Journal of Clinical & Experimental Dermatology Research
Open Access

Hiroyuki Murota

Biography

 Graduation:-1995 Favorite pursuit: motorcycle, assembling vacuume tube-audio amplifier, travel, musical instrument (electric bass, electric guitar) Unexplained events in patients with dermatoses are topics of my research, especially for… 1. understanding of the abnormal physiology in atopic dermatitis 1)         Pruritus and temperature “My pruritus worsened when I felt warmth!” This is the complaint frequently heard from patients with atopic dermatitis in our daily practice. Such warmth-provoked itch impairs patients’ QoL, and is difficult to treat. To quest for a cure of this unfavorable symptom, understanding the underlying mechanism of this symptom is required. Recently, we found a neurotrophic factor, artemin, accumulated in lesional skin of atopic dermatitis, and its involvement in warmth-provoked pruritus. Related article Murota H, et al. Artemin causes hypersensitivity to warm sensation, mimicking warmth-provoked pruritus in atopic dermatitis. J Allergy Clin Immunol. 2012 2)         Is sweat exacerbating factor of atopic dermatitis? For the dermatologist and its related researchers in outside of Japan might feel strange to hear this question. In Japan, sweat is thought to be an exacerbating factor, and is introduced as major exacerbating factor in Japanese guideline for atopic dermatitis. However, sweating is important to maintain skin in healthy condition. Thus, we are confusing how should we instruct possible countermeasures to sweat to the patients with atopic dermatitis. To investigate the pathogenic role of sweat in atopic dermatitis, we are measuring sweating volume in patients with atopic dermatitis using quantitative axon reflex test (originally generated by Prof. Jeong-Beom Lee) . Related article Kijima A, Murota H, et al. Abnormal Axon Reflex-Mediated Sweating Correlates with High State of Anxiety in Atopic Dermatitis. Allergol Int. 2012 3)         The role of cholesterol in skin barrier function and keratinocyte biology. As you all know, lipids play important role in skin barrier function and skin homeostasis. Although the role of ceramide has been well documented in many literatures, the role of cholesterol remains obscure. Now, we are investigating the role of cholesterol in keratinocyte and stratum corneum. Related article Abd El-Latif MI, Murota H, et al. Effects of a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor and low-density lipoprotein on proliferation and migration of keratinocytes. Br J Dermatol. 2010 163:128-37. 4)         Ecomonic impact, medical cost, health related Quality of life, and work and classroom productivity in allergic skin diseases. The impairment that pruritic skin diseases have on patient productivity at work, in the classroom, and in daily activities is substantial and needs to be characterized. The objective of this study was to determine how pruritic skin diseases impact patient productivity and quality of life (QOL), in order to improve the measurement of these endpoints to allow the influence of treatment options Related article Murota H, et al. Impact of sedative and non-sedative antihistamines on the impaired productivity and quality of life in patients with pruritic skin diseases. Allergol Int. 2010 59:345-54 Murota H, et al. Effects of nonsedative antihistamines on productivity of patients with pruritic skin diseases. Allergy. 2010 65:929-30. 5)         Tissue remodeling in chronic allergic dermatitis. The process known as tissue remodeling and repair is thought to be an underlying cause of refractory allergic diseases such as asthmatic diseases and atopic dermatitis. Based on a generally accepted definition by the Global Initiative for Asthma, it has been proposed that tissue remodeling contributes to (1) reconstitution and repair of inflammatory tissue injuries, (2) irreversibility or intractability of the process, and (3) persistence of allergic inflammation. In view of these considerations, tissue remodeling appears to participate in the prolongation of chronic allergic reactions rather than in repair of tissue damaged by allergic inflammation. Histamine has distinct effects on dermal fibroblasts, which are characterized by increased synthesis of type 1 collagen and glycosaminoglycans, and augmentation of fibrogenic cytokine-induced fibroblast proliferation. However, there has been little or no direct evidence as to whether the effects of histamine on fibroblasts derived from different tissues are expressed at the same level. Now, we are confirming the involvement of histamine in tissue remodeling of atopic dermatitis lesional skin.   Related article Murota H, et al. Emedastine difumarate inhibits histamine-induced collagen synthesis in dermal fibroblasts. J Investig Allergol Clin Immunol. 2008;18:245-52 Murota H, Katayama I. Emedastine difumarate: a review of its potential ameliorating effect for tissue remodeling in allergic diseases. Expert Opin Pharmacother. 2009 10:1859-67 2. Pathogenesis of scleroderma and its therapeutic perspectives Scleroderma is characterized by broad area skin sclerosis and internal organ involvement including pulmonary fibrosis, esophageal dysfunction, pulmonary arterial hypertension, renal crisis, and heart failure. These symptoms dramatically affect the prognosis for scleroderma patients. Autoaggressive immunological activation and continuous activation of fibroblasts are the key components of scleroderma, yet the mechanisms underlying these are incompletely understood. We focused on the role of several inflammatory cytokines (e.g. TNF and IL-6), proteases (e.g. TACE), and matrix protein (e.g. periostin) in pathogenesis of scleroderma, and believe we could contribute to formulating novel therapeutic approach for patients with scleroderma. Related article Yang L, et al. Periostin Facilitates Skin Sclerosis via PI3K/Akt Dependent Mechanism in a Mouse Model of Scleroderma. PLoS ONE 2012 7: e41994. Kitaba S, Murota H, et al. Blockade of interleukin-6 receptor alleviates disease in mouse model of scleroderma. Am J Pathol. 2012 180:165-76. Terao M, Murota H, et al. Tumor necrosis factor-alpha processing inhibitor-1 inhibits skin fibrosis in a bleomycin-induced murine model of scleroderma. Exp Dermatol. 2010 19:38-43 Murota H, et al. Disruption of tumor necrosis factor receptor p55 impairs collagen turnover in experimentally induced sclerodermic skin fibroblasts. Arthritis Rheum. 2003 48:1117-25. 3. Temperature and circulatory disorder 1) Livedo reticularis with summer ulceration; Why in summer? Livedo reticularis with summer ulceration (LRSU) was origin- ally defined as a syndrome associated with idiopathic livedo reticularis in which ulcerations occur only or especially during the warmer months of the year. Typical histopathological findings of LRSU are endothelial proliferation and hyaline degeneration along with thrombosis of dermal vessels and necrosis of the epidermis. The pathogenesis of livedo reticularis is partly explained by a genetic disorder, venous abnormalities and dysfunction of coagulant proteins. Although these results imply that disorder of anticoagulant process might trigger this disease, they cannot explain why LRSU occurs only in summer. Now, we are searching the thermo-sensitive disease-associated protein using proteomics.   Related article Murota H,et al. Heat-inductible turbidity precipitates in plasma samples of livedo reticularis with summer ulceration: hypothesis for abnormal coagulation in summer. Thromb Haemost. 2005 94:222-3 2) Raynaud phenomenon Now, we are searching the thermo-sensitive disease-associated protein using proteomics.    

Research Interest

 allergic inflamation, itch, kinetics of lipid in stratum corneum,allergic dermatoses, collagen diseases

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