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Eun Shin 2 Articles
Interleukin-31, Interleukin-31RA, and OSMR Expression Levels in Post-burn Hypertrophic Scars
Mi Young Lee, Eun Shin, Hyunchul Kim, In Suk Kwak, Younghee Choi
J Pathol Transl Med. 2018;52(5):307-313.   Published online August 16, 2018
DOI: https://doi.org/10.4132/jptm.2018.08.03
  • 7,138 View
  • 196 Download
  • 9 Web of Science
  • 9 Crossref
AbstractAbstract PDF
Background
Although several studies have shown the role of interleukin-31 (IL-31) and its receptors in inducing pruritus in certain skin disorders, knowledge of its role in post-burn hypertrophic scars is insufficient. Therefore, the histopathological expression levels of IL-31, IL-31 receptor alpha (IL-31RA), and oncostatin M receptor (OSMR) in post-burn hypertrophic scar tissues were investigated and compared with normal tissue expression levels.
Methods
Samples of hypertrophic scar tissue were obtained from 20 burn patients through punch biopsy. Normal samples were obtained from areas adjacent to the burn injury site of the same patients. Samples were placed in 10% neutral buffered formalin, embedded in paraplast, and processed into serial 5-μm sections. Immunohistochemistry results were semi-quantitatively evaluated for IL-31, IL-31RA, and OSMR. By hematoxylin and eosin staining, epidermal and dermal thickness were assessed with a microscope and digital camera. Intensities were rated on a scale of 1 to 4.
Results
Percentages for IL-31, IL-31RA, and OSMR in the epidermal basal layer cell cytoplasm were significantly greater in the burn scar tissue compared to normal skin, as well as the dermal and epidermal thickness (p < .05). There was a significant difference in IL-31 epidermal basal layer intensity in burn scar tissue compared to normal skin (p < .05). Besides the OSMR basal layer intensity, IL-31 and IL-31RA intensities between the burn scar and normal tissues were not significant. However, correlations were significant, indicating that the greater the infiltration percentage, the higher the intensity (p < .05).
Conclusions
IL-31, IL-31RA, and OSMR expression levels are increased in hypertrophic scars compared with normal tissue.

Citations

Citations to this article as recorded by  
  • Pharmacotherapy for Keloids and Hypertrophic Scars
    Teruo Murakami, Sadayuki Shigeki
    International Journal of Molecular Sciences.2024; 25(9): 4674.     CrossRef
  • Understanding Neural Factors in Burn-related Pruritus and Neuropathic Pain
    Dulan A Gunawardena, Edward Stanley, Andrea C Issler-Fisher
    Journal of Burn Care & Research.2023; 44(5): 1182.     CrossRef
  • Canine interleukin-31 binds directly to OSMRβ with higher binding affinity than to IL-31RA
    Yuxin Zheng, Jing Zhang, Tianling Guo, Jin Cao, Lixian Wang, Jie Zhang, Xuefei Pang, Feng Gao, Hua Sun, Haixia Xiao
    3 Biotech.2023;[Epub]     CrossRef
  • Multimodal roles of transient receptor potential channel activation in inducing pathological tissue scarification
    Yuping Zheng, Qingrui Huang, Yanfeng Zhang, Lanxin Geng, Wuqing Wang, Huimin Zhang, Xiang He, Qiannan Li
    Frontiers in Immunology.2023;[Epub]     CrossRef
  • Role of burn severity and posttraumatic stress symptoms in the co-occurrence of itch and neuropathic pain after burns: A longitudinal study
    N. E. E. Van Loey, A. E. E. de Jong, H. W. C. Hofland, A. I. M. van Laarhoven
    Frontiers in Medicine.2022;[Epub]     CrossRef
  • Trial of Nemolizumab in Moderate-to-Severe Prurigo Nodularis
    Sonja Ständer, Gil Yosipovitch, Franz J. Legat, Jean-Philippe Lacour, Carle Paul, Joanna Narbutt, Thomas Bieber, Laurent Misery, Andreas Wollenberg, Adam Reich, Faiz Ahmad, Christophe Piketty
    New England Journal of Medicine.2020; 382(8): 706.     CrossRef
  • Post-Burn Pruritus
    Bo Young Chung, Han Bi Kim, Min Je Jung, Seok Young Kang, In-Suk Kwak, Chun Wook Park, Hye One Kim
    International Journal of Molecular Sciences.2020; 21(11): 3880.     CrossRef
  • Novel Analgesics with Peripheral Targets
    Cosmin I. Ciotu, Michael J.M. Fischer
    Neurotherapeutics.2020; 17(3): 784.     CrossRef
  • Post-Burn Pruritus and Its Management—Current and New Avenues for Treatment
    Emilie Fowler, Gil Yosipovitch
    Current Trauma Reports.2019; 5(2): 90.     CrossRef
Histopathological Causes of Late Liver Allograft Dysfunction: Analysis at a Single Institution
Eun Shin, Ji Hoon Kim, Eunsil Yu
Korean J Pathol. 2013;47(1):21-27.   Published online February 25, 2013
DOI: https://doi.org/10.4132/KoreanJPathol.2013.47.1.21
  • 7,873 View
  • 66 Download
  • 4 Crossref
AbstractAbstract PDF
Background

We summarize our experience in the pathological diagnosis of late complications of liver transplantation (LT) to better understand the causes of late allograft dysfunction in a population mostly composed of patients with hepatitis B virus (HBV) infection.

Methods

We reviewed 361 post-transplant liver biopsies from 174 patients who underwent LT and first presented with liver function abnormalities 3 months post-procedure. The underlying diseases included HBV-associated liver disease (77%), toxic or alcoholic liver disease (10.3%), hepatitis C virus (HCV)-associated liver disease (8.6%), primary biliary cirrhosis (1.2%), primary sclerosing cholangitis (1.2%), and metabolic disease (1.7%).

Results

The three most common late complications were acute rejection (32.5%), recurrent disease (19.1%), and biliary complication (17.1%). Patients who underwent LT for HBV infection or for drug- or alcohol-related liver disease had a lower incidence of recurring disease than those who underwent transplantation for HCV infection. During post-transplantation months 3-12, acute rejection was the most common cause of allograft dysfunction and recurring disease was the leading cause for allograft dysfunction (p=0.039). The two primary causes of late allograft dysfunction have overlapping histological features, although acute rejection more frequently showed bile duct damage and vascular endothelialitis than recurring HBV infection, and recurring HBV infection had more frequent lobular activity and piecemeal necrosis.

Conclusions

The causes of late liver allograft dysfunction are closely associated with the original liver diseases and the period after LT. Careful attention is required for differential diagnosis between acute rejection and recurrent HBV.

Citations

Citations to this article as recorded by  
  • Liver Transplantation from a Human Leukocyte Antigen-Matched Sibling Donor: Effectiveness of Direct-Acting Antiviral Therapy against Hepatitis C Virus Infection
    Tatsuo Kanda, Naoki Matsumoto, Tomotaka Ishii, Shuhei Arima, Shinji Shibuya, Masayuki Honda, Reina Sasaki-Tanaka, Ryota Masuzaki, Shini Kanezawa, Masahiro Ogawa, Shintaro Yamazaki, Osamu Aramaki, Hirofumi Kogure, Yukiyasu Okamura
    Reports.2022; 5(4): 49.     CrossRef
  • A comparative histological analysis of early and late graft dysfunction in different time zones following living donor liver transplantation
    Archana Rastogi, Nayana Patil, Sphurti Srivastava, Gayatri Ramakrishna, Rakhi Maiwal, Guresh Kumar, Ashok K. Choudhary, Seema Alam, Chhagan Bihari, Viniyendra Pamecha
    Indian Journal of Pathology and Microbiology.2022; 65(4): 802.     CrossRef
  • Differences in risk factors for early-onset and late-onset biliary complications in liver transplant patients
    Hsiu-Lung Fan, An-Chieh Feng, Meng-Hsing Ho, Shih-Ming Kuo, Wei-Chou Chang, Teng-Wei Chen
    Journal of Medical Sciences.2015; 35(5): 201.     CrossRef
  • Vitamin C exerts beneficial hepatoprotection against Concanavalin A-induced immunological hepatic injury in mice through inhibition of NF-κB signal pathway
    Tao Liang, Xiaoyu Chen, Min Su, Hongqiu Chen, Guozhe Lu, Kun Liang
    Food & Function.2014; 5(9): 2175.     CrossRef

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