The Suppression of Non-specific Esterase Activity in Mouse Skin Sebaceous Gland by “CS” Gas

Nature ◽  
1972 ◽  
Vol 240 (5383) ◽  
pp. 560-561 ◽  
Author(s):  
D. H. BARRY ◽  
L. F. CHASSEAUD ◽  
B. HUNTER ◽  
W. E. ROBINSON
Keyword(s):  
Esterase Activity ◽  
Sebaceous Gland ◽  
Mouse Skin

scholarly journals Stem cell dynamics in sebaceous gland morphogenesis in mouse skin

2012 ◽  
Vol 363 (1) ◽  
pp. 138-146 ◽  
Author(s):  
Daniela Frances ◽  
Catherin Niemann
Keyword(s):  
Stem Cell ◽  
Sebaceous Gland ◽  
Mouse Skin ◽  
Cell Dynamics ◽  
Gland Morphogenesis

EFFECTS OF STEROID HORMONES ON DEVELOPING MOUSE SKIN IN VITRO

1975 ◽  
Vol 66 (2) ◽  
pp. 195-205 ◽  
Author(s):  
AMREEK SINGH ◽  
MARGARET H. HARDY
Keyword(s):  
Cell Differentiation ◽  
Organ Culture ◽  
Sebaceous Gland ◽  
Mouse Skin ◽  
Hair Follicles ◽  
Stratum Granulosum ◽  
Normal Medium ◽  
Hormonal Steroids ◽  
Good Differentiation

SUMMARY Pieces of skin from 13·5- to 15-day-old foetal mice were grown in organ culture in a biological medium with or without the addition of hormonal steroids. Cortisol (7·5 μg/ml) caused thinning of the non-cornified epidermis and flattening of the stratum granulosum after 3 days. By 6 days the epidermis was thinner and hair follicles were regressing, and these changes continued up to 12 days. Administration of corticosterone (5 μg/ml) also produced thinning of the epidermis and regression of the follicles after 6 days. Good differentiation of epidermis and hair follicles was obtained when testosterone (100 μg/ml) was added to the medium. The non-cornified epidermal layers were similar to those of control cultures at 3 days but less than half as thick at 6 days. Hair follicles differentiated as rapidly in medium containing testosterone as in normal medium, but, unlike in the latter medium, also developed sebaceous gland anlagen at 6 days. Some explants in testosterone medium showed signs of sebaceous cell differentiation at 9 days.

Suppression of sebaceous gland non-specific esterase activity by electrophilicαβ-unsaturated compounds

1975 ◽  
Vol 31 (10) ◽  
pp. 1196-1197 ◽  
Author(s):  
L. F. Chasseaud ◽  
B. Hunter ◽  
W. E. Robinson ◽  
D. H. Barry
Keyword(s):  
Esterase Activity ◽  
Sebaceous Gland ◽  
Unsaturated Compounds

scholarly journals Epigenomic profiling of stem cells within the pilosebaceous unit identifies PRDM16 as a regulator of sebaceous gland homeostasis

2021 ◽  
Author(s):  
Rizwan Rehimi ◽  
Giuliano Crispatzu ◽  
Carlos Andrés Chacón-Martínez ◽  
Tore Bleckwehl ◽  
Giada Mantellato ◽  
...  
Keyword(s):  
Stem Cells ◽  
Sebaceous Gland ◽  
Mouse Skin ◽  
Rna Seq ◽  
Pilosebaceous Unit ◽  
Junctional Zone ◽  
Knock Out ◽  
Interfollicular Epidermis ◽  
Sebum Production ◽  
Knock Out Mouse

AbstractThe epidermis consists of different compartments such as the hair follicle (HF), sebaceous gland (SG) and interfollicular epidermis (IFE), each containing distinct stem cell (SC) populations. However, with the exception of the SCs residing within the HF bulge, other epidermal SC populations remain less well understood. Here we used an epigenomic strategy that combines H3K27me3 ChIP-seq and RNA-seq profiling to identify major regulators of pilosebaceous unit (PSU) SC located outside the bulge. When applied to the bulk of PSU SC isolated from mouse skin our approach identified both previously known and potentially novel non-bulge PSU SC regulators. Among the latter, we found that PRDM16 was predominantly enriched within the Junctional Zone (JZ), which harbors SC that contribute to renewal of the upper HF and the SG. To investigate PRDM16 function in the PSU SC, we generated an epidermal-specific Prdm16 Knock-out mouse model (K14-Cre-Prdm16fl/fl). Notably, SG homeostasis was disturbed upon loss of PRDM16 resulting in enlarged SGs, and excessive sebum production, resembling some of the features associated with human acne and sebaceous hyperplasia. Importantly, PRDM16 is essential to shut down proliferation in differentiating sebocytes. Overall, our study provides a list of putative novel regulators of PSU SC outside the bulge and identifies PRDM16 as a major regulator of SG homeostasis.

The bulge is the source of cellular renewal in the sebaceous gland of mouse skin

2000 ◽  
Vol 292 (11) ◽  
pp. 573-576 ◽  
Author(s):  
Andrei A. Panteleyev ◽  
Thomas Rosenbach ◽  
Ralf Paus ◽  
A. M. Christiano
Keyword(s):  
Sebaceous Gland ◽  
Mouse Skin

scholarly journals Epidermal PPARγ Is a Key Homeostatic Regulator of Cutaneous Inflammation and Barrier Function in Mouse Skin

2021 ◽  
Vol 22 (16) ◽  
pp. 8634
Author(s):  
Raymond L. Konger ◽  
Ethel Derr-Yellin ◽  
Teresa A. Zimmers ◽  
Terrence Katona ◽  
Xiaoling Xuei ◽  
...  
Keyword(s):  
Barrier Function ◽  
Sebaceous Gland ◽  
Differential Expression Analysis ◽  
Mouse Skin ◽  
Skin Lesions ◽  
Transepidermal Water Loss ◽  
Epidermal Differentiation ◽  
Inflammasome Activation ◽  
Loss Of Function ◽  
Cutaneous Inflammation

Both agonist studies and loss-of-function models indicate that PPARγ plays an important role in cutaneous biology. Since PPARγ has a high level of basal activity, we hypothesized that epidermal PPARγ would regulate normal homeostatic processes within the epidermis. In this current study, we performed mRNA sequencing and differential expression analysis of epidermal scrapings from knockout mice and wildtype littermates. Pparg-/-epi mice exhibited a 1.5-fold or greater change in the expression of 11.8% of 14,482 identified transcripts. Up-regulated transcripts included those for a large number of cytokines/chemokines and their receptors, as well as genes associated with inflammasome activation and keratinization. Several of the most dramatically up-regulated pro-inflammatory genes in Pparg-/-epi mouse skin included Igfl3, 2610528A11Rik, and Il1f6. RT-PCR was performed from RNA obtained from non-lesional full-thickness skin and verified a marked increase in these transcripts, as well as transcripts for Igflr1, which encodes the receptor for Igfl3, and the 2610528A11Rik receptor (Gpr15). Transcripts for Il4 were detected in Pparg-/-epi mouse skin, but transcripts for Il17 and Il22 were not detected. Down-regulated transcripts included sebaceous gland markers and a number of genes associated with lipid barrier formation. The change in these transcripts correlates with an asebia phenotype, increased transepidermal water loss, alopecia, dandruff, and the appearance of spontaneous inflammatory skin lesions. Histologically, non-lesional skin showed hyperkeratosis, while inflammatory lesions were characterized by dermal inflammation and epidermal acanthosis, spongiosis, and parakeratosis. In conclusion, loss of epidermal Pparg alters a substantial set of genes that are associated with cutaneous inflammation, keratinization, and sebaceous gland function. The data indicate that epidermal PPARγ plays an important role in homeostatic epidermal function, particularly epidermal differentiation, barrier function, sebaceous gland development and function, and inflammatory signaling.

scholarly journals Group III secreted phospholipase A2 transgenic mice spontaneously develop inflammation

2009 ◽  
Vol 421 (1) ◽  
pp. 17-27 ◽  
Author(s):  
Hiroyasu Sato ◽  
Yoshitaka Taketomi ◽  
Yuki Isogai ◽  
Seiko Masuda ◽  
Tetsuyuki Kobayashi ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Prostaglandin E2 ◽  
Phospholipase A2 ◽  
Inflammatory Cytokines ◽  
Sebaceous Gland ◽  
Mouse Skin ◽  
Skin Inflammation ◽  
Group Iii ◽  
Extramedullary Haemopoiesis ◽  
Pro Inflammatory Cytokines

PLA2 (phospholipase A2) group III is an atypical sPLA2 (secretory PLA2) that is homologous with bee venom PLA2 rather than with other mammalian sPLA2s. In the present paper, we show that endogenous group III sPLA2 (PLA2G3) is expressed in mouse skin and that Tg (transgenic) mice overexpressing human PLA2G3 spontaneously develop skin inflammation. Pla2g3-Tg mice over 9 months of age frequently developed dermatitis with hyperkeratosis, acanthosis, parakeratosis, erosion, ulcer and sebaceous gland hyperplasia. The dermatitis was accompanied by infiltration of neutrophils and macrophages and by elevated levels of pro-inflammatory cytokines, chemokines and prostaglandin E2. In addition, Pla2g3-Tg mice had increased lymph aggregates and mucus in the airway, lymphocytic sialadenitis, hepatic extramedullary haemopoiesis, splenomegaly with increased populations of granulocytes and monocytes/macrophages, and increased serum IgG1. Collectively, these observations provide the first demonstration of spontaneous development of inflammation in mice with Tg overexpression of mammalian sPLA2.

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