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      Rho-Associated Coiled-Coil Kinase (ROCK) in Molecular Regulation of Angiogenesis

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          Abstract

          Identified as a major downstream effector of the small GTPase RhoA, Rho-associated coiled-coil kinase (ROCK) is a versatile regulator of multiple cellular processes. Angiogenesis, the process of generating new capillaries from the pre-existing ones, is required for the development of various diseases such as cancer, diabetes and rheumatoid arthritis. Recently, ROCK has attracted attention for its crucial role in angiogenesis, making it a promising target for new therapeutic approaches. In this review, we summarize recent advances in understanding the role of ROCK signaling in regulating the permeability, migration, proliferation and tubulogenesis of endothelial cells (ECs), as well as its functions in non-ECs which constitute the pro-angiogenic microenvironment. The therapeutic potential of ROCK inhibitors in angiogenesis-related diseases is also discussed.

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          Endothelial cell migration during angiogenesis.

          Laurent Lamalice, Fabrice Le Boeuf, Jacques Huot (2007)
          Endothelial cell migration is essential to angiogenesis. This motile process is directionally regulated by chemotactic, haptotactic, and mechanotactic stimuli and further involves degradation of the extracellular matrix to enable progression of the migrating cells. It requires the activation of several signaling pathways that converge on cytoskeletal remodeling. Then, it follows a series of events in which the endothelial cells extend, contract, and throw their rear toward the front and progress forward. The aim of this review is to give an integrative view of the signaling mechanisms that govern endothelial cell migration in the context of angiogenesis.
          Article 0 comments Cited 433 times – based on 0 reviews     Review now
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            Signaling from Rho to the actin cytoskeleton through protein kinases ROCK and LIM-kinase.

            M. Maekawa, T Ishizaki, S Boku … (1999)
            The actin cytoskeleton undergoes extensive remodeling during cell morphogenesis and motility. The small guanosine triphosphatase Rho regulates such remodeling, but the underlying mechanisms of this regulation remain unclear. Cofilin exhibits actin-depolymerizing activity that is inhibited as a result of its phosphorylation by LIM-kinase. Cofilin was phosphorylated in N1E-115 neuroblastoma cells during lysophosphatidic acid-induced, Rho-mediated neurite retraction. This phosphorylation was sensitive to Y-27632, a specific inhibitor of the Rho-associated kinase ROCK. ROCK, which is a downstream effector of Rho, did not phosphorylate cofilin directly but phosphorylated LIM-kinase, which in turn was activated to phosphorylate cofilin. Overexpression of LIM-kinase in HeLa cells induced the formation of actin stress fibers in a Y-27632-sensitive manner. These results indicate that phosphorylation of LIM-kinase by ROCK and consequently increased phosphorylation of cofilin by LIM-kinase contribute to Rho-induced reorganization of the actin cytoskeleton.
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              Caspase-3-mediated cleavage of ROCK I induces MLC phosphorylation and apoptotic membrane blebbing.

              M Sebbagh, C Renvoizé, J Hamelin … (2001)
              Increased phosphorylation of myosin light chain (MLC) is necessary for the dynamic membrane blebbing that is observed at the onset of apoptosis. Here we identify ROCK I, an effector of the small GTPase Rho, as a new substrate for caspases. ROCK I is cleaved by caspase-3 at a conserved DETD1113/G sequence and its carboxy-terminal inhibitory domain is removed, resulting in deregulated and constitutive kinase activity. ROCK proteins are known to regulate MLC-phosphorylation, and apoptotic cells exhibit a gradual increase in levels of phosphorylated MLC concomitant with ROCK I cleavage. This phosphorylation, as well as membrane blebbing, is abrogated by inhibition of caspases or ROCK proteins, but both processes are independent of Rho activity. We also show that expression of active truncated ROCK I induces cell blebbing. Thus, activation of ROCK I by caspase-3 seems to be responsible for bleb formation in apoptotic cells.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Theranostics
                Journal ID (iso-abbrev): Theranostics
                Journal ID (publisher-id): thno
                Title: Theranostics
                Publisher: Ivyspring International Publisher (Sydney )
                ISSN (Electronic): 1838-7640
                Publication date Collection: 2018
                Publication date (Electronic): 26 November 2018
                Volume: 8
                Issue: 21
                Pages: 6053-6069
                Affiliations
                [1 ]Laboratory of Microvascular Medicine, Medical Research Center, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, Shandong, China
                [2 ]The Research Center for Advanced Science and Technology, Isotope Science Center, The University of Tokyo, Meguro-ku, Tokyo, Japan.
                [3 ]Department of Biology, Trent University, Peterborough, Ontario, Canada
                [4 ]Department of Bioengineering, Rice University, Houston, TX 77030, USA
                Author notes
                ✉ Corresponding authors: Gang Bao, Email: gb20@ 123456rice.edu and Ju Liu, Email: ju.liu@ 123456sdu.edu.cn

                Competing Interests: The authors have declared that no competing interest exists.

                Article
                Publisher ID: thnov08p6053
                DOI: 10.7150/thno.30305
                PMC ID: 6299434
                PubMed ID: 30613282
                SO-VID: 0ca7e8b0-e98d-4911-91a9-d0a553af076d
                Copyright © © Ivyspring International Publisher
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) license ( https://creativecommons.org/licenses/by-nc/4.0/). See http://ivyspring.com/terms for full terms and conditions.

                History
                Date received : 30 September 2018
                Date accepted : 16 October 2018
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular medicine
                Keywords: rho-associated coiled-coil kinase (rock),angiogenesis,endothelial cell,microenvironment,therapeutic target
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: rho-associated coiled-coil kinase (rock), angiogenesis, endothelial cell, microenvironment, therapeutic target

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