Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0220723 (PCA)
 4,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

[3H]Glutamic acid (PCA) was followed with time after a single subcutaneous injection. PCA specific activity increased slowly, reaching a peak at 3 to 4 days after injection of the labeled amino acid, after which it slowly decline. Incorporation of [3H]glutamic acid into epidermal PCA was markedly inhibited by a single topical application of cycloheximide. Topical application of cycloheximide 2 hr prior to [3H]glutamate injection caused a significantly greater reduction in PCA specific activity (determined 3 days after injection) than cycloheximide treatment 3 hr after administration of the labeled amino acid. Ninety-seven percent of the PCA content of hairless mouse epidermis was shown to reside in the stratum corneum. These observations indicate the involvement of protein synthesis in the formation of PCA from glutamic acid rather than a direct conversion of the amino acid. The high level of PCA in mammalian epidermis appears to be caused by its accumulation in the stratum corneum accompainied by a relatively slow rate of PCA turnover in comparison to other tissues.
J Invest Dermatol 1977 May
PMID:Biosynthesis of pyrrolidone carboxylic acid in hairless mouse epidermis. 87 May 63

Recent literature has suggested that pyroglutamate (PCA) formation in stratum corneum occurs by spontaneous cyclization of glutamine residues derived from filaggrin breakdown. This paper describes an enzymatic alternative. Epidermal homogenates from hairless mice were found to catalyze the formation of PCA from both glutamine and glutamic acid at pH 6.2. Enzyme activity responsible for the first step in this reaction, gamma-glutamyl peptide formation, was partially purified using ammonium sulfate precipitation followed by ion exchange, gel filtration, and hydroxylapatite chromatography. Enzyme preparations free of gamma-glutamyl cyclotransferase activity (which forms PCA from certain gamma-glutamyl peptides) catalyzed formation of gamma-glutamyl-glutamine from glutamine and gamma-glutamyl-glutamate from glutamic acid. Enzyme preparations catalyzed hydrolysis of a variety of gamma-glutamyl peptides but did not split non-gamma-glutamyl peptides or the transpeptidase substrate gamma-glutamyl-rho-nitroanilide. Ammonium sulfate fractions containing both gamma-glutamyl peptidase and gamma-glutamyl cyclotransferase activity catalyzed linear formation of PCA from glutamic acid for periods of up to 19 h. Using gamma-glutamyl-leucine as a substrate, gamma-glutamyl peptidase activity was found to be much higher in crude extracts from epidermis than in preparations from liver, kidney, spleen, intestine, lung, brain, or heart. This activity has not, to our knowledge, been previously described in mammalian tissues.
J Invest Dermatol 1988 Apr
PMID:Gamma glutamyl peptidase: a novel enzyme from hairless mouse epidermis. 289 53

Skin biopsies from 6 patients with Jessner's lymphocytic infiltration (JLI) were studied using monoclonal antibodies in peroxidase staining, on some occasions combined with [3H]thymidine incorporation visualized by autoradiography. Ninety-one +/- two percent of all inflammatory mononuclear cells in situ were T11-positive T lymphocytes, whereas B lymphocytes were few. Forty-nine +/- nine percent of cells were Ia-positive, suggesting involvement of T cells in the local pathogenetic mechanisms, but interleukin-2 receptor-carrying cells as well as [3H]thymidine-incorporating cells accounted for less than 2% of all inflammatory cells, suggesting that T blasts account for only a small minority. Similarly, PCA-1 plasma cells were few in situ, there was no immunoglobulin or complement deposition at the dermal-epidermal junction and serum antinuclear and anti-DNA antibodies as well as complement levels were normal, and no visceral involvement was revealed during the survey period. According to our findings, JLI of the skin seems to be sufficiently distinctive to be appreciated as an entity. T lymphocytes in JLI do not seem to proliferate in the site of inflammation but are merely accumulated from the circulation.
J Invest Dermatol 1987 Aug
PMID:A long-term clinicopathologic survey of patients with Jessner's lymphocytic infiltration of the skin. 311 Mar 1

The human pilosebaceous duct was isolated and maintained for 7 days in defined medium, and defined medium supplemented with 1 microM 13-cis retinoic acid. Freshly isolated ducts retained their in vivo morphology, showing a stratified squamous keratinizing epithelium. On maintenance there was a loss of basic duct architecture, and a significant reduction in the rate of [methyl-3H] thymidine uptake. The addition of 1 microM 13-cis retinoic acid resulted in an improved duct architecture and caused a further significant reduction in the rate of [methyl-3H] thymidine uptake. [Methyl-3H] thymidine autoradiography showed that freshly isolated ducts maintained their in situ pattern of cell division. It was difficult to discern the region of cell division in ducts maintained for 7 days, but the degree of graining reflected the measured rates of [methyl-3H] thymidine uptake into PCA precipitable material. The pattern of keratin synthesis of the freshly isolated duct was similar to patterns previously described for the duct in situ. This study reports the successful isolation and maintenance of the human pilosebaceous duct, and demonstrates that 13-cis retinoic acid acts directly at the level of the duct.
Br J Dermatol 1993 Mar
PMID:Isolation and maintenance of the human pilosebaceous duct: 13-cis retinoic acid acts directly on the duct in vitro. 768 33

The pathobiology of primary cicatricial ("scarring") alopecia (PCA) remains poorly understood and underinvestigated. In this issue, Karnik et al. identify a previously unsuspected player, peroxisome proliferator-activated receptor-gamma (PPARgamma), in the pathogenesis of the most frequent form of PCA, lichen planopilaris (LPP). The authors show that PPARgamma is required for maintenance of a functional epithelial stem cell compartment in murine hair follicles, that the targeted deletion of PPARgamma in the bulge/isthmus area of the hair follicle epithelium generates a skin pathology that resembles LPP, and that LPP patients show gene expression changes that indicate a defect in lipid metabolism and peroxisome biogenesis. This study invites the revisitation of many open questions in PCA pathobiology and the exploration of new avenues for future PCA management.
J Invest Dermatol 2009 May
PMID:Scarring alopecia and the PPAR-gamma connection. 1905 58

Autoimmune diseases are rare, but their incidence has increased over the past decades. Interestingly, the co-occurrence of autoimmune diseases is well documented; however, data on the presence of more than one specific autoantibody in healthy individuals are not available. Here, we investigated the prevalence of several autoantibodies in a cohort of over 6000 healthy persons. While individual autoantibodies were rarely detected (i.e. ranging from 0.3% for ANCA to 4.6% for anti-TPO), the cumulative prevalence of the tested autoantibodies was as high as 10%. Furthermore, our results demonstrate co-occurrence of ANA with specific autoantibodies that target TPO, CCP and Dsg1/3, while ANCA and autoantibodies to PCA and BP180/BP230 were not more frequent in ANA-positive compared to ANA-negative samples. This indicates that shared and independent mechanisms influence loss of tolerance to distinct sets of self-antigens.
Exp Dermatol 2014 Jul
PMID:Co-occurrence of autoantibodies in healthy blood donors. 2481 28

Seborrheic dermatitis (SD) is a chronic, recurrent, inflammatory skin disorder occurring in areas rich in sebaceous glands. It manifests clinically as erythematous macules or plaques with varying levels of scaling and associated pruritus. Although the pathogenesis of SD has yet to be fully understood, Malassezia yeasts, hormones, sebum levels, and immune response are known to play important roles. Additional factors including drugs, winter temperatures, and stress may exacerbate SD. Current available treatments include antifungal agents, topical low-potency steroids, and calcineurin inhibitors. We aimed to evaluate the effectiveness of a topical non-steroidal cream in treating facial seborrheic dermatitis (FSD). We performed a case series of 11 patients with mild or moderate FSD and a history of several previous treatments without improvement. The patients were treated for 8 weeks with a topical non-steroidal facial cream (NSFC) containing zinc PCA, piroctone olamine, hydroxyphenyl propamidobenzoic acid, biosaccharide gum-2, and stearyl glycyrrhetinate. Signs and symptoms and tolerance were assessed before, during, and at the end of treatment. All of the patients had improved symptoms of FSD (desquamation, pruritus, erythema, and stinging sensation); 81.8% showed an excellent response and 18.1% showed a good response. None of the patients had adverse effects. J Drugs Dermatol. 2020;19(6): doi:10.36849/JDD.2020.5121.
J Drugs Dermatol 2020 Jun 01
PMID:Non-Steroidal Topical Therapy for Facial Seborrheic Dermatitis. 3257 15