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      Hyaluronic acid-curcumin conjugate suppresses the fibrotic functions of myofibroblasts from contractive joint by the PTGER2 demethylation

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          Abstract

          Joint contracture is a fibrotic complication induced by joint immobilization and trauma, which is characterized as excessive myofibroblast proliferation in joint capsule. The treatments of joint contracture are unsatisfied and patients are suffered from joint dysfunction. Our previous study has shown that curcumin can inhibit myofibroblast proliferation in vitro, but the major challenge is the low aqueous solubility and biological activity of curcumin. In this study, hyaluronic acid-curcumin (HA-Cur) conjugate was synthesized to suppress myofibroblasts in joint contracture. Cells were isolated from the joint capsules of joint contracture patients and induced to active myofibroblasts by transforming growth factor-β (TGF-β). The anti-fibrotic function and mechanisms of HA-Cur were investigated by immunohistochemistry, reverse transcription-quantitative polymerase chain reaction (PCR), methylation-specific PCR, western blot, transwell migration assay and proliferation assay. Results showed that 30 μM HA-Cur significantly attenuated the fibrotic functions of myofibroblast in joint contracture in vitro by regulating the methylation of prostaglandin E receptor 2 (PTGER2) and inhibiting TGF-β signaling. This may provide a mechanism for the treatment of joint contracture, and provide a molecular target PTGER2 for therapy during the pathogenesis of joint contracture.

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          Curcumin: the story so far.

          R A Sharma, A Gescher, W Steward (2005)
          Curcumin is a polyphenol derived from the herbal remedy and dietary spice turmeric. It possesses diverse anti-inflammatory and anti-cancer properties following oral or topical administration. Apart from curcumin's potent antioxidant capacity at neutral and acidic pH, its mechanisms of action include inhibition of several cell signalling pathways at multiple levels, effects on cellular enzymes such as cyclooxygenase and glutathione S-transferases, immuno-modulation and effects on angiogenesis and cell-cell adhesion. Curcumin's ability to affect gene transcription and to induce apoptosis in preclinical models is likely to be of particular relevance to cancer chemoprevention and chemotherapy in patients. Although curcumin's low systemic bioavailability following oral dosing may limit access of sufficient concentrations for pharmacological effect in certain tissues, the attainment of biologically active levels in the gastrointestinal tract has been demonstrated in animals and humans. Sufficient data currently exist to advocate phase II clinical evaluation of oral curcumin in patients with invasive malignancy or pre-invasive lesions of the gastrointestinal tract, particularly the colon and rectum.
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            Curcumin nanoformulations: a review of pharmaceutical properties and preclinical studies and clinical data related to cancer treatment.

            Ornchuma Naksuriya, Siriporn Okonogi, Raymond Schiffelers … (2014)
            Curcumin, a natural yellow phenolic compound, is present in many kinds of herbs, particularly in Curcuma longa Linn. (turmeric). It is a natural antioxidant and has shown many pharmacological activities such as anti-inflammatory, anti-microbial, anti-cancer, and anti-Alzheimer in both preclinical and clinical studies. Moreover, curcumin has hepatoprotective, nephroprotective, cardioprotective, neuroprotective, hypoglycemic, antirheumatic, and antidiabetic activities and it also suppresses thrombosis and protects against myocardial infarction. Particularly, curcumin has demonstrated efficacy as an anticancer agent, but a limiting factor is its extremely low aqueous solubility which hampers its use as therapeutic agent. Therefore, many technologies have been developed and applied to overcome this limitation. In this review, we summarize the recent works on the design and development of nano-sized delivery systems for curcumin, including liposomes, polymeric nanoparticles and micelles, conjugates, peptide carriers, cyclodextrins, solid dispersions, lipid nanoparticles and emulsions. Efficacy studies of curcumin nanoformulations using cancer cell lines and in vivo models as well as up-to-date human clinical trials are also discussed. Copyright © 2014 Elsevier Ltd. All rights reserved.
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              Epigenetic gene silencing in cancer: the DNA hypermethylome.

              Manel Esteller (2007)
              Epigenetic gene inactivation in transformed cells involves many 'belts of silencing'. One of the best-known lesions of the malignant cell is the transcriptional repression of tumor-suppressor genes by promoter CpG island hypermethylation. We are in the process of completing the molecular dissection of the entire epigenetic machinery involved in methylation-associated silencing, such as DNA methyltransferases, methyl-CpG binding domain proteins, histone deacetylases, histone methyltransferases, histone demethylases and Polycomb proteins. The first indications are also starting to emerge about how the combination of cellular selection and targeted pathways leads to abnormal DNA methylation. One thing is certain already, promoter CpG island hypermethylation of tumor-suppressor genes is a common hallmark of all human cancers. It affects all cellular pathways with a tumor-type specific profile, and in addition to classical tumor-suppressor and DNA repair genes, it includes genes involved in premature aging and microRNAs with growth inhibitory functions. The importance of hypermethylation events is already in evidence at the bedside of cancer patients in the form of cancer detection markers and chemotherapy predictors, and in the approval of epigenetic drugs for the treatment of hematological malignancies. In the very near future, the synergy of candidate gene approaches and large-scale epigenomic technologies, such as methyl-DIP, will yield the complete DNA hypermethylome of cancer cells.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Regen Biomater
                Journal ID (iso-abbrev): Regen Biomater
                Journal ID (publisher-id): rb
                Title: Regenerative Biomaterials
                Publisher: Oxford University Press
                ISSN (Print): 2056-3418
                ISSN (Electronic): 2056-3426
                Publication date (Print): October 2019
                Publication date (Electronic): 22 April 2019
                Publication date PMC-release: 22 April 2019
                Volume: 6
                Issue: 5
                Pages: 269-277
                Affiliations
                [1 ]Department of Orthopedic Surgery, The Third Affiliated Hospital of Sun Yat-sen University , Guangzhou, China
                [2 ]National Engineering Research Center for Biomaterials, Sichuan University , Chengdu, China
                Author notes
                Correspondence address. No. 600 Tianhe Road, Tianhe District, 510000, Guangzhou, China. Tel: +86 020-85252229; Fax: +86 020-85253336; E-mail: wangk@ 123456mail.sysu.edu.cn and herh3@ 123456mail.sysu.edu.cn

                Dongjie Yu, Ze Zhuang and Jianhua Ren authors contributed equally to this work.

                Author information
                http://orcid.org/0000-0003-1396-6325
                Article
                Publisher ID: rbz016
                DOI: 10.1093/rb/rbz016
                PMC ID: 6783700
                PubMed ID: 31616564
                SO-VID: cd801f21-976c-4aa5-ab6a-96578e3f39a5
                Copyright © © The Author(s) 2019. Published by Oxford University Press.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 25 January 2019
                Date revision received : 25 February 2019
                Date accepted : 11 March 2019
                Page count
                Pages: 9
                Funding
                Funded by: National Natural Science Foundation of China 10.13039/501100001809
                Award ID: 81772368
                Award ID: 81802184
                Funded by: Natural Science Foundation of Guangdong 10.13039/501100003453
                Award ID: 2017A030310226
                Funded by: Guangdong Traditional Chinese Medicine Bureau Research Fund
                Award ID: 20181061
                Funded by: Medical Research Foundation of Guangdong
                Award ID: A2017003
                Categories
                Subject: Research Articles

                Keywords: curcumin,ptger2,methylation,joint contracture
                Data availability:
                Keywords: curcumin, ptger2, methylation, joint contracture

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