Hair Follicle Growth Controls

Stenn, Kurt S.; Combates, Nicholas J.; Eilertsen, Kenneth J.; Gordon, Joel S.; Pardinas, José R.; Parimoo, Satish; Prouty, Stephen M.

doi:10.1016/s0733-8635(05)70383-1

Cited by 136 publications

(138 citation statements)

References 148 publications

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“…irse, inner root sheath end; cts, perifollicular connective tissue sheath; other legends same as in this apparently tightly controlled system. [1][2][3][4] Thus, the normal hr gene product may not be a catagen repressor, but rather an essential regulator of the earliest events associated with normal HF regression, during which the stepwise down-regulation of matrix cell proliferation must be carefully coordinated with an up-regulation of apoptosis in selected matrix cells.…”

Section: Discussionmentioning

confidence: 99%

“…However, little is understood about the exact nature, sequence, and interplay of the molecular signals that govern the cyclic transformations of the HF between rest (telogen), growth (anagen), and regression (catagen). [1][2][3][4] Several lines of evidence point to the hairless (hr) gene as one potentially important regulatory molecule in hair cycle control. An autosomal recessive mutation of the hairless (hr) gene in mice evokes severe, irreversible HF abnormalities.…”

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confidence: 99%

“…Also, these studies did not address the earliest stages of hr phenotype development in neonatal hr/hr mice undergoing their first synchronized, spontaneous HF regression (catagen). 1,3,20,21 Therefore, in the current study, we have systematically characterized the chronology of HF transformation in HRS/J hr/hr hairless mutant mice by routine histology, histochemistry, and immunohistology throughout the period of postnatal skin development when the macroscopic phenotype is first evident and when the hair shafts are shed (ie, during days 14 -20 postpartum). This was compared to age-matched, heterozygous ϩ/hr mice, which develop and maintain an apparently normal fur coat.…”

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confidence: 99%

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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: Discussionmentioning

confidence: 99%

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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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“…It has been reported that the hair growth cycle is controlled by a number of receptor-protein tyrosine kinases (PTKs), such as epidermal growth factor receptor (EGFR), insulin-like growth factor receptor (IGFR) and nerve growth factor receptor (NGFR) (Peus and Pittelkow, 1996;Stenn et al, 1996;Botchkarev et al, 1998;Paus and Cotsarelis, 1999). It has also been reported that hair pigmentation, which requires c-Kit as a receptor protein tyrosine kinase (Nishikawa et al, 1991), may be coupled to the anagen phase of the hair cycle (Slominski and Paus, 1993;Slominski et al, 1994;Ortonne and Prora, 1993), although not all anagen phases accompany pigmentation.…”

Section: Introductionmentioning

confidence: 99%

RET tyrosine kinase enhances hair growth in association with promotion of melanogenesis

et al. 2001

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We ®rst demonstrated that c-Ret protein is transiently expressed mainly in the inner and outer root sheaths of hair follicles soon after birth in the skin of normal C57BL/6 and BALB/c mice. A longer-lasting expression of activated RET protein overlapped the c-Ret expression with some preferential expression in the outer root sheath in close association with increase in the number of S-100 protein-containing cells in the area and excess melanogenesis in and around hair bulbs in the skin of RFP-RET-transgenic mice on a C57BL/6 background (RFP-RET/B6). Hair follicles in the skin of the transgenic mice continuously showed histology of the anagen phase, and the recovery period for the hair of the transgenic mice after shaving was shortened. Such growth promotion was not observed in the case of white hairs of RFP-RET-transgenic mice on a BALB/c background. These results suggest that RET works to extend the anagen phase in association with upregulation of melanin production. Oncogene (2001) 20, 7536 ± 7541.

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“…During the last decade, it has been shown that the expression patterns of many cytokines, transcription factors, and adhesion molecules are subject to significant changes during normal HF morphogenesis and cycling 8,9 thus suggesting a role in the regulation of HF transformation. Although informative, these studies are somewhat limited in that they do not illuminate the molecular pathways of gene activity and their functional role in HF biology.…”

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Patterns of Hairless (hr) Gene Expression in Mouse Hair Follicle Morphogenesis and Cycling

Panteleyev¹,

Paus

Christiano

2000

The American Journal of Pathology

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The hr (hairless) gene encodes a putative transcription factor with restricted expression in the skin and brain. Mutations in the hr locus cause papular atrichia in humans and complete hair loss in mice and other mammals. To further elucidate the role of hr in skin biology, and to identify potential target cells for hr regulation, we studied hr mRNA localization during hair follicle (HF) morphogenesis and cycling in normal C57BL/6J mice. In situ hybridization revealed that hr expression was present in the suprabasal cell layers of the epidermis, whereas the basal and highly differentiated keratinocytes of the granular layer were hr-negative. During the early stages of HF morphogenesis, hr mRNA was detected in the developing hair peg. Later, it became concentrated in the HF infundibulum, in the HF matrix, and in the inner root sheath (IRS), whereas the dermal papilla (DP) and outer root sheath were consistently hr mRNA-negative. During catagen, hr gene expression gradually declined in the regressing IRS, shortly but dramatically increased in the zone of developing club hair, and became up-regulated in the epithelial cells adjacent to the DP. The co-localization of hr mRNA with the site of the morphological defects in mutant skin implicates hr as a key factor in regulating basic cellular processes during catagen, including club hair formation, maintenance of DP-epithelial integrity, IRS disintegration, and keratinocyte apoptosis in the HF matrix.

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Hair Follicle Growth Controls

Cited by 136 publications

References 148 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

RET tyrosine kinase enhances hair growth in association with promotion of melanogenesis

Patterns of Hairless (hr) Gene Expression in Mouse Hair Follicle Morphogenesis and Cycling

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