scholarly journals A role for disulfide bonding in keratin intermediate filament organization and dynamics in skin keratinocytes

2015 ◽  
Vol 209 (1) ◽  
pp. 59-72 ◽  
Author(s):  
Xia Feng ◽  
Pierre A. Coulombe
Keyword(s):  
Primary Cultures ◽  
Mouse Skin ◽  
Disulfide Bonding ◽  
Skin Keratinocytes ◽  
Keratin Filaments ◽  
Keratinocyte Cell ◽  
Mouse Skin Keratinocytes ◽  
Sizable Fraction ◽  
Trans Dimer

We recently reported that a trans-dimer, homotypic disulfide bond involving Cys367 in keratin 14 (K14) occurs in an atomic-resolution structure of the interacting K5/K14 2B domains and in keratinocyte cell lines. Here we show that a sizable fraction of the K14 and K5 protein pools participates in interkeratin disulfide bonding in primary cultures of mouse skin keratinocytes. By comparing the properties of wild-type K14 with a completely cysteine-free variant thereof, we found that K14-dependent disulfide bonding limited filament elongation during polymerization in vitro but was necessary for the genesis of a perinuclear-concentrated network of keratin filaments, normal keratin cycling, and the sessile behavior of the nucleus and whole cell in keratinocytes studied by live imaging. Many of these phenotypes were rescued when analyzing a K14 variant harboring a single Cys residue at position 367. These findings establish disulfide bonding as a novel and important mechanism regulating the assembly, intracellular organization, and dynamics of K14-containing intermediate filaments in skin keratinocytes.

Early changes in gene expression induced by tumour promoters in mouse skin keratinocytes

1987 ◽  
Vol 23 (11) ◽  
pp. 1736-1737
Author(s):  
S. Bohm ◽  
C. Pereswetoff-Morath ◽  
A. Berghard ◽  
K. Hyvönen ◽  
R. Toftgård
Keyword(s):  
Gene Expression ◽  
Mouse Skin ◽  
Skin Keratinocytes ◽  
Tumour Promoters ◽  
Mouse Skin Keratinocytes

scholarly journals Forced Expression of Keratin 16 Alters the Adhesion, Differentiation, and Migration of Mouse Skin Keratinocytes

2000 ◽  
Vol 11 (10) ◽  
pp. 3315-3327 ◽  
Author(s):  
Matthew Wawersik ◽  
Pierre A. Coulombe
Keyword(s):  
Mouse Skin ◽  
Cellular Level ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Keratin 16 ◽  
Skin Keratinocytes ◽  
Steady State Levels ◽  
And Migration ◽  
Mouse Skin Keratinocytes ◽  
The Impact

Injury to the skin results in an induction of keratins K6, K16, and K17 concomitant with activation of keratinocytes for reepithelialization. Forced expression of human K16 in skin epithelia of transgenic mice causes a phenotype that mimics several aspects of keratinocyte activation. Two types of transgenic keratinocytes, with forced expression of either human K16 or a K16-C14 chimeric cDNA, were analyzed in primary culture to assess the impact of K16 expression at a cellular level. High K16-C14-expressing and low K16-expressing transgenic keratinocytes behave similar to wild type in all aspects tested. In contrast, high K16-expressing transgenic keratinocytes show alterations in plating efficiency and calcium-induced differentiation, but proliferate normally. Migration of keratinocytes is reduced in K16 transgenic skin explants compared with controls. Finally, a subset of high K16-expressing transgenic keratinocytes develops major changes in the organization of keratin filaments in a time- and calcium concentration-dependent manner. These changes coincide with alterations in keratin content while the steady-state levels of K16 protein remain stable. We conclude that forced expression of K16 in progenitor skin keratinocytes directly impacts properties such as adhesion, differentiation, and migration, and that these effects depend upon determinants contained within its carboxy terminus.

scholarly journals Onset of re-epithelialization after skin injury correlates with a reorganization of keratin filaments in wound edge keratinocytes: defining a potential role for keratin 16.

1996 ◽  
Vol 132 (3) ◽  
pp. 381-397 ◽  
Author(s):  
R D Paladini ◽  
K Takahashi ◽  
N S Bravo ◽  
P A Coulombe
Keyword(s):  
Cultured Cells ◽  
Structural Function ◽  
Cell Periphery ◽  
Post Injury ◽  
Wound Edge ◽  
Keratin 16 ◽  
Skin Keratinocytes ◽  
Keratin Filaments ◽  
10 Nm Filaments

Injury to stratified epithelia causes a strong induction of keratins 6 (K6) and 16 (K16) in post-mitotic keratinocytes located at the wound edge. We show that induction of K6 and K16 occurs within 6 h after injury to human epidermis. Their subsequent accumulation in keratinocytes correlates with the profound reorganization of keratin filaments from a pan-cytoplasmic distribution to one in which filaments are aggregated in a juxtanuclear location, opposite to the direction of cell migration. This filament reorganization coincides with additional cytoarchitectural changes and the onset of re-epithelialization after 18 h post-injury. By following the assembly of K6 and K16 in vitro and in cultured cells, we find that relative to K5 and K14, a well-characterized keratin pair that is constitutively expressed in epidermis, K6 and K16 polymerize into short 10-nm filaments that accumulate near the nucleus, a property arising from K16. Forced expression of human K16 in skin keratinocytes of transgenic mice causes a retraction of keratin filaments from the cell periphery, often in a polarized fashion. These results imply that K16 may not have a primary structural function akin to epidermal keratins. Rather, they suggest that in the context of epidermal wound healing, the function of K16 could be to promote a reorganization of the cytoplasmic array of keratin filaments, an event that precedes the onset of keratinocyte migration into the wound site.

scholarly journals A Method for the Immortalization of Newborn Mouse Skin Keratinocytes

2015 ◽  
Vol 5 ◽  
Author(s):  
Brianna O. Hammiller ◽  
Taghrid Bahig El-Abaseri ◽  
Andrzej A. Dlugosz ◽  
Laura A. Hansen
Keyword(s):  
Mouse Skin ◽  
Newborn Mouse ◽  
Skin Keratinocytes ◽  
Mouse Skin Keratinocytes

Gsdma3 is a new factor needed for TNF-α-mediated apoptosis signal pathway in mouse skin keratinocytes

2012 ◽  
Vol 138 (3) ◽  
pp. 385-396 ◽  
Author(s):  
Mingxing Lei ◽  
Xiufeng Bai ◽  
Tian Yang ◽  
Xiangdong Lai ◽  
Weiming Qiu ◽  
...  
Keyword(s):  
Mouse Skin ◽  
Signal Pathway ◽  
Skin Keratinocytes ◽  
Tnf Α ◽  
Mouse Skin Keratinocytes

Synthetic epidermal pentapeptide and related growth regulatory peptides inhibit proliferation and enhance differentiation in primary and regenerating cultures of human epidermal keratinocytes

1990 ◽  
Vol 97 (1) ◽  
pp. 51-58 ◽  
Author(s):  
P.K. Jensen ◽  
K. Elgjo ◽  
O.D. Laerum ◽  
L. Bolund
Keyword(s):  
Primary Cultures ◽  
Mouse Skin ◽  
Regulatory Peptides ◽  
Epidermal Keratinocytes ◽  
Synthetic Analog ◽  
Proliferating Cells ◽  
Human Epidermal Keratinocytes ◽  
Epidermal Pentapeptide

A pentapeptide that inhibits proliferation of mouse epidermal keratinocytes in vivo and in vitro has been purified from mouse skin extracts. In the present study the effect of a synthetic analog of the epidermal pentapeptide on proliferation and differentiation of cultured human epidermal keratinocytes was investigated. In young, rapidly growing primary cultures the pentapeptide caused a dramatic decrease in mitotic activity and also induced pronounced changes in the balance between kinetically defined subpopulations of proliferating cells. A dipeptide derived from the pentapeptide was found to be at least as potent. A serine derivative of a hemoregulatory peptide also seemed to be active. When tested in epidermal cultures regenerating after removal of the suprabasal cell layers, both the pentapeptide and the dipeptide were shown to cause a delay in the proliferative response. Both peptides were also able to stimulate early (increase in cell size) and late (cornified envelope formation) events in the differentiation pathway of the keratinocyte. The apparent stimulatory effect on differentiation was most clearly seen in regenerating cultures, whereas the effect on primary cultures varied with the experimental set-up. It is suggested that homologous epidermal peptide(s) may play a major role in the regulation of human epidermal homeostasis.

scholarly journals Targeted Deletion of Rad9 in Mouse Skin Keratinocytes Enhances Genotoxin-Induced Tumor Development

2008 ◽  
Vol 68 (14) ◽  
pp. 5552-5561 ◽  
Author(s):  
Zhishang Hu ◽  
Yuheng Liu ◽  
Chunbo Zhang ◽  
Yun Zhao ◽  
Wei He ◽  
...  
Keyword(s):  
Tumor Development ◽  
Mouse Skin ◽  
Targeted Deletion ◽  
Skin Keratinocytes ◽  
Mouse Skin Keratinocytes
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