Differential control of cell death in the skin

Norris, David A.

doi:10.1001/archderm.131.8.945

Cited by 26 publications

(22 citation statements)

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“…It has been suggested that programmed cell death is part of the normal process of keratinocyte differentiation in the epidermis, matrix, and root sheath of hair follicles [27][28][29]. In our model, we were not able to detect apoptotic cells in normal skin.…”

Section: Discussioncontrasting

confidence: 68%

Increased apoptosis during papilloma development in mice susceptible to tumor progression

et al. 1997

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Programmed cell death (apoptosis) is known to occur not only during normal development and tissue remodeling but also during neoplasia. Despite the suggested role of apoptosis in preventing the proliferation of malignant cells, a positive correlation between tumor progression and the presence of apoptotic cells has been found in different types of cancer, including epithelial tumors. In normal mouse skin, the role of apoptosis is not completely understood, and it has been suggested that terminal differentiation may be a special case of apoptosis. In the work reported here, we counted apoptotic cells in mouse skin tumors generated with a two-stage chemical carcinogenesis protocol. We analyzed papillomas from outbred SENCAR mice at different times during promotion, and to better determine the correlation between apoptosis and tumor progression, we compared papillomas generated from two inbred strains derived from the SENCAR stock that differ in their susceptibility to tumor progression. Our results showed that in mouse skin chemical carcinogenesis, the number of apoptotic cells was greater in papillomas that may have been in the process of progressing to squamous cell carcinomas. This conclusion is also supported by the fact that papillomas from SENCAR P/Bt. mice, a tumor progression-susceptible strain derived from outbred SENCAR mice, had more apoptotic cells than papillomas from progression-resistant SSIN mice.

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Section: Discussioncontrasting

confidence: 68%

Increased apoptosis during papilloma development in mice susceptible to tumor progression

et al. 1997

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“…Other cell types may be affected, notably inflammatory cells, which are difficult to identify once the process of apoptosis has occurred, which may lead to the inexact identification of the cells undergoing apoptosis. In a previous study of apoptosis in the skin, Norris (1995) suggested multiple triggers of apoptosis, which work through a variety of signaling pathways. Therefore, another possible reason is that some caspase-3-independent pathway mediates the apoptosis observed in normal healed flat scars of S2 and S3.…”

Section: Akasaka Et Almentioning

confidence: 99%

Enhanced Expression of Caspase-3 in Hypertrophic Scars and Keloid: Induction of Caspase-3 and Apoptosis in Keloid Fibroblasts In Vitro

Akasaka

Ishikawa

Ono

et al. 2000

Laboratory Investigation

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SUMMARY:Recent studies have suggested that the regulation of apoptosis during wound healing is important in scar establishment and development of pathological scarring. To examine the phenomenon of apoptosis and its involvement in the process of pathological scarring, we immunohistochemically quantified differential levels of expression of caspase-3 and -2, which are activated during apoptosis in vitro, in surgical resected scar tissues. We divided 33 cases of normally healed flat scars and 18 cases of pathological scars (15 cases of hypertrophic scars and 3 cases of keloid) into three groups (S1 ϭ Ͻ10 months' duration; S2 ϭ 10 to 40 months' duration; and S3 ϭ Ͼ40 months' duration) according to the duration of scar. In all three groups examined, the semiquantitative scores for caspase-3 staining were significantly higher for the combination of hypertrophic scars and keloid as a group compared with normally healed flat scars, suggesting reduced cell survival and increased apoptotic cell death in hypertrophic scars and keloid. Apoptosis and caspase proteolytic activities were examined in vitro using two flat scar-derived fibroblast lines (FSFB-1 and -2) and two keloid-derived fibroblast lines (KFB-1 and -2). After 24 hours of serum deprivation, apoptotic cells were significantly increased in both KFB lines, whereas serum deprivation of FSFB-1 cells did not result in a significant increase in apoptotic cell number. After serum deprivation, significant increases in caspase-3 proteolytic activities were detected in both KFB lines compared with both FSFB lines. In contrast, no significant differences with caspase-8 activity were observed between similarly treated KFB and FSFB lines. Furthermore, serum deprivation-induced apoptosis of KFB-2 cells was significantly inhibited by the caspase-3 inhibitor Ac-Asp-Glu-Val-Asp-fluoromethyl ketone (DEVD-FMK), indicating that caspase-3 is important for serum deprivation-induced apoptosis in KFB-2 cells. Considering the role of caspase-3 as a key effector molecule in the execution of apoptotic stimuli, our results suggested that enhanced expression of caspase-3 in hypertrophic scars and keloid induces apoptosis of fibroblasts, which may play a role in the process of pathological scarring. (Lab Invest 2000, 80:345-357).

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“…In the skin, apoptotic cells can be detected under a wide variety of conditions, including inflammatory dermatoses (Teraki and Shiohara 1999) and skin neoplasms (Kerr et al 1972;Sen 1992;Thompson 1995;Weedon 1990). It is also involved in the homeostasis of healthy skin, where terminal differentiation of keratinocytes is thought to be a special form of apoptosis (McCall and Cohen 1991) and is present in the matrix and root sheath of cycling hair follicles (Norris 1995). Its role in physical and, particularly, mechanical trauma has also been demonstrated both in animal experimentation and in humans.…”

Section: Introductionmentioning

confidence: 99%

Demonstration of apoptosis in human skin injuries as an indicator of vital reaction

et al. 2002

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Demonstrating the vital character of an injury and estimation of the age are routine tasks in forensic pathology and although many different techniques have been applied to this problem none have been found to be completely satisfactory. Apoptosis, an active genetically controlled process, is the major mechanism by which homeostasis of a number of physiological systems in the body is regulated and changes in the rate following different kinds of stimuli have prompted us to test it as an indicator of vitality. We used an in situ end-labelling technique (Apop-Tag) in 30 human surgical skin injuries with age since injury ranging from 3 min to 8 h and found that apoptotic keratinocytes are found in over 50% of the cases with a post-infliction interval of at least 120 min. Apoptosis was not seen in injuries less than 120 min old or in normal skin, which was used as an external control. These results suggest that apoptosis could be a useful indicator for the intravital occurrence of injuries and could help to estimate the date of the skin injuries in some cases. The importance of strict technical control is stressed and the necessity of a complementary technique to confirm apoptosis is discussed.

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Differential control of cell death in the skin

Cited by 26 publications

References 0 publications

Increased apoptosis during papilloma development in mice susceptible to tumor progression

Increased apoptosis during papilloma development in mice susceptible to tumor progression

Enhanced Expression of Caspase-3 in Hypertrophic Scars and Keloid: Induction of Caspase-3 and Apoptosis in Keloid Fibroblasts In Vitro

Demonstration of apoptosis in human skin injuries as an indicator of vital reaction

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