Recombinant adenovirus encoding vasohibin prevents tumor angiogenesis and inhibits tumor growth

Li, Dajiang; Zhou, Kun; Wang, Shuguang; Zhong, Shuming; Yang, Zhao

doi:10.1111/j.1349-7006.2009.01388.x

Cited by 24 publications

(22 citation statements)

References 29 publications

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“…Similar to our findings, several previous reports had demonstrated that an elevated expression of VASH1 predicted a worse clinical outcome in patients with cancer [54], [55], [56], [57], [58], [59]. In various experimental disease models including those of cancer and diabetic nephropathy, the administration of adenoviral vectors encoding VASH1 resulted in therapeutic effects [19], [21], [22], [23], [24], [25], [26], [60]. More recent findings have demonstrated the role of VASH1 in enhancing the stress resistance of endothelial cells [20].…”

Section: Discussionsupporting

confidence: 91%

“…However, the cell surface receptor(s) for VASH1 have not yet been identified. The therapeutic efficacy of VASH1 against tumor growth and atherosclerosis models has been reported [19], [21], [22], [23], [24]. We previously reported the therapeutic effects of the adenoviral transfer of human VASH1 in mouse type 1 and 2 diabetic nephropathy models [25], [26].…”

Section: Introductionmentioning

confidence: 93%

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Exacerbation of Diabetic Renal Alterations in Mice Lacking Vasohibin-1

et al. 2014

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Vasohibin-1 (VASH1) is a unique endogenous inhibitor of angiogenesis that is induced in endothelial cells by pro-angiogenic factors. We previously reported renoprotective effect of adenoviral delivery of VASH1 in diabetic nephropathy model, and herein investigated the potential protective role of endogenous VASH1 by using VASH1-deficient mice. Streptozotocin-induced type 1 diabetic VASH1 heterozygous knockout mice (VASH1+/−) or wild-type diabetic mice were sacrificed 16 weeks after inducing diabetes. In the diabetic VASH1+/− mice, albuminuria were significantly exacerbated compared with the diabetic wild-type littermates, in association with the dysregulated distribution of glomerular slit diaphragm related proteins, nephrin and ZO-1, glomerular basement membrane thickning and reduction of slit diaphragm density. Glomerular monocyte/macrophage infiltration and glomerular nuclear translocation of phosphorylated NF-κB p65 were significantly exacerbated in the diabetic VASH1+/− mice compared with the diabetic wild-type littermates, accompanied by the augmentation of VEGF-A, M1 macrophage-derived MCP-1 and phosphorylation of IκBα, and the decrease of angiopoietin-1/2 ratio and M2 macrophage-derived Arginase-1. The glomerular CD31+ endothelial area was also increased in the diabetic VASH1+/− mice compared with the diabetic-wild type littermates. Furthermore, the renal and glomerular hypertrophy, glomerular accumulation of mesangial matrix and type IV collagen and activation of renal TGF-β1/Smad3 signaling, a key mediator of renal fibrosis, were exacerbated in the diabetic VASH1+/− mice compared with the diabetic wild-type littermates. In conditionally immortalized mouse podocytes cultured under high glucose condition, transfection of VASH1 small interfering RNA (siRNA) resulted in the reduction of nephrin, angiopoietin-1 and ZO-1, and the augmentation of VEGF-A compared with control siRNA. These results suggest that endogenous VASH1 may regulate the development of diabetic renal alterations, partly via direct effects on podocytes, and thus, a strategy to recover VASH1 might potentially lead to the development of a novel therapeutic approach for diabetic nephropathy.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 93%

Exacerbation of Diabetic Renal Alterations in Mice Lacking Vasohibin-1

et al. 2014

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“…Watanabe et al (2004) proposed that VASH1 is an endothelium-derived negative feedback regulator of angiogenesis. VASH1 has been reported to be expressed predominantly in the endothelial cells of the artery, corneal, retina, lymph node, endometrium, glomerulus, and tumors in humans , Yoshinaga et al 2008, Hosaka et al 2009, Tamaki et al 2009) and mice , Heishi et al 2010, Li et al 2010. Expression studies in human endothelial cells revealed that VASH1 protein localized to the nucleus and cytoplasm (Watanabe et al 2004, Kern et al 2008.…”

Section: Discussionmentioning

confidence: 99%

Possible action of vasohibin-1 as an inhibitor in the regulation of vascularization of the bovine corpus luteum

et al. 2012

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The development of the corpus luteum (CL), which secretes large amounts of progesterone to establish pregnancy, is accompanied by active angiogenesis, vascularization, and lymphangiogenesis. Negative feedback regulation is a critical physiological mechanism. Vasohibin-1 (VASH1) was recently discovered as a novel endothelium-derived negative feedback regulator of vascularization. We therefore investigated the expression of VASH1 in the bovine CL. Expression of VASH1 mRNA and protein was predominantly localized to luteal endothelial cells (LECs). VASH1 expression in the CL was constant through the early to late luteal phases and decreased during CL regression relating with the action of luteolytic prostaglandin F 2a in vivo. To investigate the role of VASH1, we determined whether VASH1 treatment affects angiogenesis and/or lymphangiogenesis using LECs and lymphatic endothelial cells (LyECs) in vitro. Vascular endothelial growth factor A (VEGFA) stimulated the expression of VASH1 in LECs but not in LyECs, and VASH1 completely blocked VEGFA-induced formation of capillary-like tube structures of LECs and LyECs in vitro. In summary, VASH1 is predominantly located on LECs in the bovine CL and inhibits the angiogenic and lymphangiogenic actions of VEGFA. Bovine CL therefore has a VEGFA-VASH1 system that may be involved in regulation of luteal function, especially in the development of the CL. The results indicate that VASH1 has the potential to act as a negative feedback regulator of angiogenesis and lymphangiogenesis in the CL in cows.

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“…Furthermore, VASH1 is not only expressed in normal tissue, but VASH1 expression in vascular ECs around malignant tumors has also been documented in various carcinomas. In addition to expression in malignant tumors, the relationship to prognosis, tumor growth, metastasis, and more has been examined; VASH1 is gaining attention as a new target or biomarker for predicting prognosis (Li et al 2010;Chan et al 2012;Coch et al 2014). For example, current studies report cases of poor prognosis having high expression of VASH1 in breast carcinoma and non-small cell lung carcinoma (NSCLC) (Hosaka et al 2009;Tamaki et al 2009).…”

Section: Introductionmentioning

confidence: 99%

Vasohibin-1 Is a Poor Prognostic Factor of Ovarian Carcinoma

Sano

Kanomata

Suzuki

et al. 2017

Tohoku J. Exp. Med.

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Vasohibin-1 (VASH1) is an identified negative feedback inhibitor of angiogenesis induced by vascular endothelial growth factor (VEGF) in vascular endothelial cells (ECs). Expression of VASH1 has been reported not only in ECs of normal tissue, but also in ECs surrounding malignant tumors. In malignant tumors, VASH1 is also gaining attention as a prognosis prediction marker. The aim of this study is to investigate the correlation between VASH1 expression and vascular-related factors and various clinicopathological outcomes in clinical cases of ovarian carcinoma. We retrospectively analyzed clinical records of 58 patients with ovarian carcinoma. The expression patterns of VASH1 and other vascularrelated factors (CD31 as markers of microvessel density (MVD), VEGF receptor type 2 (VEGFR2), D2-40 as markers of lymphovessel density), and Ki67 (as proliferation markers of cancer cells) were examined immunohistochemically. We studied the correlation between immunohistochemical expression and overall survival. VASH1 expression pattern significantly differed between Federation of Obstetrics and Gynecology (FIGO) Stages. Numbers of VASH1-positive vessels had a significant positive correlation with MVD (Speaman's correlation coefficient (ρ) was 0.51, p < 0.001), VEGFR2-positive vessels (ρ = 0.61, p < 0.001), and percentage of Ki67 (ρ = 0.28, p = 0.034). The Cox univariable analyses revealed that the group of high VASH1 expression (> 14.6 vessels per mm 2 ) at Stages I-III is a prognostic factor (HR = 3.3, 95%CI = 0.4-8.4; p = 0.013). Our results indicate that VASH1 expression in ovarian carcinoma is significantly associated with vascular-related factors and Ki67 expression. We propose that VASH1 is a prognostic marker in ovarian carcinoma.

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Recombinant adenovirus encoding vasohibin prevents tumor angiogenesis and inhibits tumor growth

Cited by 24 publications

References 29 publications

Exacerbation of Diabetic Renal Alterations in Mice Lacking Vasohibin-1

Exacerbation of Diabetic Renal Alterations in Mice Lacking Vasohibin-1

Possible action of vasohibin-1 as an inhibitor in the regulation of vascularization of the bovine corpus luteum

Vasohibin-1 Is a Poor Prognostic Factor of Ovarian Carcinoma

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