Patterns of cell death: the significance of apoptosis for dermatology

Paus, R.; Rosenbach, Thomas; Haas, Norbert; Czarnetzki, Beate M.

doi:10.1111/j.1600-0625.1993.tb00192.x

Cited by 80 publications

(52 citation statements)

References 82 publications

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“…This is in striking contrast to catagen HF in ϩ/hr ( Figure 5I) or C57BL/6 mice, 23 and further demonstrates that the absence of a functional hr gene product causes severe disturbances in normal catagen-associated HF transformation. 23,32,33 During the final stage of hr/hr HF transformation (stage 9), the epithelial cells that remained associated with the detached DP remnants were Ki-67-positive, suggesting a high proliferative activity in this ectopic epithelial compartment of hr/hr skin ( Figure 5, J and K). The epithelial nature of these cells was confirmed by their expression of IL-1R1 ( Figure 4I), which is a useful and reliable marker for distinguishing HF keratinocytes from the follicle-associated mesenchyme.…”

Section: Patterns Of Proliferation and Apoptosismentioning

confidence: 98%

The Role of the Hairless (hr) Gene in the. Regulation of Hair Follicle Catagen Transformation

Panteleyev¹,

Botchkareva²,

Sundberg³

et al. 1999

The American Journal of Pathology

153

136

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Mice that carry a mutation at the hairless (hr) locus develop seemingly normal hair follicles (HF) but shed their hairs completely soon after birth. Histologically , their HFs degenerate into characteristic utriculi and dermal cysts shortly after the entry of the HF into the first regression phase (catagen) , during the initiation of HF cycling. Here , we show that at least nine distinct stages of HF disintegration can be distinguished in hr/hr mice. Toward the end of HF morphogenesis (day 15 postpartum) the proximal hair bulb in hr/hr skin undergoes premature and massive apoptosis. This is associated with a dyscoordination of cell proliferation in defined HF compartments, malpositioning of the proximal inner root sheath, striking atrophy of outer root sheath , and failure of trichilemmal keratinization in the developing club hair. Rather than undergoing their normal catagenassociated involution , the hair bulb and central outer root sheath disintegrate into separate cell clusters, thus disrupting all epithelial contact with the dermal papilla. Dermal papilla fibroblasts fail to migrate upward , and break up into clusters of shrunken cells stranded in the reticular dermis as dermal cyst precursors , while the upper HF epithelium transforms into utriculi. Some dermal papilla cells , which normally never undergo apoptosis , also become TUNEL؉ in hr/hr skin , and their normally high expression of a key adhesion molecule , neural cell adhesion molecule , declines. Thus , loss of a functional hr gene product (a putative zinc finger transcription factor) initiates a premature , highly dysregulated catagen, which results in the destruction of the normal HF architecture and abrogates the HF's ability to cycle. This provides new insights into the pathobiology of the hr mutation , and suggests that the normal hr gene product is a crucial element of catagen control. (Am J Pathol 1999, 155:159 -171)

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Section: Patterns Of Proliferation and Apoptosismentioning

confidence: 98%

The Role of the Hairless (hr) Gene in the. Regulation of Hair Follicle Catagen Transformation

Panteleyev¹,

Botchkareva²,

Sundberg³

et al. 1999

The American Journal of Pathology

153

136

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“…A number of different growth factors and cytokines are involved in the regulation of apoptosis in the epidermis and in the regressing hair follicle (61).…”

Section: Role Of Growth Factors/cytokines In Apoptosismentioning

confidence: 99%

Hormonal control of programmed cell death/apoptosis

Kieß

Gallaher

1998

European Journal of Endocrinology

123

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Apoptosis or programmed cell death is a physiological form of cell death that occurs in embryonic development and during involution of organs. It is characterized by distinct biochemical and morphological changes such as DNA fragmentation, plasma membrane blebbing and cell volume shrinkage. Many hormones, cytokines and growth factors are known to act as general and/or tissuespecific survival factors preventing the onset of apoptosis. In addition, many hormones and growth factors are also capable of inducing or facilitating programmed cell death under physiological or pathological conditions, or both. Steroid hormones are potent regulators of apoptosis in steroiddependent cell types and tissues such as the mammary gland, the prostate, the ovary and the testis. Growth factors such as epidermal growth factor, nerve growth factor, platelet-derived growth factor (PDGF) and insulin-like growth factor-I act as survival factors and inhibit apoptosis in a number of cell types such as haematopoietic cells, preovulatory follicles, the mammary gland, phaeochromocytoma cells and neurones. Conversely, apoptosis modulates the functioning and the functional integrity of many endocrine glands and of many cells that are capable of synthesizing and secreting hormones. In addition, exaggeration of the primarily natural process of apoptosis has a key role in the pathogenesis of diseases involving endocrine tissues. Most importantly, in autoimmune diseases such as autoimmune thyroid disease and type 1 diabetes mellitus, new data suggest that the immune system itself may not carry the final act of organ injury: rather, the target cells (i.e. thyrocytes and b cells of the islets) commit suicide through apoptosis. The understanding of how hormones influence programmed cell death and, conversely, of how apoptosis affects endocrine glands, is central to further design strategies to prevent and treat diseases that affect endocrine tissues. This short review summarizes the available evidence showing where and how hormones control apoptosis and where and how programmed cell death exerts modulating effects upon hormonally active tissues. European Journal of Endocrinology 138 482-491

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“…Furthermore, programmed cell death plays an important role during many inflammatory and malignant pathological processes (9), including skin diseases (10). In particular, Fas-induced keratinocyte apoptosis plays a recognized pathogenetic role in eczematous dermatitis (11), toxic epidermal necrolysis (12), acantholytic bullous dermatosis (13) and cutaneous lupus erythematosus (14).…”

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confidence: 99%

The Role of Apoptosis in the Pathogenesis of Dermatitis Herpetiformis

Caproni

Torchia

Antiga

et al. 2005

Int J Immunopathol Pharmacol

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Apoptosis is a form of cell death that is claimed to be involved in a number of chronic inflammatory and malignant skin diseases. The aim of this study was to investigate whether apoptosis may contribute to the pathogenesis of epidermal changes in dermatitis herpetiformis (DR) and, in particular, whether certain apoptosis-related markers such as Bax, Bcl-2, Fas and Fas ligand (FasL) take part in this process. For the detection of apoptotic nuclei, terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labelling technique (TUNEL) was employed on cryostat sections. Skin lesions from six and perilesional skin from four DH patients were stained with monoclonal antibodies to Bax, Bcl-2, Fas and FasL. The same evaluation was also performed on three patients affected by bullous pemphigoid (BP) and in two healthy donors. Using TUNEL technique, a remarkable increase in the apoptotic rate within the epidermal compartment was observed in DH and BP patients in comparison with normal controls. In our immunohistochemical analysis, Bax/Bcl-2 ratio was almost the same in the epidermis of perilesional/lesional DH, BP and healthy skin specimens. In DH and BP specimens both Bax and Bcl-2 proteins were increased in the dermal perivascular compartment. Fas showed a prevalently epidermal staining, both in DH and BP lesions, while FasL was distributed in perivascular and subjunctional dermis; some FasL+ cells infiltrated the DEJ and the basal layer of epidermis. This study allowed us to highlight conspicuous apoptotic phenomena in basal and suprabasal keratinocytes within lesional and perilesional skin ofDH. We conclude that in DH, as well as in BP, apoptosis plays a role in the pathogenesis of cutaneous lesions in concert with other pathogenetic mechanisms.Dermatitis herpetiformis (DH) is an autoimmune subepidermal blistering disease characterized by chronic and recurrent eruptions of erythematous, urticarial, papular, vesicular and bullous lesions. Granular IgA deposits at the dermal papillae represent the immunological marker of the disease, that is strictly associated with a gluten-sensitive enteropathy (GSE), indistinguishable from coeliac disease (CD) (1). To date, immunopathological mechanisms that lead to blister formation in DH are only partially known. In this respect, granular IgA deposition at the dermo-epidermal junction (DEJ), neutrophils and eosinophils together with activated CD4+ Th2 lymphocytes are supposed to represent the main immune mechanisms involved in the pathogenesis of the disease (1-2).Apoptosis is a sequence of events based on cellular metabolism that lead to cell shrinkage,

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Patterns of cell death: the significance of apoptosis for dermatology

Cited by 80 publications

References 82 publications

The Role of the Hairless (hr) Gene in the. Regulation of Hair Follicle Catagen Transformation

The Role of the Hairless (hr) Gene in the. Regulation of Hair Follicle Catagen Transformation

Hormonal control of programmed cell death/apoptosis

The Role of Apoptosis in the Pathogenesis of Dermatitis Herpetiformis

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