HGF Gene Therapy for Therapeutic Angiogenesis in Peripheral Artery Disease

Muratsu, Jun; Sanada, Fumihiro; Taniyama, Yoshiaki; Ikeda-Iwabu, Yuka; Otsu, Rei; Shibata, Katsushi; Brulé, May Kanako; Rakugi, Hiromi; Morishita, Ryuichi

doi:10.1007/978-981-10-2744-4_9

Cited by 3 publications

(3 citation statements)

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“…Originally discovered as a potent mitogen for adult rat hepatocytes, HGF is a pleiotropic cytokine that exhibits a variety of cellular effects upon tyrosine phosphorylation of its receptor, c-Met [52,53]. HGF is secreted as a glycoprotein precursor, activated upon proteolytic cleavage.…”

Section: Hepatocyte Growth Factormentioning

confidence: 99%

“…The composite structure of the receptor is completed by a transmembrane helix [54]. The receptor is expressed by endothelial cells, smooth muscle cells, and bone marrow-derived endothelial progenitor cells [52]. The binding of the HGF and c-Met promotes different cellular signaling pathways, which is involved in the regulation of tissue homeostasis under physiological conditions.…”

Section: Hepatocyte Growth Factormentioning

confidence: 99%

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Tumor Angiogenesis and Anti-Angiogenic Strategies for Cancer Treatment

Teleanu

Chircov

Grumezescu

et al. 2019

JCM

353

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: Hepatocyte Growth Factormentioning

confidence: 99%

Section: Hepatocyte Growth Factormentioning

confidence: 99%

Tumor Angiogenesis and Anti-Angiogenic Strategies for Cancer Treatment

Teleanu

Chircov

Grumezescu

et al. 2019

JCM

353

251

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“…In response, diverse approaches have been attempted to enhance the therapeutic efficacy of hMSCs in treating MI. For instance, genetically engineered hMSCs overexpressing a number of antiapoptotic proteins (6,7), growth factors, or prosurvival genes-such as vascular endothelial growth factor (VEGF) (8), insulin-like growth factor 1 (IGF-1) (9), and hepatocyte growth factor (HGF) (10)showed increased survival and retention in vivo resulting in improved cardiac function and myocardial angiogenesis in MI-induced hearts. However, these approaches require genetic modification and, therefore, are incompatible with clinical applications.…”

Section: Introductionmentioning

confidence: 99%

In vivo priming of human mesenchymal stem cells with hepatocyte growth factor–engineered mesenchymal stem cells promotes therapeutic potential for cardiac repair

et al. 2020

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The clinical use of human bone marrow–derived mesenchymal stem cells (BM-MSCs) has been hampered by their poor performance after transplantation into failing hearts. Here, to improve the therapeutic potential of BM-MSCs, we developed a strategy termed in vivo priming in which BM-MSCs are primed in vivo in myocardial infarction (MI)–induced hearts through genetically engineered hepatocyte growth factor–expressing MSCs (HGF-eMSCs) that are encapsulated within an epicardially implanted 3D cardiac patch. Primed BM-MSCs through HGF-eMSCs exhibited improved vasculogenic potential and cell viability, which ultimately enhanced vascular regeneration and restored cardiac function to the MI hearts. Histological analyses further demonstrated that the primed BM-MSCs survived longer within a cardiac patch and conferred cardioprotection evidenced by substantially higher numbers of viable cardiomyocytes in the MI hearts. These results provide compelling evidence that this in vivo priming strategy can be an effective means to enhance the cardiac repair of MI hearts.

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