For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
4
views
28
references
 Top references
cited by
11
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      592
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Hyperbaric oxygen treatment on keloid tumor immune gene expression

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background:

          Hyperbaric oxygen treatment (HBOT) has been demonstrated to influence the keloid recurrence rate after surgery and to relieve keloid symptoms and other pathological processes in keloids. To explore the mechanism of the effect of HBOT on keloids, tumor immune gene expression and immune cell infiltration were studied in this work.

          Methods:

          From February 2021 to April 2021, HBOT was carried out on keloid patients four times before surgery. Keloid tissue samples were collected and divided into an HBOT group (keloid with HBOT before surgery [HK] group, n = 6) and a non-HBOT group (K group, n = 6). Tumor gene expression was analyzed with an Oncomine Immune Response Research Assay kit. Data were mined with R package. The differentially expressed genes between the groups were compared. Hub genes between the groups were determined and verified with Quantitative Real-time PCR. Immune cell infiltration was analyzed based on CIBERSORT deconvolution algorithm analysis of gene expression and verified with immunohistochemistry (IHC).

          Results:

          Inflammatory cell infiltration was reduced in the HK group. There were 178 upregulated genes and 217 downregulated genes. Ten hub genes were identified, including Integrin Subunit Alpha M ( ITGAM), interleukin ( IL)- 4, IL-6, IL-2, Protein Tyrosine Phosphatase Receptor Type C ( PTPRC), CD86, transforming growth factor ( TGF), CD80, CTLA4, and IL-10. CD80, ITGAM, IL-4, and PTPRC with significantly downregulated expression were identified. IL-10 and IL-2 were upregulated in the HK group but without a significant difference. Infiltration differences of CD8 lymphocyte T cells, CD4 lymphocyte T-activated memory cells, and dendritic resting cells were identified with gene CIBERSORT deconvolution algorithm analysis. Infiltration levels of CD4 lymphocyte T cell in the HK group were significantly higher than those of the K group in IHC verification.

          Conclusion:

          HBOT affected tumor gene expression and immune cell infiltration in keloids. CD4 lymphocyte T cell, especially activated memory CD4 +T, might be the key regulatory immune cell, and its related gene expression needs further study.

          Related collections

          Most cited references28

          • Record: found
          • Abstract: found
          • Article: found
          Is Open Access

          Keloid and Hypertrophic Scars Are the Result of Chronic Inflammation in the Reticular Dermis

          Rei Ogawa (2017)
          Keloids and hypertrophic scars are caused by cutaneous injury and irritation, including trauma, insect bite, burn, surgery, vaccination, skin piercing, acne, folliculitis, chicken pox, and herpes zoster infection. Notably, superficial injuries that do not reach the reticular dermis never cause keloidal and hypertrophic scarring. This suggests that these pathological scars are due to injury to this skin layer and the subsequent aberrant wound healing therein. The latter is characterized by continuous and histologically localized inflammation. As a result, the reticular layer of keloids and hypertrophic scars contains inflammatory cells, increased numbers of fibroblasts, newly formed blood vessels, and collagen deposits. Moreover, proinflammatory factors, such as interleukin (IL)-1α, IL-1β, IL-6, and tumor necrosis factor-α are upregulated in keloid tissues, which suggests that, in patients with keloids, proinflammatory genes in the skin are sensitive to trauma. This may promote chronic inflammation, which in turn may cause the invasive growth of keloids. In addition, the upregulation of proinflammatory factors in pathological scars suggests that, rather than being skin tumors, keloids and hypertrophic scars are inflammatory disorders of skin, specifically inflammatory disorders of the reticular dermis. Various external and internal post-wounding stimuli may promote reticular inflammation. The nature of these stimuli most likely shapes the characteristics, quantity, and course of keloids and hypertrophic scars. Specifically, it is likely that the intensity, frequency, and duration of these stimuli determine how quickly the scars appear, the direction and speed of growth, and the intensity of symptoms. These proinflammatory stimuli include a variety of local, systemic, and genetic factors. These observations together suggest that the clinical differences between keloids and hypertrophic scars merely reflect differences in the intensity, frequency, and duration of the inflammation of the reticular dermis. At present, physicians cannot (or at least find it very difficult to) control systemic and genetic risk factors of keloids and hypertrophic scars. However, they can use a number of treatment modalities that all, interestingly, act by reducing inflammation. They include corticosteroid injection/tape/ointment, radiotherapy, cryotherapy, compression therapy, stabilization therapy, 5-fluorouracil (5-FU) therapy, and surgical methods that reduce skin tension.
          Article 0 comments Cited 259 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Hypertrophic scars and keloids--a review of their pathophysiology, risk factors, and therapeutic management.

            Dolores Wolfram, Alexandar Tzankov, Petra Pülzl … (2009)
            Hypertrophic scars and keloids result from an abnormal fibrous wound healing process in which tissue repair and regeneration-regulating mechanism control is lost. These abnormal fibrous growths present a major therapeutic dilemma and challenge to the plastic surgeon because they are disfiguring and frequently recur. To provide updated clinical and experimental information on hypertrophic scars and keloids so that physicians can better understand and properly treat such lesions. A Medline literature search was performed for relevant publications and for diverse strategies for management of hypertrophic scars and keloids. The growing understanding of the molecular processes of normal and abnormal wound healing is promising for discovery of novel approaches for the management of hypertrophic scars and keloids. Although optimal treatment of these lesions remains undefined, successful healing can be achieved only with combined multidisciplinary therapeutic regimens.
            Article 0 comments Cited 153 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: found
              Is Open Access

              Signal Transducer and Activator of Transcription (STATs) Proteins in Cancer and Inflammation: Functions and Therapeutic Implication

              Chin-Yap Loh, Aditya Arya, Ahmed Fadhil Naema … (2019)
              Signal Transducer and Activator of Transcription (STAT) pathway is connected upstream with Janus kinases (JAK) family protein and capable of integrating inputs from different signaling pathways. Each family member plays unique functions in signal transduction and crucial in mediating cellular responses to different kind of cytokines. STAT family members notably STAT3 and STAT5 have been involved in cancer progression whereas STAT1 plays opposite role by suppressing tumor growth. Persistent STAT3/5 activation is known to promote chronic inflammation, which increases susceptibility of healthy cells to carcinogenesis. Here, we review the role of STATs in cancers and inflammation while discussing current therapeutic implications in different cancers and test models, especially the delivery of STAT3/5 targeting siRNA using nanoparticulate delivery system.
              Article 0 comments Cited 133 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): Chin Med J (Engl)
                Journal ID (iso-abbrev): Chin Med J (Engl)
                Journal ID (publisher-id): CM9
                Title: Chinese Medical Journal
                Publisher: Lippincott Williams & Wilkins (Hagerstown, MD )
                ISSN (Print): 0366-6999
                ISSN (Electronic): 2542-5641
                Publication date (Print): 20 September 2021
                Publication date (Electronic): 13 September 2021
                Volume: 134
                Issue: 18
                Pages: 2205-2213
                Affiliations
                [1 ]17th Department of Plastic Surgery, Plastic Surgery Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100144, China
                [2 ]Department of Plastic Surgery, Peking Union Medical College Hospital, Beijing 100730, China
                [3 ]Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China
                [4 ]Department of Pathology, Peking Union Medical College Hospital, Beijing 100730, China.
                Author notes
                Correspondence to: You-Bin Wang, Department of Plastic Surgery, Peking Union Medical College Hospital, Beijing 100730, China E-Mail: wybenz@ 123456sina.com
                Article
                Publisher ID: CMJ-2021-2168
                DOI: 10.1097/CM9.0000000000001780
                PMC ID: 8478393
                PubMed ID: 34553702
                SO-VID: 1b803087-8d18-420d-9f26-10cb881f1334
                Copyright © Copyright © 2021 The Chinese Medical Association, produced by Wolters Kluwer, Inc. under the CC-BY-NC-ND license.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. http://creativecommons.org/licenses/by-nc-nd/4.0

                History
                Date received : 05 July 2021
                Categories
                Subject: Original Articles
                Custom metadata
                OPEN-ACCESS TRUE

                Keywords: keloid,hyperbaric oxygen treatment,tumor immune gene,immune cell
                Data availability:
                Keywords: keloid, hyperbaric oxygen treatment, tumor immune gene, immune cell

                Comments

                Comment on this article

                scite_

                Similar content592

                See all similar

                Cited by11

                See all cited by

                Most referenced authors271

                See all reference authors