Controlling skin morphogenesis: hope and despair

Brouard, Michel; Barrandon, Yann

doi:10.1016/j.copbio.2003.09.005

Cited by 52 publications

(36 citation statements)

References 49 publications

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“…E4F1 might also exert other, as-yet unidentified cellular functions independent from Bmi1 and the Arf-p53 axis, as suggested by our finding that targeting the Bmi1-Arf-p53 axis did not fully restore ESC clonal outgrowth and normal skin phenotype. Thus, it could be proposed that E4F1 also impinges on other molecular circuitries that orchestrate ESC maintenance, including TGFβ/BMP-, Wnt/β-catenin-, Notch-, and p63-initiated signaling cascades (10,(12)(13)(14). Indeed, E4F1 might act as a transcriptional regulator of the p63 gene or as a posttranslational modifier of p63 activity, as has been described for p53.…”

Section: Discussionmentioning

confidence: 99%

“…ESCs fuel the highly proliferative transit amplifying compartments (TACs) in the basal layer of the IFE and in the bulbs of HFs. TAC cells then embark on differentiation programs to generate the spinous, granular, and cornified layers in the IFE or the different lineages of mature HFs (12)(13)(14). Several essential molecular circuitries that orchestrate ESC maintenance, including p63-, BMP-, TGF-β-, Wnt/β-catenin-, and Notchinitiated signaling cascades, have been described (12,15,16).…”

mentioning

confidence: 99%

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Transcription factor E4F1 is essential for epidermal stem cell maintenance and skin homeostasis

Lacroix

Caramel

Goguet-Rubio

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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A growing body of evidence suggests that the multifunctional protein E4F1 is involved in signaling pathways that play essential roles during normal development and tumorigenesis. We generated E4F1 conditional knockout mice to address E4F1 functions in vivo in newborn and adult skin. E4F1 inactivation in the entire skin or in the basal compartment of the epidermis induces skin homeostasis defects, as evidenced by transient hyperplasia in the interfollicular epithelium and alteration of keratinocyte differentiation, followed by loss of cellularity in the epidermis and severe skin ulcerations. E4F1 depletion alters clonogenic activity of epidermal stem cells (ESCs) ex vivo and ends in exhaustion of the ESC pool in vivo, indicating that the lesions observed in the E4F1 mutant skin result, at least in part, from cell-autonomous alterations in ESC maintenance. The clonogenic potential of E4F1 KO ESCs is rescued by Bmi1 overexpression or by Ink4a/Arf or p53 depletion. Skin phenotype of E4F1 KO mice is also delayed in animals with Ink4a/Arf and E4F1 compound gene deficiencies. Our data identify a regulatory axis essential for ESC-dependent skin homeostasis implicating E4F1 and the Bmi1–Arf–p53 pathway.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Transcription factor E4F1 is essential for epidermal stem cell maintenance and skin homeostasis

Lacroix

Caramel

Goguet-Rubio

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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“…Previous studies using lineage tracing and mouse models revealed that stem cells of both the epidermis and the hair follicles contribute to skin wound repair (Ito et al 2005;Levy et al 2007;Nowak et al 2008;Snippert et al 2010). Because there are more sweat glands than hair follicles in the majority area of human skin, it has been hypothesized that another source of progenitors or stem cells within the sweat apparatus (duct and gland) can contribute to skin wound repair (Brouard and Barrandon 2003;Biedermann et al 2010). How the cells in the sweat apparatus maintain homeostasis and respond to different types of injury has been studied at the histological level.…”

Section: Homeostasis and Wound Repair Of The Sweat Apparatusmentioning

confidence: 99%

Sweat Gland Progenitors in Development, Homeostasis, and Wound Repair

Fuchs

2014

Cold Spring Harbor Perspectives in Medicine

134

116

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The human body is covered with several million sweat glands. These tiny coiled tubular skin appendages produce the sweat that is our primary source of cooling and hydration of the skin. Numerous studies have been published on their morphology and physiology. Until recently, however, little was known about how glandular skin maintains homeostasis and repairs itself after tissue injury. Here, we provide a brief overview of sweat gland biology, including newly identified reservoirs of stem cells in glandular skin and their activation in response to different types of injuries. Finally, we discuss how the genetics and biology of glandular skin has advanced our knowledge of human disorders associated with altered sweat gland activity.

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“…These 2 stem cell compartments are well characterized by their capacity to self renew and maintain specific functions over an individual's lifetime. The cell types' accessibility, ability to survive in ex vivo cell culture, and transplantability are advantageous for their use in gene therapy; in fact, over 20 years of research on ex vivo manipulation of these stem cell compartments (in HSCT and burn repairs, respectively) has enabled rapid advances in the gene therapy field (6)(7)(8)(9)(10).…”

mentioning

confidence: 99%

Gene therapy for severe combined immunodeficiency: are we there yet?

Cavazzana‐Calvo¹,

Fischer²

2007

J. Clin. Invest.

196

110

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Inherited and acquired diseases of the hematopoietic system can be cured by allogeneic hematopoietic stem cell transplantation. This treatment strategy is highly successful when an HLA-matched sibling donor is available, but if not, few therapeutic options exist. Gene-modified, autologous bone marrow transplantation can circumvent the severe immunological complications that occur when a related HLA-mismatched donor is used and thus represents an attractive alternative. In this review, we summarize the advantages and limitations associated with the use of gene therapy to cure SCID. Insertional mutagenesis and technological improvements aimed at increasing the safety of this strategy are also discussed.Nonstandard abbreviations used: AAV, adeno-associated virus; ADA, adenosine deaminase; γc, γ common; GALV, gibbon ape leukemia virus; HIV-1, HIV type 1; HSCT, HSC transplantation; IN, integrase; LMO2, LIM domain only 2; LTR, long-term repeat; MLV, murine leukemia virus; SCID-X1, X-linked SCID; ZFN, zinc finger nuclease; ZFP, zinc finger protein.

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Controlling skin morphogenesis: hope and despair

Cited by 52 publications

References 49 publications

Transcription factor E4F1 is essential for epidermal stem cell maintenance and skin homeostasis

Transcription factor E4F1 is essential for epidermal stem cell maintenance and skin homeostasis

Sweat Gland Progenitors in Development, Homeostasis, and Wound Repair

Gene therapy for severe combined immunodeficiency: are we there yet?

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