Detection of programmed cell death in anagen hair follicles of guinea pig skin by labeling of nick ends of fragmented DNA

1997 ◽  
Vol 289 (10) ◽  
pp. 603-605 ◽  
Author(s):  
S. Kishimoto ◽  
Makoto Nagata ◽  
Hideya Takenaka ◽  
R. Shibagaki ◽  
Hirokazu Yasuno

1964 ◽  
Vol 12 (7) ◽  
pp. 538-544 ◽  
Author(s):  
MAX WACHSTEIN ◽  
ELIZABETH MEISEL

By using an improved benzidine technique, peroxidase activity can be demonstrated in various locations in mammalian tissues. A relatively formalin resistant enzyme is found in hemoglobin and is also associated with mitochondria of striated muscle and heart. A somewhat less formalin resistant peroxidase occurs in the granules of myeloid and mast cells. A relatively formalin sensitive peroxidase is present in a number of additional locations, e.g. the acinar cells in thyroid and salivary gland, the medulla of the kidney, in hair follicles of the guinea pig skin and Kupffer cells of the liver.



Author(s):  
Honoree Fleming

Pyknosis, karyorrhexis and karyolysis, harbingers of programmed cell death in many systems, appear to be driving forces that transform Ishikawa monolayer epithelial cells into differentiated dome cells. The heterochromatin affected by these process is contained in multiple nuclei aggregated in the syncytia that form when Ishikawa monolayers are stimulated to differentiate (Fleming, 2016a). The nuclear aggregates are enveloped in a double membrane staining for the endogenous biotin in mitochondrial carboxylases. The structure called a mitonucleon becomes vacuolated, along with the heterochromatin it envelops, and this structure elevates with the apical membrane of the syncytium 6 to 8 hours into the 20 hour differentiation, becoming increasingly pyknotic. This phase of the differentiation comes to an end when the mitonucleon membranes are breached and nuclei emerging from the aggregated state can be seen to fragment explosively. Fragmented DNA associates with an array of microtubules, filling the large central clearing of the predome. Some chromatin remains unfragmented and can be seen of the edges of the predome clearing. Cell death does not occur. Instead, the fragmented DNA coalesces into an irregular mass within the apical and basal membranes of the predome under which fluid has been accumulating. From the chromatin sheet, nuclei emerge amitotically as described in Part 3 of this series (Fleming, 2016c).



2016 ◽  
Author(s):  
Honoree Fleming

Pyknosis, karyorrhexis and karyolysis, harbingers of programmed cell death in many systems, appear to be driving forces that transform Ishikawa monolayer epithelial cells into differentiated dome cells. The heterochromatin affected by these process is contained in multiple nuclei aggregated in the syncytia that form when Ishikawa monolayers are stimulated to differentiate (Fleming, 2016a). The nuclear aggregates are enveloped in a double membrane staining for the endogenous biotin in mitochondrial carboxylases. The structure called a mitonucleon becomes vacuolated, along with the heterochromatin it envelops, and this structure elevates with the apical membrane of the syncytium 6 to 8 hours into the 20 hour differentiation, becoming increasingly pyknotic. This phase of the differentiation comes to an end when the mitonucleon membranes are breached and nuclei emerging from the aggregated state can be seen to fragment explosively. Fragmented DNA associates with an array of microtubules, filling the large central clearing of the predome. Some chromatin remains unfragmented and can be seen of the edges of the predome clearing. Cell death does not occur. Instead, the fragmented DNA coalesces into an irregular mass within the apical and basal membranes of the predome under which fluid has been accumulating. From the chromatin sheet, nuclei emerge amitotically as described in Part 3 of this series (Fleming, 2016c).



Author(s):  
MASOUD ALI KARAMI ◽  
MARZIE JALILI RAD ◽  
BEHZAD SHARIF MAKHMAL ZADEH ◽  
ANAYATOLLAH SALIMI

Objective: Alopecia aretea is associated with an increase in free radicals causing damage to hair follicles. Superoxide dismutase (SOD) with sufficient penetration through hair follicles, can prevent their death by its strong antioxidant effects. SOD with high molecular weight underwent limitation in follicular delivery. The aim of this study was the improvement of SOD localization into hair follicles. Methods: SOD-loaded niosomes were prepared by thin layer hydration method and were used as a vehicle for delivery to hair follicles through guinea pig skin and the synthetic membrane. Particle size, entrapment efficiency, drug release, and permeability parameters through hairly and non-hairly pig skin compared with a synthetic membrane were evaluated. Results: Niosomes demonstrated 152-325 nm particle size and the SOD burst and sustained release from niosomes were mainly controlled by diffusion and dissolution phenomena. SOD was protected against degradation by niosomes and after six months, enzyme content and activity decreased less than 5%. In comparison with free SOD, niosomes increased SOD affinity to penetration through follicles by interaction with sebum. Likewise, niosome's characters such as type of surfactant, solid lipid/liquid lipid ratio played critical roles on SOD deposition on hair follicles. Conclusion: Synthetic membrane and hairy guinea pig skin demonstrated similar barrier property against free-SOD thereby implying that free SOD does not interact with guinea pig sebum. Niosomes can introduce a suitable carrier for SOD localization into the hair follicles.



2000 ◽  
Vol 68 (2) ◽  
pp. 877-883 ◽  
Author(s):  
Kathleen M. George ◽  
Lisa Pascopella ◽  
Diane M. Welty ◽  
P. L. C. Small

ABSTRACT Mycobacterium ulcerans is the causative agent of Buruli ulcer, a tropical ulcerative skin disease. One of the most intriguing aspects of this disease is the presence of extensive tissue damage in the absence of an acute inflammatory response. We recently purified and characterized a macrolide toxin, mycolactone, from M. ulcerans. Injection of this molecule into guinea pig skin reproduced cell death and lack of acute inflammatory response similar to that seen following the injection of viable bacteria. We also showed that mycolactone causes a cytopathic effect on mouse fibroblast L929 cells that is characterized by cytoskeletal rearrangements and growth arrest within 48 h. However, these results could not account for the extensive cell death which occurs in Buruli ulcer. The results presented here demonstrate that L929 and J774 mouse macrophage cells die via apoptosis after 3 to 5 days of exposure to mycolactone. Treatment of cells with a pan-caspase inhibitor can inhibit mycolactone-induced apoptosis. We demonstrate that injection of mycolactone into guinea pig skin results in cell death via apoptosis and that the extent of apoptosis increases as the lesion progresses. These results may help to explain why tissue damage in Buruli ulcer is not accompanied by an acute inflammatory response.



2009 ◽  
Vol 337 (3) ◽  
pp. 429-438 ◽  
Author(s):  
Masashi Shin ◽  
Lars-Inge Larsson ◽  
David M. Hougaard ◽  
Kunio Fujiwara


2006 ◽  
Vol 131 (4) ◽  
pp. 521-524 ◽  
Author(s):  
Y. TAMADA ◽  
H. TAKAMA ◽  
T. KITAMURA ◽  
K. YOKOCHI ◽  
Y. NITTA ◽  
...  


1998 ◽  
Vol 16 ◽  
pp. S116
Author(s):  
Saburo Kishimoto ◽  
Makoto Nagata ◽  
Ryo Shibagaki ◽  
Hideya Takenaka ◽  
Hirokazu Yasuno
Keyword(s):  


Author(s):  
Emil Bernstein

An interesting method for examining structures in g. pig skin has been developed. By modifying an existing technique for splitting skin into its two main components—epidermis and dermis—we can in effect create new surfaces which can be examined with the scanning electron microscope (SEM). Although this method is not offered as a complete substitute for sectioning, it provides the investigator with a means for examining certain structures such as hair follicles and glands intact. The great depth of field of the SEM complements the technique so that a very “realistic” picture of the organ is obtained.



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