C Yasui

Publications (12)38.59 Total impact

• Article: Mucous membrane pemphigoid with generalized blisters: IgA and IgG autoantibodies target both laminin-332 and type XVII collagen.

  I Hayashi, S Shinkuma, S Shimizu, K Natsuga, H Ujiie, C Yasui, K Tsuchiya, W Nishie, H Shimizu
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  ABSTRACT: Mucous membrane pemphigoid (MMP) is a mucous membrane-dominated, subepidermal autoimmune blistering disease in which autoantibodies usually react with the C-terminal domain of type XVII collagen (COL17) or with laminin-332. Only a few cases of MMP with widespread blisters have been reported. Serologically, IgA and IgG class autoantibodies directed against COL17 or IgG autoantibodies directed against laminin-332 in patients with MMP have been well documented. MMP cases in which IgA reacts with laminin-332, however, are extremely rare. We report a case of MMP in a 67-year-old man. Clinical examination revealed extensive mucosal lesions as well as generalized blisters and erosions that healed with scar formation. The disease was intractable to treatment with systemic steroids. Interestingly, in addition to IgG directed against laminin-332 and the noncollagenous 16A (NC16A) and C-terminal domains of COL17, circulating IgA reacting with laminin-332 and with the NC16A domain of COL17 was also detected. This is the first MMP case with circulating IgA and IgG autoantibodies against both laminin-332 and COL17.
  British Journal of Dermatology 12/2011; 166(5):1116-20. · 3.67 Impact Factor
• Article: Subcutaneous nodules on the buttocks as a manifestation of dialysis-related amyloidosis: a clinicopathological entity?

  S Shimizu, C Yasui, K Yasukawa, H Nakamura, H Shimizu, K Tsuchiya
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  ABSTRACT: While beta 2-microglobulin amyloidosis occurring in patients undergoing long-term dialysis is frequently associated with joint involvement, skin lesions have rarely been encountered. We report a 57-year-old man with extensive subcutaneous amyloid deposition forming large nodules on the buttocks; the patient had been on maintenance dialysis for 28 years. Although this condition is rare, a review of the literature indicates that the majority of such lesions occur around the buttock region.
  British Journal of Dermatology 09/2003; 149(2):400-4. · 3.67 Impact Factor
• Article: Substance P induces inositol 1,4,5-trisphosphate and intracellular free calcium increase in cultured normal human epidermal keratinocytes.

  H Koizumi, C Yasui, T Fukaya, T Ueda, A Ohkawara
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  ABSTRACT: Substance P is a neuropeptide which is present in peripheral C nerve endings and released from them. Free nerve endings of C nerve are present in human epidermis. The effects of substance P on the transmembrane signaling system of pig epidermal sheets were previously reported. In these studies, a small amount of cells other than keratinocytes contaminated the epidermal sheets and the species difference from human was also noticed. Therefore we investigated the effects of substance P on cultured normal human epidermal keratinocytes. Alteration of intracellular free calcium (Ca2+) in single living keratinocytes was studied using an inverted fluorescence microscope and Ca(2+)-sensitive dye, Fura 2-AM. Treatment of normal human epidermal keratinocytes with substance P resulted in an increase in inositol 1,4,5-trisphosphate and in intracellular Ca2+. Substance P inhibited DNA synthesis of the keratinocytes in a dose-dependent manner. These results are consistent with the view that substance P stimulates phosphatidylinositol-4,5-bisphosphate hydrolysis of human keratinocytes, resulting in inositol 1,4,5-trisphosphate-Ca2+ signal.
  Experimental Dermatology 03/1994; 3(1):40-4. · 3.54 Impact Factor
• Article: Adenylate cyclase induces intracellular calcium increase in single human epidermal keratinocytes measured by fluorescence microscopy using Fura 2-AM.

  C Yasui, H Koizumi, T Fukaya, M Kumakiri, A Ohkawara, T Ueda
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  ABSTRACT: Intracellular calcium ([Ca2+]i) is an important second messenger of extracellular signals to induce various cellular responses. Extracellular and intracellular Ca2+ are considered to be important for cellular differentiation and proliferation of epidermal keratinocytes. Several mechanisms which increase [Ca2+]i have been demonstrated in various tissues, but in epidermal keratinocytes these mechanisms are poorly understood. In epidermal keratinocytes the adenylate cyclase-cyclic AMP response is thought to regulate cell proliferation and differentiation. However, the series of reactions which follow the cyclic AMP response remain unknown. Beta-adrenergic agonists increase [Ca2+]i in cultured epidermal keratinocytes, and we have therefore studied whether stimulation of keratinocyte adenylate cyclase could induce [Ca2+]i increase, by using fluorescence microscopy with Fura 2-AM. Adenosine and histamine, which are known to be keratinocyte adenylate cyclase receptor agonists, induced transient [Ca2+]i increase, as did epinephrine. In addition, forskolin, a direct adenylate cyclase activator, and dibutyryl-cyclic AMP also induced an increase in [Ca2+]i. In a calcium-free medium epinephrine, adenosine, histamine and dibutyryl-cyclic AMP induced an increase in [Ca2+]i. These results suggest that cyclic AMP in human epidermal keratinocytes regulates [Ca2+]i, which is released from intracellular stores.
  British Journal of Dermatology 01/1993; 127(6):589-94. · 3.67 Impact Factor
• Article: HTLV-I-associated myelopathy in a patient with adult T-cell leukemia.

  C Yasui, T Fukaya, H Koizumi, H Kobayashi, A Ohkawara
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  ABSTRACT: Disseminated erythematous papules and plaques developed in a 60-year-old man 3 years before the appearance of neurologic manifestations. A biopsy specimen of the plaque revealed Pautrier's microabscess and a dense mononuclear cell infiltration with atypical convoluted nuclei in the papillary dermis. These cells were helper/inducer T lymphocytes that expressed the interleukin 2 receptor. The patient's white blood cell count was normal, but 1% atypical lymphocytes and a high titer of anti-human T-lymphotropic virus (HTLV)-I antibody were detected in his serum. A smoldering type of adult T-cell leukemia was diagnosed. While he was being treated with PUVA, a gait disturbance developed. A high titer of anti-HTLV-I antibody, characteristic of HTLV-I-associated myelopathy, was demonstrated in his cerebrospinal fluid.
  Journal of the American Academy of Dermatology 05/1991; 24(4):633-7. · 3.99 Impact Factor
• Article: [Changes in the intracellular free calcium of cultured human epidermal keratinocytes].

  C Yasui
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  ABSTRACT: Changes in the intracellular free calcium ([Ca2+]i) of cultured normal human epidermal keratinocytes (NHEK) were investigated in order to determine whether the adenylate cyclase cAMP (AC) system and phospholipase C activating system are involved in increasing [Ca2+]i. NHEK were obtained from neonatal foreskin and grown in serum-free medium (K-GM) supplemented with 2% bovine pituitary extract. [Ca2+]i was measured by fluorescence ratio imaging microscopy using Fura-2 as the indicator. In the case of the AC system, transient increases in [Ca2+]i were observed in response to stimulation with epinephrine, norepinephrine, isoproterenol and salbutamol. Methoxamine, clonidine and dobutamine did not induce any [Ca2+]i increase. The [Ca2+]i increase evoked by epinephrine was inhibited by pretreatment with propranolol, but not by prazosin or yohimbine, indicating that epinephrine-induced [Ca2+]i elevation via beta 2-adrenergic stimulation. Similar changes were observed when NHEK were stimulated with histamine, adenosine, GTP gamma S, forskolin and dibutyryl cAMP respectively. The absence of extracellular Ca2+ had no effect on the epinephrine-induced [Ca2+]i increase. It appears that activated protein kinase A, based on cAMP accumulation via stimulatory GTP binding protein, elicited the release of Ca2+ from intracellular stores. On the other hand, when drugs known to activate phospholipase C in a wide variety of cell types were tested, a transient increase in [Ca2+]i was demonstrated in response to the addition of thrombin, bradykinin and substance P. This reaction was not affected by the presence of EGTA, suggesting that these drugs raise [Ca2+]i via phosphatidylinositol breakdown. Vasopressin, angiotensin II, serotonin and acetylcholine did not induce any increase in [Ca2+]i. On the basis of these studies, it was concluded that NHEK possess the mechanism which increase [Ca2+]i via AC system and phospholipase C activating system. It seems probable that this rise in [Ca2+]i initiates a calcium-dependent cellular response, such as activation of calcium/calmodulin dependent kinase, and subsequently regulates the proliferation and differentiation of human epidermal keratinocytes.
  [Hokkaido igaku zasshi] The Hokkaido journal of medical science 04/1991; 66(2):111-21.
• Article: Beta-adrenergic stimulation induces intracellular Ca++ increase in human epidermal keratinocytes.

  H Koizumi, C Yasui, T Fukaya, A Ohkawara, T Ueda
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  ABSTRACT: Intracellular Ca++ ([Ca++]i) is one of the most important second messengers of extracellular signals that induce cellular responses. In epidermal keratinocytes, both extracellular and intracellular Ca++ are reported to be important to cell differentiation and proliferation. Several mechanisms that increase [Ca++]i have been elicited in various tissues; however, in epidermal keratinocytes they remain unknown. Thus, we investigated the [Ca++]i modulation in cultured human epidermal keratinocytes and the stimulation that increases the concentration. The [Ca++]i concentration of keratinocytes was increased immediately and transiently by epinephrine. Methoxamine hydrochloride and clonidine (alpha-1- and 2-adrenergic agonists) did not induce an increase in [Ca++]i. The beta-antagonist, propranolol, inhibited the [Ca++]i increase induced by epinephrine and salbutamol (a beta-2-agonist). These results reveal that the beta-adrenergic stimulation induces an immediate and transient [Ca++]i increase in human keratinocytes. Beta-adrenergic stimulation is known to induce adenylate cyclase activation, which results in cyclic AMP accumulation through stimulatory guanosine 5-triphosphate (GTP) binding proteins in the keratinocytes. Also, epinephrine is reported to inhibit cultured epidermal cell proliferation. The effect of epinephrine has been demonstrated by cyclic AMP accumulation; however, beta-adrenergic stimulation revealed a [Ca++]i increase in keratinocytes in our study. One of epinephrine's regulatory effects on epidermal cell proliferation is assumed to occur through the [Ca++]i increase as well.
  Journal of Investigative Dermatology 03/1991; 96(2):234-7. · 6.31 Impact Factor
• Article: Effect of 1,25-dihydroxyvitamin D3 on adenylate cyclase and protein kinase C in pig epidermis.

  H Koizumi, C Yasui, A Ohkawara
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  ABSTRACT: 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) is suggested to be involved in the regulation of keratinocyte proliferation and differentiation. Recent evidence also indicates its potential value for the treatment of psoriasis, where the alteration of various transmembrane signalling systems has been well documented. Using porcine epidermis, we investigated the effect of 1,25(OH)2D3 on adenylate cyclase and protein kinase C systems, both of which are markedly altered in the psoriatic hyperproliferative epidermis. The effect was compared with that of another anti-psoriatic agent, hydrocortisone. Neither 1,25(OH)2D3 nor hydrocortisone revealed any effect on cyclic AMP levels or adenylate cyclase responses of epidermis. Long-term (24 h) hydrocortisone treatment, however, resulted in increased beta-adrenergic-, and prostaglandin E-adenylate cyclase responses. 1,25(OH)2D3-treatment had no effect on the epidermal adenylate cyclase responses following 24 h of incubation. The addition of both 1,25(OH)2D3 and hydrocortisone to the incubation medium resulted in the attenuation of the hydrocortisone-induced beta-adrenergic-, and prostaglandin E-adenylate cyclase responses of the epidermis. Neither agent had any effect on the cholera toxin-induced and forskolin-induced cyclic AMP accumulations of the epidermis. Neither 1,25(OH)2D3 nor hydrocortisone had any effect on the epidermal protein kinase C activity. It has been suggested that various anti-psoriatic agents might reveal their effect through the modulation of the adenylate cyclase system. Since 1,25(OH)2D3 had no effect when it was added singly to the incubation medium and rather inhibited hydrocortisone-induced adenylate cyclase stimulation, it is suggested that 1,25(OH)2D3 reveals its therapeutic efficacy through the mechanism, probably independently of the adenylate cyclase system.
  Acta Dermato Venereologica 02/1991; 71(1):6-10. · 3.18 Impact Factor
• Article: Adenylate cyclase induces intracellular Ca2+ increase in single human epidermal keratinocytes of the epidermal sheet as measured by digital imaging microscopy using Fura 2-AM.

  Y Osawa, H Koizumi, T Fukaya, C Yasui, A Ohkawara, T Ueda
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  ABSTRACT: Intracellular Ca2+ ([Ca2+]i) is thought to act as a second messenger of transmembrane signalling systems. However, no measurement of [Ca2+]i has been made in intact epidermal keratinocytes. We have developed a method for measuring [Ca2+]i in human keratinocytes from pure epidermal sheet by the application of digital imaging fluorescence microscopy with the use of Fura 2-AM. Normal human pure epidermal sheets were obtained by dispase treatment. Epinephrine and salbutamol induced transient [Ca2+]i increases. Propranolol, a beta-antagonist, inhibited this response, while prazosin and yohimbine (alpha 1- and alpha 2-antagonists, respectively) did not affect the response. Histamine and adenosine, also receptor agonists of the epidermal adenylate cyclase system, induced a similar [Ca2+]i increase, as did forskolin, a direct activator of adenylate cyclase. These data coincide with those previously presented for cultured human epidermal keratinocytes, and reveal that adenylate cyclase activation induces an increase of [Ca2+]i in intact epidermal cells. This technique enables the kinetics of [Ca2+]i in various skin disorders to be investigated.
  Archives for Dermatological Research 02/1991; 283(2):91-5. · 2.28 Impact Factor
• Article: Ultraviolet action spectrum for intracellular free Ca2+ increase in human epidermal keratinocytes.

  T Nakagaki, J Oda, H Koizumi, T Fukaya, C Yasui, T Ueda
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  ABSTRACT: Effects of UV on normal human epidermal keratinocytes were studied by measuring the intracellular free Ca2+ concentration ([Ca2+]i) using fluorescence ratio imaging (fura-2-AM). Upon UV irradiation the [Ca2+]i increased sharply after a certain lag time, and the UV sensitivity was higher at lower temperatures. Statistically the distribution of [Ca2+]i became broader as the mean values became larger, and the number of affected cells increased sharply above a certain fluence (light intensity x time [photons/cm2]) at all wavelengths studied (200-400 nm). The action spectrum showed a single peak at about 230 nm and decreased gradually toward longer-wavelength UV regions.
  Cell Structure and Function 09/1990; 15(4):175-9. · 2.29 Impact Factor
• Article: Translocation of protein kinase C from cytosol to membrane fractions in human epidermal keratinocytes by recombinant human interferon-gamma.

  H Koizumi, H Tanaka, T Fukaya, C Yasui, A Ohkawara
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  ABSTRACT: The activation of protein kinase C involves its translocation from a cytosol fraction to a membrane fraction. Effects of interferon-gamma (IFN-gamma) on the epidermal protein kinase C were investigated. The treatment of recombinant human IFN-gamma on intact human epidermis resulted in the translocation of protein kinase C from a cytosol to a membrane fraction. The human IFN-gamma had no translocation effect on pig epidermal protein kinase C. Tumor promoter, 12-o-tetradecanoylphorbol-13-acetate (TPA), and a membrane-permeable diacylglycerol analogue, 1-oleoyl-2-acetylglycerol (OAG), both of which are well-known activators of protein kinase C, translocated the epidermal protein kinase C. The IFN-gamma had no direct effect on the epidermal protein kinase C; the addition of the IFN-gamma to partially-purified pig epidermal protein kinase C had no effect on its activity. The effect of the IFN-gamma on human epidermal protein kinase C appears to be through the species specific IFN-gamma receptors. It has been reported that the epidermal beta-adrenergic adenylate cyclase response is decreased following the TPA- (and OAG-) induced activation of protein kinase C. Human recombinant IFN-gamma, however, had no effect on the beta-adrenergic response of the human epidermis. Our results indicate that IFN-gamma affects intact keratinocytes in vitro, resulting in the activation of protein kinase C, which might be related to the physiological effect of IFN-gamma on keratinocyte.
  Journal of Dermatological Science 08/1990; 1(4):297-302. · 3.72 Impact Factor
• Article: Stimulation of prostaglandin E adenylate cyclase response in pig epidermis by hydrocortisone.

  H Koizumi, C Yasui, T Shimizu, A Ohkawara
  Archives for Dermatological Research 02/1989; 281(3):215-7. · 2.28 Impact Factor