found in the placenta, thyroid, and lungs, the exact role of PlGF is unclear, with studies showing that it can act as an endogenous competitive inhibitor [34].…”

Section: Vascular Endothelial Growth Factormentioning

confidence: 99%

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Tumor Angiogenesis and Anti-Angiogenic Strategies for Cancer Treatment

Teleanu

Chircov

Grumezescu

et al. 2019

JCM

320

251

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Angiogenesis is the process through which novel blood vessels are formed from pre-existing ones and it is involved in both physiological and pathological processes of the body. Furthermore, tumor angiogenesis is a crucial factor associated with tumor growth, progression, and metastasis. In this manner, there has been a great interest in the development of anti-angiogenesis strategies that could inhibit tumor vascularization. Conventional approaches comprise the administration of anti-angiogenic drugs that target and block the activity of proangiogenic factors. However, as their efficacy is still a matter of debate, novel strategies have been focusing on combining anti-angiogenic agents with chemotherapy or immunotherapy. Moreover, nanotechnology has also been investigated for the potential of nanomaterials to target and release anti-angiogenic drugs at specific sites. The aim of this paper is to review the mechanisms involved in angiogenesis and tumor vascularization and provide an overview of the recent trends in anti-angiogenic strategies for cancer therapy.

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Section: Vascular Endothelial Growth Factormentioning

confidence: 99%

Section: Vascular Endothelial Growth Factormentioning

confidence: 99%

Section: Vascular Endothelial Growth Factormentioning

confidence: 99%

Section: Vascular Endothelial Growth Factormentioning

confidence: 99%

See 2 more Smart Citations

Tumor Angiogenesis and Anti-Angiogenic Strategies for Cancer Treatment

Teleanu

Chircov

Grumezescu

et al. 2019

JCM

320

251

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“…This is supported by past reports that implicate these proteins in fibrogenesis. VEGF is a biomarker for angiogenesis and is the target of several IPF therapies [37]. TIMP1 is a protein expressed on macrophages and epithelial cells that promotes cell proliferation [38][39][40].…”

Section: Discussionmentioning

confidence: 99%

Bleomycin mouse model with active-phase pulmonary fibrosis and no acute mortality

Kadam¹,

Faix²,

Schnitzer³

2020

Preprint

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Background The bleomycin mouse model is the most prevalent animal model used to study idiopathic pulmonary fibrosis (IPF), ranging from basic pathophysiological mechanisms to therapeutic modalities. High mortality rates, inconsistencies in disease induction, and great severity of the disease phenotype have limited its utility and clinical relevance. In this study, we identify conditions in the mouse bleomycin model that maintain the desired IPF phenotype found in patients while avoiding the usual, associated rapid mouse mortality. Methods In two independent studies, we analyzed the effects of incremental intratracheal (IT) high (1-3 U/kg) and low (0.05-0.5 U/kg) bleomycin doses on pulmonary fibrosis in mice. We observed dose effects on weight loss, morbidity and mortality, inflammation, lung collagen content, presence of various biomarkers in bronchoalveolar lavage fluid (BALf), and histology 14 days post-treatment, when the animals were in the active phase of fibrosis. Results We characterize the fibrotic effects of various bleomycin doses in mice on pulmonary inflammation, myofibroblast activation, vascular leakiness, angiogenesis, and extracellular tissue remodeling. Higher bleomycin doses induced acute disease with severe and saturated responses, extreme and progressive weight loss, and high morbidity and mortality rates. In contrast, lower doses of bleomycin induced a milder and chronic response, featuring robust, active-phase fibrosis with mild weight loss and no mortality. Conclusion Here we demonstrate that the bleomycin mouse model can be used to reproduce symptoms of IPF patients in an animal by using low doses of bleomycin. Low concentrations of bleomycin induce chronic and progressive fibrosis with no mortality.

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β‐Elemene suppresses the proliferation of human airway granulation fibroblasts via attenuation of TGF‐β/Smad signaling pathway

Xue

Lin

Zhang

et al. 2019

J of Cellular Biochemistry

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Background Benign airway stenosis is easily to recur as a result of hyperplastic airway granulation tissues. Our previous study proved that a Chinese drug, β‐elemene, could inhibit the proliferation of fibroblasts cultured from these tissues, which could decrease the recurrence rate of this disease. Methods To find out the mechanism for this effect, we first cultured normal human airway fibroblasts and human airway granulation fibroblasts with different concentrations of β‐elemene for the same time or the same dose of β‐elemene for different times to explore the dose/time‐effect relationship between the drug and these cells. Then we used gene microarray to screen out the most important pathway by which the drug influenced human airway granulation fibroblasts. At last, we assessed the condition of this pathway in human airway granulation fibroblasts and verified the effect of this drug on this pathway. Results β‐Elemene inhibited the proliferation of human airway granulation fibroblasts in a dose but no time‐dependent manner and did not affect normal human airway fibroblasts. Affecting the expression of transforming growth factor β (TGF‐β)/Smad pathway may be the key mechanism for this effect. This pathway was activated in human airway granulation fibroblasts and β‐elemene inhibited it in a dose‐dependent manner. This effect was similar to the pathway inhibitor, SB431542, and exogenous TGF‐β could attenuate this effect. Conclusion These results indicated that suppressing TGF‐β/Smad pathway was possibly the key mechanism by which β‐elemene inhibits the proliferation of human airway granulation fibroblasts. This pathway may be a promising target to treat benign airway stenosis.

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VEGF (Vascular Endothelial Growth Factor) and Fibrotic Lung Disease

Cited by 81 publications

References 144 publications

Tumor Angiogenesis and Anti-Angiogenic Strategies for Cancer Treatment

Tumor Angiogenesis and Anti-Angiogenic Strategies for Cancer Treatment

Bleomycin mouse model with active-phase pulmonary fibrosis and no acute mortality

β‐Elemene suppresses the proliferation of human airway granulation fibroblasts via attenuation of TGF‐β/Smad signaling pathway

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