Upregulation of MicroRNA-210 Regulates Renal Angiogenesis Mediated by Activation of VEGF Signaling Pathway under Ischemia/Perfusion Injury in vivo and in vitro

Liu, Fen; Lou, Yuanlei; Wu, Jue; Ruan, Qiongfang; Xie, An; Guo, Fei; Cui, Suping; Deng, Zhifeng; Wang, Yan

doi:10.1159/000331054

Cited by 126 publications

(97 citation statements)

References 65 publications

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“…Thus, by inhibiting Ptp1b and Efna3, both negative regulators of angiogenesis, miR-210 could promote angiogenesis. This mechanism is further supported by recent findings that the overexpression of miR-210 in HUVECs can enhance VEGF and VEGFR2 expression to augment angiogenesis despite no miR-210 targets having been identified in the study [149]. Interestingly, a recent study also suggested a positive feedback mechanism from VEGF to miR-210, in which umbilical cord blood CD34 þ cells, expanded in a VEGFcontaining medium, had a significant upregulation of miR-210 expression, and when these cells were transplanted into ischemic mouse hind limbs, the tissue perfusion and capillary density were significantly improved, while a miR-210 inhibitor abolished such an effect [150].…”

Section: Mir-210 Regulates Angiogenesissupporting

confidence: 82%

Emerging roles of miR-210 and other non-coding RNAs in the hypoxic response

Huang

Zuo

2014

ABBS

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Hypoxia is a key component of the tumor microenvironment and represents a well-documented source of therapeutic failure in clinical oncology. Recent work has provided support for the idea that non-coding RNAs, and in particular, microRNAs, may play important roles in the adaptive response to low oxygen in tumors. Specifically, all published studies agree that the induction of microRNA-210 (miR-210) is a consistent feature of the hypoxic response in both normal and malignant cells. miR-210 is a robust target of hypoxia-inducible factors, and its overexpression has been detected in a variety of diseases with a hypoxic component, including most solid tumors. High levels of miR-210 have been linked to an in vivo hypoxic signature and to adverse prognosis in breast and pancreatic cancer patients. A wide variety of miR-210 targets have been identified, pointing to roles in mitochondrial metabolism, angiogenesis, DNA damage response, apoptosis, and cell survival. Such targets are suspected to affect the development of tumors in multiple ways; therefore, an increased knowledge about miR-210's functions may lead to novel diagnostic and therapeutic approaches in cancer.

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Section: Mir-210 Regulates Angiogenesissupporting

confidence: 82%

Emerging roles of miR-210 and other non-coding RNAs in the hypoxic response

Huang

Zuo

2014

ABBS

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“…5). miR-210 overexpression in normoxic endothelial cells stimulates the formation of capillary-like structures, and VEGF-driven cell migration, whereas miR-210 blockade inhibits these events (40,80,87,147). In keeping with these findings, antiangiogenic effect of WSS25 sulfated polysaccharide is, at least in part, mediated by miR-210 down-modulation (147).…”

Section: Hypoxamir and Angiogenesissupporting

confidence: 53%

HypoxamiR Regulation and Function in Ischemic Cardiovascular Diseases

Greco

Gaetano

Martelli

2014

Antioxidants & Redox Signaling

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Significance: MicroRNAs (miRNAs) are deregulated and play a causal role in numerous cardiovascular diseases, including myocardial infarction, coronary artery disease, hypertension, heart failure, stroke, peripheral artery disease, kidney ischemia-reperfusion. Recent Advances: One crucial component of ischemic cardiovascular diseases is represented by hypoxia. Indeed, hypoxia is a powerful stimulus regulating the expression of a specific subset of miRNAs, named hypoxia-induced miRNAs (hypoxamiR). These miRNAs are fundamental regulators of the cell responses to decreased oxygen tension. Certain hypoxamiRs seem to have a particularly pervasive role, such as miR-210 that is virtually induced in all ischemic diseases tested so far. However, its specific function may change according to the physiopathological context. Critical Issues: The discovery of HypoxamiR dates back 6 years. Thus, despite a rapid growth in knowledge and attention, a deeper insight of the molecular mechanisms underpinning hypoxamiR regulation and function is needed. Future Directions: An extended understanding of the function of hypoxamiR in gene regulatory networks associated with cardiovascular diseases will allow the identification of novel molecular mechanisms of disease and indicate the development of innovative therapeutic approaches.

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“…miR-210 and miR-135a also augmented tumor growth and metastasis (31,41), while miR-20b displayed an oncogenic role in normoxia (27). Similarly, angiomirs, miR-17-92 cluster, miR-378, miR-210, and miR-135, were down-regulated (7,24,30,35).…”

Section: Discussionmentioning

confidence: 95%

Interplay Between Heme Oxygenase-1 and miR-378 Affects Non-Small Cell Lung Carcinoma Growth, Vascularization, and Metastasis

Skrzypek

Tertil

Gołda

et al. 2013

Antioxidants & Redox Signaling

131

133

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Aims: Heme oxygenase-1 (HO-1, HMOX1) can prevent tumor initiation; while in various tumors, it has been demonstrated to promote growth, angiogenesis, and metastasis. Here, we investigated whether HMOX1 can modulate microRNAs (miRNAs) and regulate human non-small cell lung carcinoma (NSCLC) development. Results: Stable HMOX1 overexpression in NSCLC NCI-H292 cells up-regulated tumor-suppressive miRNAs, whereas it significantly diminished the expression of oncomirs and angiomirs. The most potently down-regulated was miR-378. HMOX1 also up-regulated p53, down-regulated angiopoietin-1 (Ang-1) and mucin-5AC ( MUC5AC), reduced proliferation, migration, and diminished angiogenic potential. Carbon monoxide was a mediator of HMOX1 effects on proliferation, migration, and miR-378 expression. In contrast, stable miR-378 overexpression decreased HMOX1 and p53; while enhanced expression of MUC5AC, vascular endothelial growth factor (VEGF), interleukin-8 (IL-8), and Ang-1, and consequently increased proliferation, migration, and stimulation of endothelial cells. Adenoviral delivery of HMOX1 reversed miR-378 effect on the proliferation and migration of cancer cells. In vivo, HMOX1 overexpressing tumors were smaller, less vascularized and oxygenated, and less metastatic. Overexpression of miR-378 exerted opposite effects. Accordingly, in patients with NSCLC, HMOX1 expression was lower in metastases to lymph nodes than in primary tumors. Innovation and Conclusion: In vitro and in vivo data indicate that the interplay between HMOX1 and miR-378 significantly modulates NSCLC progression and angiogenesis, suggesting miR-378 as a new therapeutic target. Rebound Track: This work was rejected during standard peer review and rescued by Rebound Peer Review (Antioxid Redox Signal 16, 293-296, 2012) with the following serving as open reviewers:

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Upregulation of MicroRNA-210 Regulates Renal Angiogenesis Mediated by Activation of VEGF Signaling Pathway under Ischemia/Perfusion Injury in vivo and in vitro

Cited by 126 publications

References 65 publications

Emerging roles of miR-210 and other non-coding RNAs in the hypoxic response

Emerging roles of miR-210 and other non-coding RNAs in the hypoxic response

HypoxamiR Regulation and Function in Ischemic Cardiovascular Diseases

Interplay Between Heme Oxygenase-1 and miR-378 Affects Non-Small Cell Lung Carcinoma Growth, Vascularization, and Metastasis

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