Disease relevance of Sebaceous Glands

• Overexpression of wild type rat erbB2 in the basal layer of epidermis led to alopecia, follicular hyperplasia and sebaceous gland enlargement as well as hyperplasia of the interfollicular epidermis [1].
• The urocortin antigen could be immunolocalized to normal keratinocytes of the epidermis and hair follicle, epithelium of sweat and sebaceous glands, dermal skeletal muscle, and nevocytes; it was also detected in melanoma and basal cell carcinoma cells [2].
• Glutathione, glutathione S-transferase and reactive oxygen species of human scalp sebaceous glands in male pattern baldness [3].
• Aminolevulinic acid plus red light causes phototoxicity to sebaceous follicles, prolonged suppression of sebaceous gland function, and apparent decrease in follicular bacteria after photodynamic therapy [4].
• In examination of mice with 7 other mutations affecting the integument, TCDD produced similar histologic skin changes in cryptothrix, nude, plucked, and atrichosis; a marginal squamous metaplasia of sebaceous glands in Repeated epilation, and had no effect in fur deficient and Naked mutants [5].

Psychiatry related information on Sebaceous Glands

• Regardless of SNJ's occurrence as either an isolated lesion or as the fully developed syndrome, including mental retardation and epilepsy, this congenital malformation of the skin, its hair, and sebaceous glands presents rare and histologically intriguing problems for the practitioner [6].

High impact information on Sebaceous Glands

• Scd1 is expressed in sebaceous glands and is disrupted in the asebia mouse [7].
• High levels of MC5-R was found in multiple exocrine tissues, including Harderian, preputial, lacrimal, and sebaceous glands, and was also shown to be required for production and stress-regulated synthesis of porphyrins by the Harderian gland and ACTH/MSH-regulated protein secretion by the lacrimal gland [8].
• The mechanism of action of 13-cis-retinoic acid in the therapy of acne probably involves a direct inhibitory effect of the drug on the sebaceous gland [9].
• Remarkably, however, KGF stimulated proliferation and differentiation of early progenitor cells within hair follicles and sebaceous glands in the wound bed and adjacent dermis [10].
• The shorter mean transit times of plasma cholesterol on skin areas rich in sebaceous glands (22-24 days on the head) than on those poor in these glands (38 days on forearms and 72 days on feet) suggest that cholesterol passes faster through the sebaceous glands than through the epidermis, and faster through thin than thick epidermis [11].

Chemical compound and disease context of Sebaceous Glands

• Investigation revealed smaller sebaceous glands, a reduced sebum excretion rate, decreased number of Corynebacterium acnes in the pilosebaceous ducts and a reduced conversion of testosterone to 5 alphadihydrotestosterone in the areas which were free of acne compared with acne-bearing skin [12].
• Inhibition of dihydrotestosterone-mediated hamster sebaceous gland hypertrophy by progesterone [13].
• Treatment of female OVX rats with DHEA resulted in a similar mild to moderate hyperplasia of the sebaceous glands of both dorsal (site of application) and ventral skin, as illustrated by an increase in the number and size of the acini [14].
• Keratoacanthomas have been associated with multiple carcinomas, discoid lupus erythematosus, and multiple sebaceous gland tumors with colonic and gastric carcinoma [15].
• Topical daily application of citral (15.4%) solution for 3 months produced an increase in the number of sebaceous gland lobules and hyperplasia of sebaceous cells in each gland [16].

Biological context of Sebaceous Glands

• However, this provides the first demonstration that 13-cis retinoic acid acts on human sebaceous glands directly, reducing the rate of cell division and the rate of lipogenesis, which shows that the maintained human sebaceous gland might provide a useful model for studying the effect of 13-cis retinoic acid on human sebocytes [17].
• Another effect of bacterial action on sebaceous gland lipids was the esterification of sebaceous cholesterol to cholesteryl esters [18].
• The sebaceous gland activity, which was expressed by the ratio of wax esters/[cholesterol + cholesterol esters] (WE/[C + CE]), showed a distinct change from infancy through maturity to senescence; the curve of the ratio made a peak in our subjects's 20s [19].
• Lipid metabolism in sebaceous glands and preputial glands of rodents is regulated by alpha-melanocyte stimulating hormone, the major agonist for melanocortin receptors [20].
• Transgene constructs containing the enhancer expressed high levels of apolipoprotein E mRNA in the germinative cell layer of the sebaceous gland and in epithelial cells of the hair follicle root sheath [21].

Anatomical context of Sebaceous Glands

• Results of the immunohistochemical staining showed that nestin, GFP, keratin 5/8, and keratin 15 colocalize in the hair follicle bulge cells, outer-root sheath cells, and basal cells of the sebaceous glands [22].
• Among normal tissues, PML was characteristically up-regulated in activated epithelioid histiocytes and fibroblasts in a variety of pathological conditions, columnar epithelium in small active thyroid follicles, well differentiated foamy cells in the center of sebaceous glands, and hypersecretory endometria (Arias-Stella) [23].
• The ACAT-1-/- mice had decreased openings of the eyes because of atrophy of the meibomian glands, a modified form of sebaceous glands normally expressing high ACAT activities [24].
• The sebaceous glands secrete continuously, producing sebum that consists predominantly of triglycerides, wax esters, and squalene [25].
• Its activity could be related to the regulation of lipid and cholesterol synthesis in keratinocytes and sebaceous glands and to the secretion of sweat in sweat glands [26].

Associations of Sebaceous Glands with chemical compounds

• Values of f were lower on skin areas rich in sebaceous glands (0.29-0.46 on forehead) than on areas poor in these glands (0.41-0.70 for forearms; 0.60 on feet) and lower for esterified (0.27-0.33) than for free (0.39-0.48) cholesterol [11].
• In the androgen-treated group, sebaceous gland volume (micron 3 X 10(-3) increased from 896 +/- 194 to 3,233 +/- 754 (P less than 0.001), sebaceous cell area (micron 2) increased from 167 +/- 12 to 243 +/- 19 (P less than 0.001), and labeling index (percentage) increased from 2.7 +/- 0.7 to 6.4 +/- 0.9 (P less than 0.01) [27].
• A close correlation was found between the carcinogenicities and destructive activities of nitrofuran derivatives on the sebaceous glands [28].
• Specific carcinogenic effect of N-methyl-N-nitrosourea on the midventral sebaceous gland of the gerbil (Meriones unguiculatus) [29].
• Under similar conditions, the potent carcinogen 7,12-dimethylbenz(alpha)athracene almost completely destroyed the sebaceous glands at a dose of 0.05 mg/mouse, but dimethyl sulfoxide (used as solvent for the test compounds) had no effect [28].

Gene context of Sebaceous Glands

• We conclude that ERV3 env is most strongly expressed in adrenal and sebaceous glands as well as in placenta [30].
• Sebaceous glands were stained for BGP only [31].
• Glycoproteins of the carcinoembryonic antigen (CEA) family are expressed in sweat and sebaceous glands of human fetal and adult skin [31].
• Within human skin, Delta-6 desaturase/FADS2 mRNA and protein expression is restricted to differentiating sebocytes located in the suprabasal layers of the sebaceous gland [32].
• In rc mice, the loxl mRNA was reduced in the skin and the LOXL protein in the heart, dermis, atrophic hair follicles, and sebaceous glands [33].

Analytical, diagnostic and therapeutic context of Sebaceous Glands

• In situ hybridization revealed a 5-LO mRNA-containing epidermal cell (EC) population that was predominantly located in the midportion of the spinous layer, in outer hair root sheaths, and in the epithelial compartment of sebaceous glands [34].
• Thymidine autoradiography demonstrates that transecting follicles beneath the sebaceous gland leads to an increase in DNA synthesis of the cells in the external root sheath, but does not alter DNA synthesis of the cells in the follicle matrix [35].
• The present data show that the topical administration of finasteride, in analogy with flutamide, causes local inhibition of sebaceous gland growth in both the costovertebral organs and ears [36].
• At a light schedule of 8 h the testes shrink, plasma testosterone levels and sebaceous gland areas show a significant reduction ("photoperiodic castration") [37].
• Presence of the melanocortin 5 receptor protein in human sebaceous glands and rat preputial glands was further verified by Western blotting [20].

References