The Experts below are selected from a list of 16833 Experts worldwide ranked by ideXlab platform
Rainer Voegeli - One of the best experts on this subject based on the ideXlab platform.
-
Stratum corneum proteases and dry skin conditions
Cell and Tissue Research, 2013Co-Authors: Anthony V. Rawlings, Rainer VoegeliAbstract:This paper reviews the role of stratum corneum (SC) proteases and their inhibitors in normal and xerotic skin conditions. The importance of the corneodesmosome for SC integrity is also discussed, and the effect of proteases on its disassembly. The relevance of each enzyme class is outlined, as well as their potential inhibitors. It is becoming much clearer, however, that the LEKTI family of inhibitors are critical for SC enzyme control. Delayed Desquamation is the accumulation of corneocytes on the surface of the SC that leads ultimately to the cosmetic condition commonly termed as “dry skin”. The reductions of serine protease activity are a consistent theme in dry skin, and non-eczematous atopic dermatitis otherwise known as atopic xerosis leading to retention hyperkeratosis. Flaky skin is normally seen on the body whereas a rough skin is observed on the face. Increased protease activity occurs in most, if not all, inflammatory dermatoses, ranging from the genetic disorders, psoriasis and eczematous atopic dermatitis to sub-clinical barrier abnormalities induced by surfactants or by environmental influences as a result of premature Desquamation. In some of these conditions a thinner SC is apparent, e.g., eczematous atopic skin or on photodamaged facial skin. A better understanding of the proteolytic events and of the regulatory mechanisms involved in Desquamation should enable the design of new treatments for skin disorders associated with faulty Desquamation. This new knowledge will be an important basis for new developments in ‘corneotherapy’ and ‘corneocare’.
-
Stratum corneum proteases and dry skin conditions
Cell and Tissue Research, 2013Co-Authors: Anthony V. Rawlings, Rainer VoegeliAbstract:This paper reviews the role of stratum corneum (SC) proteases and their inhibitors in normal and xerotic skin conditions. The importance of the corneodesmosome for SC integrity is also discussed, and the effect of proteases on its disassembly. The relevance of each enzyme class is outlined, as well as their potential inhibitors. It is becoming much clearer, however, that the LEKTI family of inhibitors are critical for SC enzyme control. Delayed Desquamation is the accumulation of corneocytes on the surface of the SC that leads ultimately to the cosmetic condition commonly termed as “dry skin”. The reductions of serine protease activity are a consistent theme in dry skin, and non-eczematous atopic dermatitis otherwise known as atopic xerosis leading to retention hyperkeratosis. Flaky skin is normally seen on the body whereas a rough skin is observed on the face. Increased protease activity occurs in most, if not all, inflammatory dermatoses, ranging from the genetic disorders, psoriasis and eczematous atopic dermatitis to sub-clinical barrier abnormalities induced by surfactants or by environmental influences as a result of premature Desquamation. In some of these conditions a thinner SC is apparent, e.g., eczematous atopic skin or on photodamaged facial skin. A better understanding of the proteolytic events and of the regulatory mechanisms involved in Desquamation should enable the design of new treatments for skin disorders associated with faulty Desquamation. This new knowledge will be an important basis for new developments in ‘corneotherapy’ and ‘corneocare’.
-
Desquamation: It Is Almost All About Proteases
Treatment of Dry Skin Syndrome, 2012Co-Authors: Rainer Voegeli, Anthony V. RawlingsAbstract:This chapter reviews the structure, function, and formation of the stratum corneum, how it is perturbed in a variety of conditions. In particular it discusses the role of proteases such as the kallikreins, plasmin, and urokinase and their inhibitors that play a role in Desquamation of healthy and pathological skin. Faulty Desquamation is the accumulation of corneocytes on the surface of the stratum corneum that leads ultimately to the cosmetic condition commonly termed as “dry skin.” This can be flaky skin as is normally seen on the body or rough skin observed on the face. Changes in the proteolytic balance of the skin can also result in inflammation, which leads to the typical clinical signs of redness, scaling, and itching. Reduced protease activity is known in soap-induced dry skin, but increased serine protease activity occurs in most, if not all, inflammatory dermatoses, ranging from genetic disorders, such as Netherton syndrome, psoriasis, and atopic dermatitis, to subclinical barrier abnormalities induced, e.g., surfactants, or by environmental influences. Serine proteases might represent key markers for underlying and sometimes nonobservable skin abnormalities. The biology of skin moisturization, of which hydration is only one benefit, is highly complex. The future of all new moisturizers lies in the fully understanding of the control and impairment of Desquamation. Better understanding of the multistep proteolytic events and of the regulatory mechanisms involved in Desquamation should enable the design of new treatments for the skin disorders associated with disturbance in the stratum corneum turnover. This will be the ultimate approach to corneocare.
Anthony V. Rawlings - One of the best experts on this subject based on the ideXlab platform.
-
Stratum corneum proteases and dry skin conditions
Cell and Tissue Research, 2013Co-Authors: Anthony V. Rawlings, Rainer VoegeliAbstract:This paper reviews the role of stratum corneum (SC) proteases and their inhibitors in normal and xerotic skin conditions. The importance of the corneodesmosome for SC integrity is also discussed, and the effect of proteases on its disassembly. The relevance of each enzyme class is outlined, as well as their potential inhibitors. It is becoming much clearer, however, that the LEKTI family of inhibitors are critical for SC enzyme control. Delayed Desquamation is the accumulation of corneocytes on the surface of the SC that leads ultimately to the cosmetic condition commonly termed as “dry skin”. The reductions of serine protease activity are a consistent theme in dry skin, and non-eczematous atopic dermatitis otherwise known as atopic xerosis leading to retention hyperkeratosis. Flaky skin is normally seen on the body whereas a rough skin is observed on the face. Increased protease activity occurs in most, if not all, inflammatory dermatoses, ranging from the genetic disorders, psoriasis and eczematous atopic dermatitis to sub-clinical barrier abnormalities induced by surfactants or by environmental influences as a result of premature Desquamation. In some of these conditions a thinner SC is apparent, e.g., eczematous atopic skin or on photodamaged facial skin. A better understanding of the proteolytic events and of the regulatory mechanisms involved in Desquamation should enable the design of new treatments for skin disorders associated with faulty Desquamation. This new knowledge will be an important basis for new developments in ‘corneotherapy’ and ‘corneocare’.
-
Stratum corneum proteases and dry skin conditions
Cell and Tissue Research, 2013Co-Authors: Anthony V. Rawlings, Rainer VoegeliAbstract:This paper reviews the role of stratum corneum (SC) proteases and their inhibitors in normal and xerotic skin conditions. The importance of the corneodesmosome for SC integrity is also discussed, and the effect of proteases on its disassembly. The relevance of each enzyme class is outlined, as well as their potential inhibitors. It is becoming much clearer, however, that the LEKTI family of inhibitors are critical for SC enzyme control. Delayed Desquamation is the accumulation of corneocytes on the surface of the SC that leads ultimately to the cosmetic condition commonly termed as “dry skin”. The reductions of serine protease activity are a consistent theme in dry skin, and non-eczematous atopic dermatitis otherwise known as atopic xerosis leading to retention hyperkeratosis. Flaky skin is normally seen on the body whereas a rough skin is observed on the face. Increased protease activity occurs in most, if not all, inflammatory dermatoses, ranging from the genetic disorders, psoriasis and eczematous atopic dermatitis to sub-clinical barrier abnormalities induced by surfactants or by environmental influences as a result of premature Desquamation. In some of these conditions a thinner SC is apparent, e.g., eczematous atopic skin or on photodamaged facial skin. A better understanding of the proteolytic events and of the regulatory mechanisms involved in Desquamation should enable the design of new treatments for skin disorders associated with faulty Desquamation. This new knowledge will be an important basis for new developments in ‘corneotherapy’ and ‘corneocare’.
-
Desquamation: It Is Almost All About Proteases
Treatment of Dry Skin Syndrome, 2012Co-Authors: Rainer Voegeli, Anthony V. RawlingsAbstract:This chapter reviews the structure, function, and formation of the stratum corneum, how it is perturbed in a variety of conditions. In particular it discusses the role of proteases such as the kallikreins, plasmin, and urokinase and their inhibitors that play a role in Desquamation of healthy and pathological skin. Faulty Desquamation is the accumulation of corneocytes on the surface of the stratum corneum that leads ultimately to the cosmetic condition commonly termed as “dry skin.” This can be flaky skin as is normally seen on the body or rough skin observed on the face. Changes in the proteolytic balance of the skin can also result in inflammation, which leads to the typical clinical signs of redness, scaling, and itching. Reduced protease activity is known in soap-induced dry skin, but increased serine protease activity occurs in most, if not all, inflammatory dermatoses, ranging from genetic disorders, such as Netherton syndrome, psoriasis, and atopic dermatitis, to subclinical barrier abnormalities induced, e.g., surfactants, or by environmental influences. Serine proteases might represent key markers for underlying and sometimes nonobservable skin abnormalities. The biology of skin moisturization, of which hydration is only one benefit, is highly complex. The future of all new moisturizers lies in the fully understanding of the control and impairment of Desquamation. Better understanding of the multistep proteolytic events and of the regulatory mechanisms involved in Desquamation should enable the design of new treatments for the skin disorders associated with disturbance in the stratum corneum turnover. This will be the ultimate approach to corneocare.
Eleftherios P Diamandis - One of the best experts on this subject based on the ideXlab platform.
-
a potential role for multiple tissue kallikrein serine proteases in epidermal Desquamation
Journal of Biological Chemistry, 2006Co-Authors: Carla Borgoňo, Nahoko Komatsu, Ravi M Kapadia, Gary L Clayman, Iacovos P Michael, Georgia Sotiropoulou, Arumugam Jayakumar, Eleftherios P DiamandisAbstract:Abstract Desquamation of the stratum corneum is a serine protease-dependent process. Two members of the human tissue kallikrein (KLK) family of (chymo)tryptic-like serine proteases, KLK5 and KLK7, are implicated in Desquamation by digestion of (corneo)desmosomes and inhibition by Desquamation-related serine protease inhibitors (SPIs). However, the epidermal localization and specificity of additional KLKs also supports a role for these enzymes in Desquamation. This study aims to delineate the probable contribution of KLK1, KLK5, KLK6, KLK13, and KLK14 to Desquamation by examining their interactions, in vitro, with: 1) colocalized SPI, lympho-epithelial Kazal-type-related inhibitor (LEKTI, four recombinant fragments containing inhibitory domains 1–6 (rLEKTI(1–6)), domains 6–8 and partial domain 9 (rLEKTI(6–9′)), domains 9–12 (rLEKTI(9–12)), and domains 12–15 (rLEKTI(12–15)), secretory leukocyte protease inhibitor, and elafin and 2) their ability to digest the (corneo)desmosomal cadherin, desmoglein 1. KLK1 was not inhibited by any SPI tested. KLK5, KLK6, KLK13, and KLK14 were potently inhibited by rLEKTI(1–6), rLEKTI(6–9′), and rLEKTI(9–12) with Ki values in the range of 2.3–28.4 nm, 6.1–221 nm, and 2.7–416 nm for each respective fragment. Only KLK5 was inhibited by rLEKTI(12–15) (Ki = 21.8 nm). No KLK was inhibited by secretory leukocyte protease inhibitor or elafin. Apart from KLK13, all KLKs digested the ectodomain of desmoglein 1 within cadherin repeats, Ca2+ binding sites, or in the juxtamembrane region. Our study indicates that multiple KLKs may participate in Desquamation through cleavage of desmoglein 1 and regulation by LEKTI. These findings may have clinical implications for the treatment of skin disorders in which KLK activity is elevated.
K Jezernik - One of the best experts on this subject based on the ideXlab platform.
-
Succession of events in Desquamation of superficial urothelial cells as a response to stress induced by prolonged constant illumination.
Tissue and Cell, 2001Co-Authors: P. Veranič, K JezernikAbstract:Abstract The effect of moderate stress induced by prolonged illumination was analysed on urothelial cells of female mouse urinary bladders at ultrastructural and cytochemical levels. This study demonstrates that the urothelium responds to moderate stress with Desquamation which involves two subsequent steps. The first step includes a local detachment of tight junctions and consequently the loss of the permeability barrier leading to expanded intercellular spaces among urothelial cells. During the second step, the disjunction of desmosomes accompanied by exocytosis of lysosomal enzymes (NADPase) in the intercellular space results in exfoliation of superficial cells. It is evident thatmoderate stress elicits an enhanced Desquamation of only superficial cells by a subsequent dysfunction of first tight junctions and after that adherens-type junctions. A rapid restoration of the newtight junctions prevents a long-term malfunction of the blood–urine barrier.
-
Desquamation of urinary bladder epithelial cells.
Pflugers Archiv : European journal of physiology, 1996Co-Authors: K JezernikAbstract:Desquamation of urothelial cells is brought about by various specific inductions. Moderate stress in mouse female adults induced by constant illumination for 96 hours results in Desquamation of superficial and intermediate cells. Application of endotoxin LPS involves Desquamation of single cells as well as whole sheets of cells from the underlying lamina propria. Cell detachment involves interruption of tight junctions between neighbouring cells, reorganisation of intermediate filaments and concentration of different vacuoles or multivesicular bodies. These results clearly demonstrate the involvement of specific adhesion mechanisms during detachment and Desquamation of uroepithelial cells.
-
A COMPARATIVE STUDY OF THE Desquamation OF UROTHELIAL CELLS DURING GESTATION AND IN ADULTS MICE FOLLOWING MODERATE STRESS OR ENDOTOXIN TREATMENT
Cell Biology International, 1995Co-Authors: K Jezernik, O. Medalia, M. AronsonAbstract:Abstract The present paper deals with the comparative EM study of the detachment of mouse urinary bladder epithelial cells under various physiological conditions, namely, during gestation and in adult mice following induction by endotoxin or by exposure to moderate stress. It has been shown that Desquamation during gestation involves two distinct modes, shedding of single cells and formation of apoptotic bodies. Moderate stress in adult female mice induced by constant illumination for 72 or 96 hours, results in Desquamation of superficial and intermediate cells. Application of LPS is followed by Desquamation of single cells and whole sheets of cells. Cell detachment involves interruption of tight junctions between neighbouring cells and formation of numerous cup shaped vesicles, multivesicular bodies and vacuoles at the base of desquamating cells. LPS induces Desquamation entails delivery of lysosomal enzymes extracellulary into the intercellular space. In the areas of sloughing the bladder epithelium lack permeability barrier. Desquamated cells in the bladder lumen are mostly alive. These results clearly demonstrate the existence of specific adhesion mechanisms of detachment and Desquamation of uroepithelial cells.
Carla Borgoňo - One of the best experts on this subject based on the ideXlab platform.
-
a potential role for multiple tissue kallikrein serine proteases in epidermal Desquamation
Journal of Biological Chemistry, 2006Co-Authors: Carla Borgoňo, Nahoko Komatsu, Ravi M Kapadia, Gary L Clayman, Iacovos P Michael, Georgia Sotiropoulou, Arumugam Jayakumar, Eleftherios P DiamandisAbstract:Abstract Desquamation of the stratum corneum is a serine protease-dependent process. Two members of the human tissue kallikrein (KLK) family of (chymo)tryptic-like serine proteases, KLK5 and KLK7, are implicated in Desquamation by digestion of (corneo)desmosomes and inhibition by Desquamation-related serine protease inhibitors (SPIs). However, the epidermal localization and specificity of additional KLKs also supports a role for these enzymes in Desquamation. This study aims to delineate the probable contribution of KLK1, KLK5, KLK6, KLK13, and KLK14 to Desquamation by examining their interactions, in vitro, with: 1) colocalized SPI, lympho-epithelial Kazal-type-related inhibitor (LEKTI, four recombinant fragments containing inhibitory domains 1–6 (rLEKTI(1–6)), domains 6–8 and partial domain 9 (rLEKTI(6–9′)), domains 9–12 (rLEKTI(9–12)), and domains 12–15 (rLEKTI(12–15)), secretory leukocyte protease inhibitor, and elafin and 2) their ability to digest the (corneo)desmosomal cadherin, desmoglein 1. KLK1 was not inhibited by any SPI tested. KLK5, KLK6, KLK13, and KLK14 were potently inhibited by rLEKTI(1–6), rLEKTI(6–9′), and rLEKTI(9–12) with Ki values in the range of 2.3–28.4 nm, 6.1–221 nm, and 2.7–416 nm for each respective fragment. Only KLK5 was inhibited by rLEKTI(12–15) (Ki = 21.8 nm). No KLK was inhibited by secretory leukocyte protease inhibitor or elafin. Apart from KLK13, all KLKs digested the ectodomain of desmoglein 1 within cadherin repeats, Ca2+ binding sites, or in the juxtamembrane region. Our study indicates that multiple KLKs may participate in Desquamation through cleavage of desmoglein 1 and regulation by LEKTI. These findings may have clinical implications for the treatment of skin disorders in which KLK activity is elevated.