E-Mail Alert

Add your e-mail address to receive forthcoming issues of this journal:

Journal Browser

Journal Browser

Special Issue "Hepatocyte Growth Factor (HGF), II"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 31 October 2019

Special Issue Editors

Guest Editor
Prof. Dr. Eiichi Gohda

Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 700-8530, Japan
Website | E-Mail
Interests: HGF expression; HGF function; antitumor immune response; immune tolerance; neuronal differentiation
Guest Editor
Prof. Dr. Hirohito Tsubouchi

Department of HGF liver regeneration and tissue repair, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima 890-8520, Japan and Kagoshima City Hospital, Kagoshima 890-8760, Japan
Interests: HGF pathophysiology; HGF therapeutic application; liver regeneration

Special Issue Information

Dear Colleagues,

Hepatocyte growth factor (HGF), also known as hepatopoietin-A (HPTA), scatter factor (SF), and fibroblast-derived tumor cytotoxic factor (F-TCF), is a pleiotropic growth factor that is secreted mainly from mesenchymal cells and acts on epithelial cells, endothelial cells, and other types of cells. The receptor of HGF is the product of c-met proto-oncogene with tyrosine kinase activity that mediates the transduction of multiple biological signals of HGF. Since HGF was purified and HGF cDNA was molecularly cloned in the late 1980s, extensive studies have been carried out in the fields of not only tissue regeneration but also cell biology, tumor biology, neurology, immunology, and others. 

This Special Issue of the International Journal of Molecular Sciences will focus on recent advances in “Hepatocyte Growth Factor (HGF)” research, including new insights into liver regeneration, activation, biological and pharmacological activities, signaling pathways, structure-function relationships, regulation of expression, therapeutic and diagnostic applications, and other aspects of HGF. Original research papers and review articles relevant to those topics are welcome.

You may wish to check the previous volume.

Prof. Dr. Eiichi Gohda
Prof. Dr. Hirohito Tsubouchi
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Published Papers (1 paper)

View options order results:
result details:
Displaying articles 1-1
Export citation of selected articles as:


Open AccessArticle
Anti-Apoptotic Effects of Recombinant Human Hepatocyte Growth Factor on Hepatocytes Were Associated with Intrahepatic Hemorrhage Suppression Indicated by the Preservation of Prothrombin Time
Int. J. Mol. Sci. 2019, 20(8), 1821; https://doi.org/10.3390/ijms20081821
Received: 20 March 2019 / Revised: 10 April 2019 / Accepted: 11 April 2019 / Published: 12 April 2019
PDF Full-text (4530 KB) | HTML Full-text | XML Full-text
Hepatocyte growth factor (HGF) is an endogenously expressed bioactive substance that has a strong anti-apoptotic effect. In this study, we biochemically and histologically characterized the effects of rh-HGF on in vitro human hepatocyte injury and mouse acute liver failure (ALF) models, both of [...] Read more.
Hepatocyte growth factor (HGF) is an endogenously expressed bioactive substance that has a strong anti-apoptotic effect. In this study, we biochemically and histologically characterized the effects of rh-HGF on in vitro human hepatocyte injury and mouse acute liver failure (ALF) models, both of which were induced by antibody-mediated Fas signaling. rh-HGF inhibited intracellular caspase-3/7 activation and cytokeratin 18 (CK-18) fragment release in both models. Histologically, rh-HGF dramatically suppressed parenchymal damage and intrahepatic hemorrhage. Among the laboratory parameters, prothrombin time (PT) was strongly preserved by rh-HGF, and PT was well correlated with the degree of intrahepatic hemorrhage. These results showed that the anti-apoptotic effect of rh-HGF on hepatocytes coincided strikingly with the suppression of intrahepatic hemorrhage. PT was considered to be the best parameter that correlated with the intrahepatic hemorrhages associated with hepatocellular damage. The action of rh-HGF might derive not only from its anti-apoptosis effects on liver parenchymal cells but also from its stabilization of structural and vasculature integrity. Full article
(This article belongs to the Special Issue Hepatocyte Growth Factor (HGF), II)

Figure 1

Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top