Nucleoside/nucleotide reverse transcriptase inhibitors attenuate angiogenesis and lymphangiogenesis by impairing receptor tyrosine kinases signalling in endothelial cells

Lin, Shi; Ding, Sha; Ge, Zhen; Zhu, Xiaolong; Qiu, Cong; Wang, Yuewen; Lai, Enyin; Yang, Weijun; Sun, Yi; Chow, Samson A.; Yu, Luyang

doi:10.1111/bph.14036

Cited by 22 publications

(16 citation statements)

References 81 publications

(97 reference statements)

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“…Lamivudine attenuated laser-induced choroidal neovascularization in mice (Mizutani et al, 2015. A recent study also revealed that lamivudine and tenofovir inhibit VEGFR-2 phosphorylation in VEGF-stimulated human dermal microvascular endothelial cells (Song et al, 2018). In this study, compatible with the previous studies, the VEGFR-2 phosphorylation was significantly downregulated in NUCs-treated Fig.…”

Section: Discussionsupporting

confidence: 91%

“…It is thought that the NUCs attenuate liver cirrhosis by suppressing HBVrelated liver damage. However, NUCs have been known to exert effects other than viral suppression, such as NO production (Zídek et al, 1999;Kostecká et al, 2012) and angiogenesis (Mizutani et al, 2015;Song et al, 2018). This study, therefore, assessed the therapeutic potential of NUCs on nonviral cirrhosis.…”

Section: Discussionmentioning

confidence: 99%

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Nucleos(t)ide Analogs Do Not Independently Influence Hepatic Fibrosis and Portal Hypertension beyond Viral Suppression in CBDL-Induced Cirrhotic Rat

Hsieh

Chang

Chuang

et al. 2018

J Pharmacol Exp Ther

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Chronic hepatitis is the major cause of liver cirrhosis and portal hypertension. Several factors affect portal pressure, including liver fibrosis, splanchnic vasodilatation, and pathologic angiogenesis. Nucleos(t)ide analogs (NUCs), the oral antiviral agents, effectively attenuate chronic hepatitis B-related liver cirrhosis and portal hypertension via viral suppression and alleviation of hepatitis. On the other hand, NUCs affect tumor necrosis factor (TNF)-, vascular endothelial growth factor (VEGF), and nitric oxide, which participate in fibrogenesis, vasodilatation, and angiogenesis. However, whether NUCs independently influence liver fibrosis and portal hypertension beyond viral suppression is unknown. This study thus aimed to evaluate the influences of three frequently used NUCs in rats with nonviral cirrhosis. Male Sprague-Dawley rats received common bile duct ligation (CBDL) to induce cholestatic cirrhosis and portal hypertension. The rats were randomly allocated into four groups, treated by mouth with lamivudine (30 mg/kg per day), entecavir (0.09 mg/kg per day), tenofovir (50 mg/kg per day), or distilled water (vehicle control) from the 15th day after CBDL. On the 29th day, liver cirrhosis- and portal hypertension-related parameters were evaluated. The results showed that chronic NUCs treatment did not affect hemodynamic parameters, plasma TNF- concentration, and hepatic fibrogenesis protein expressions in rats with nonviral cirrhosis. Though the mesenteric VEGF receptor 2 phosphorylation was downregulated in NUCs-treated groups, the splanchnic angiogenesis was not influenced. In conclusion, lamivudine, entecavir, and tenofovir had no additional effects on liver cirrhosis and portal hypertension in rats with nonviral cirrhosis.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Nucleos(t)ide Analogs Do Not Independently Influence Hepatic Fibrosis and Portal Hypertension beyond Viral Suppression in CBDL-Induced Cirrhotic Rat

Hsieh

Chang

Chuang

et al. 2018

J Pharmacol Exp Ther

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“…The HIV-reverse transcriptase inhibitors zidovudine and lamivudine can downregulate MMP-9 expression in normal or tumor cells, weaken MAPK/ERK or PI3K/AKT phosphorylation, reduce nitric oxide production and impair angiogenesis [ 174 , 216 , 217 , 218 ]. In contrast, other HIV-reverse transcriptase inhibitors (e.g., tenofovir and efavirenz) are able to exert either pro- or anti- tumor activities [ 217 , 219 ].…”

Section: Mmp-9 Inhibitorsmentioning

confidence: 99%

The Impact of Matrix Metalloproteinase-9 on the Sequential Steps of the Metastatic Process

Barillari

2020

IJMS

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In industrialized countries, cancer is the second leading cause of death after cardiovascular disease. Most cancer patients die because of metastases, which consist of the self-transplantation of malignant cells in anatomical sites other than the one from where the tumor arose. Disseminated cancer cells retain the phenotypic features of the primary tumor, and display very poor differentiation indices and functional regulation. Upon arrival at the target organ, they replace preexisting, normal cells, thereby permanently compromising the patient’s health; the metastasis can, in turn, metastasize. The spread of cancer cells implies the degradation of the extracellular matrix by a variety of enzymes, among which the matrix metalloproteinase (MMP)-9 is particularly effective. This article reviews the available published literature concerning the important role that MMP-9 has in the metastatic process. Additionally, information is provided on therapeutic approaches aimed at counteracting, or even preventing, the development of metastasis via the use of MMP-9 antagonists.

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“…DAPI staining was used to assess the positions of the nuclei after staining for 10 min at 37°C. Finally, the red fluorescence intensity was measured under an FV1000 Olympus confocal microscope (Olympus) at excitation/emission wavelengths of 510 nm/580 nm (Song et al ., ).…”

Section: Methodsmentioning

confidence: 97%

Icariin protects cardiomyocytes against ischaemia/reperfusion injury by attenuating sirtuin 1‐dependent mitochondrial oxidative damage

Feng

et al. 2018

British J Pharmacology

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Nucleoside/nucleotide reverse transcriptase inhibitors attenuate angiogenesis and lymphangiogenesis by impairing receptor tyrosine kinases signalling in endothelial cells

Abstract: This article is part of a themed section on Spotlight on Small Molecules in Cardiovascular Diseases. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.8/issuetoc.

Cited by 22 publications

References 81 publications

Nucleos(t)ide Analogs Do Not Independently Influence Hepatic Fibrosis and Portal Hypertension beyond Viral Suppression in CBDL-Induced Cirrhotic Rat

Nucleos(t)ide Analogs Do Not Independently Influence Hepatic Fibrosis and Portal Hypertension beyond Viral Suppression in CBDL-Induced Cirrhotic Rat

The Impact of Matrix Metalloproteinase-9 on the Sequential Steps of the Metastatic Process

Icariin protects cardiomyocytes against ischaemia/reperfusion injury by attenuating sirtuin 1‐dependent mitochondrial oxidative damage

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