Defective stratum corneum and early neonatal death in mice lacking the gene for transglutaminase 1 (keratinocyte transglutaminase)

Matsuki, Masato; Ishida‐Yamamoto, Akemi; Yamada, Kazutaka; Tabata, Kohichi; Yasuno, Hirokazu; Iizuka, Hideko; Yamanishi, Kiyofumi

doi:10.1016/s0923-1811(98)83082-x

Cited by 28 publications

(50 citation statements)

References 25 publications

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“…74 TG1 crosslinks proteins and is important for the correct assembly of the cornified envelope. 113,114 Desquamin, a protease of which the molecular identity remains to be determined, is expressed at the transition zone between the granular and cornified layer. It has been suggested that desquamin is involved in the degradation of the nuclear matrix.…”

Section: Discussionmentioning

confidence: 99%

“…113 A similar phenotype is observed in mice lacking the TG1 gene. 114 These mice have defects in the formation of the epidermal barrier and the cornified envelopes, and die shortly after birth; however, no effects on apoptosis have been reported. TG2 knockout mice do not have any defects in the keratinocyte differentiation program, and its role in apoptosis remains unclear.…”

Section: Transglutaminasesmentioning

confidence: 99%

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Death penalty for keratinocytes: apoptosis versus cornification

et al. 2005

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Homeostasis implies a balance between cell growth and cell death. This balance is essential for the development and maintenance of multicellular organisms. Homeostasis is controlled by several mechanisms including apoptosis, a process by which cells condemned to death are completely eliminated. However, in some cases, total destruction and removal of dead cells is not desirable, as when they fulfil a specific function such as formation of the skin barrier provided by corneocytes, also known as terminally differentiated keratinocytes. In this case, programmed cell death results in accumulation of functional cell corpses. Previously, this process has been associated with apoptotic cell death. In this overview, we discuss differences and similarities in the molecular regulation of epidermal programmed cell death and apoptosis. We conclude that despite earlier confusion, apoptosis and cornification occur through distinct molecular pathways, and that possibly antiapoptotic mechanisms are implicated in the terminal differentiation of keratinocytes.

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Section: Discussionmentioning

confidence: 99%

Section: Transglutaminasesmentioning

confidence: 99%

Death penalty for keratinocytes: apoptosis versus cornification

et al. 2005

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“…157,158 In recent years, it has become evident that this most critical SC functionethe permeability barriereis impaired in most ichthyosis forms. 11,60,[159][160][161][162][163][164] Several murine knockout models for ichthyosis [Spink5 (e/e), Tgm1 (e/e), Abca12 (e/e) mice, [165][166][167] Alox12b (e/e), 168 Cldn1(e/e) 169 ] have demonstrated neonatal lethality as a result of dehydration, underscoring the critical role of these genes in permeability barrier competence. Mutations that either alter the lipid composition of the SC membranesedisorders of lipid metabolismeor affect the function of the corneocyte structural proteinsedisorders of keratinocyte proteinseresult in increased water movement through the intercellular pathway.…”

Section: Concept Of the Impaired Permeability Barrier And Homeostaticmentioning

confidence: 99%

Revised nomenclature and classification of inherited ichthyoses: Results of the First Ichthyosis Consensus Conference in Sorèze 2009

Oji

Tadini

Akiyama

et al. 2010

Journal of the American Academy of Dermatology

687

704

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“…Data from Turksen and Troy showed that mice with defective CE caused by overexpressing claudin6 exhibited neonatal death due to unquenchable infection, outflow of water and temperature instability [5]. Similarly, mice with the GTase1 gene knockout died as neonates, lacking the normal insoluble cornified envelope and having impaired barrier function [6]. However, the knockout of genes encoding some CE proteins such as involucrin, loricrin and envoplakin did not abolish CE formation and only slightly affected CE function, suggesting the existence of some compensatory mechanisms preventing a more severe skin phenotype [7][8][9].…”

Section: Introductionmentioning

confidence: 99%

Gene expression pattern and hormonal regulation of Small Proline-Rich Protein 2 family members in the female mouse reproductive system during the estrous cycle and pregnancy

Tan

Sun

et al. 2006

Reprod. Nutr. Dev.

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-Small proline-rich proteins (SPRR) are known to construct the cornified cell envelope (CE) in the stratified squamous epithelial cell. Their functions in the simple epithelium such as the uterine epithelium are not clear hitherto. In the present study, the mRNA expression patterns of sprr2 family members in the mouse uterus and vagina during the estrous cycle and pregnancy as well as their regulation by steroids were investigated. Using semi-quantitative RT-PCR, it was revealed that the transcripts of sprr2b, 2e and 2g genes were up-regulated in the proestrous and estrous uteri, and sprr2d was up-regulated only in the estrous uterus. In the vagina, transcription of sprr2a, 2b, 2d, 2e and 2k genes were up-regulated at the metestrous stage. Northern blot analysis demonstrated that the overall expression of sprr2 was highly up-regulated in the estrous uterus and the metestrous vagina. During pregnancy, the sprr2 mRNA in the uterus was sharply repressed from day 3 postcoitus on, and began to be induced around labor time. In situ hybridization showed that the sprr2 transcripts were localized in uterine luminal and glandular epithelial cells as well as vaginal stratified epithelial cells. In ovariectomized mice, the expression of sprr2a, 2d, 2e and 2f genes in the uterus were induced by estrogen, and the effect of estrogen on sprr2d and 2e expression could be partly abolished by progesterone. The data indicate that the sprr2 genes have unique regulation patterns in different reproductive tissues under different physiological conditions, and the encoded proteins might play diverse functions in the female reproductive system. small proline-rich protein / uterus / estrous cycle / pregnancy / stress

show abstract

Defective stratum corneum and early neonatal death in mice lacking the gene for transglutaminase 1 (keratinocyte transglutaminase)

Cited by 28 publications

References 25 publications

Death penalty for keratinocytes: apoptosis versus cornification

Death penalty for keratinocytes: apoptosis versus cornification

Revised nomenclature and classification of inherited ichthyoses: Results of the First Ichthyosis Consensus Conference in Sorèze 2009

Gene expression pattern and hormonal regulation of Small Proline-Rich Protein 2 family members in the female mouse reproductive system during the estrous cycle and pregnancy

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