Effects of the Selective Protein Kinase C Inhibitor, Ro 31-7549, on the Proliferation of Cultured Mouse Epidermal Keratinocytes

Bollag, Wendy B.; Ducote, Janet; Harmon, Charles S.

doi:10.1111/1523-1747.ep12468992

Cited by 30 publications

(34 citation statements)

References 23 publications

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“…With the same inhibitor Le Panse et al (19) demonstrated that PKC controlled negatively keratinocyte growth in response to EGF and KGF. Using Ro 31-7549, another selective PKC inhibitor, it has been shown that the loss of proliferative capacity in differentiating epidermal keratinocyte cultures may be mediated, at least in part, by PKC (20). Inhibition or downregulation of PKC could lead to increased DNA synthesis (21).…”

Section: Pkc Has Antiproliferation Properties In Keratinocytesmentioning

confidence: 99%

Signal transduction in keratinocytes

Mitev

Miteva

1999

Experimental Dermatology

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Signal transduction in keratinocytesand their proliferation and differentiation are stimulated by a variety of biological factors. The major mechanism by which cells (keratinocytes) respond to extracellular signals, is changing in protein phosphorylation. Key words: keratinocytes -proliferation -The protein phosphorylation is a consequence of the ligand/receptor binddifferentiation -protein kinases -STAT ing which leads to activation of several transduction systems. In this review we emphasize on different signal transduction pathways in kera-

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Section: Pkc Has Antiproliferation Properties In Keratinocytesmentioning

confidence: 99%

Signal transduction in keratinocytes

Mitev

Miteva

1999

Experimental Dermatology

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“…Primary epidermal keratinocytes were prepared from 1-to 3-day-old neonatal CD1 mice and cultured as described (6). Briefly, after trypsinization of the Downloaded from https://academic.oup.com/carcin/article-abstract/20/4/569/2526632 by guest on 07 June 2019 skin, the epidermis was mechanically separated from the dermis, and epidermal cells were released by scraping.…”

Section: Cell Culturementioning

confidence: 99%

“…One such agent is bradykinin, which increases cellular inositol phosphates (2)(3)(4)(5) and DAG (4) and can presumably activate PKC. We (6) and others have provided evidence that PKC activity, in turn, is involved in terminal differentiation of these cells (reviewed in 1). PKC can also be activated directly by tumor-promoting phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate (TPA), which has been shown to inhibit proliferation and stimulate differentiation of keratinocytes (7)(8)(9).…”

Section: Introductionmentioning

confidence: 99%

Sustained phospholipase D activation is associated with keratinocyte differentiation

et al. 1999

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Our previous results and data in the literature have suggested a potential role for phospholipase D (PLD) in the regulation of epidermal keratinocyte growth and differentiation. Therefore, we investigated the effect of agents reported to modulate keratinocyte growth and differentiation on PLD activation. The purported protein kinase C (PKC) 'inhibitor', staurosporine (Stsp), has been reported to activate PKC in keratinocytes, eliciting many of the same effects as active tumor promoters such as 12-Otetradecanoylphorbol-13-acetate (TPA). Stsp also induces a programmed pattern of differentiation similar to that seen in keratinocytes in vivo; TPA, on the other hand, appears to preferentially elicit markers consistent with late (granular) differentiation. In contrast, bradykinin is reported to stimulate keratinocyte proliferation. We found that these three agents had different effects on PLD activation in primary mouse epidermal keratinocytes. TPA increased PLD activity acutely and in a sustained fashion. In contrast, Stsp did not acutely activate PLD and inhibited acute TPA-induced activation of PLD. However, treatment of keratinocytes with Stsp for longer time periods (3-5 h) induced sustained PLD activation and this long-term effect was additive with that of TPA. Bradykinin activated PLD acutely but transiently. Both TPA and Stsp increased transglutaminase activity, a marker of late differentiation, whereas bradykinin had little or no effect on either cell proliferation or transglutaminase activity. These results suggest that a sustained activation of PLD is associated with the induction of keratinocyte differentiation. We hypothesize that PLD activity mediates late keratinocyte differentiation through generation of diacylglycerol and activation of specific PKC isoforms. Furthermore, we propose that the profound and immediate TPA-induced stimulation of PLD activity 'drives' the keratinocytes to late differentiation steps. However, the less efficacious (and more gradual) sustained activation of PLD by Stsp may allow a patterned differentiation more like that observed in skin.

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“…It is well known that keratinocyte differentiation plays an important role in activating the intracellular signal transduction system by delivering external stimuli. For example, keratinocyte differentiation-promoting factors, such as calcium, are known to activate protein kinase C and affect downstream signaling systems (Matsui et al, 1992;Dlugosz & Yuspa, 1993;Bollag et al, 1993;O'Driscoll et al, 1994). The activation of mitogen-activated protein kinases, such as ERK1/2 and p38, has also been shown to play a pivotal role in keratinocyte differentiation (Efimova et al, 2003;Eckert et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Sophora japonica extracts accelerates keratinocyte differentiation through miR-181a

Kim¹,

Jun

Joo³

et al. 2018

biomed dermatol

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Background: The Sophora japonica extracts contain flavonol triglycoside, isoflavonol, coumarone chromone, saponin, triterpene glucoside, phospholipids, alkaloids, amino acids, polysaccharides, and fatty acids. These components have physiological effects such as anti-infertility and anti-cancer activities. This study investigated the regulation of keratinocyte differentiation upon treatment with the S. japonica extracts in keratinocyte and the molecular cell biological mechanism involved. Methods: To determine whether the S. japonica extracts or troxerutin, which is its main component, regulates keratinocyte differentiation, quantitative real-time polymerase chain reaction (qRT-PCR) was performed on keratinocyte differentiation markers such as keratin 1 (K1), keratin 10 (K10), involucrin, and filaggrin after treatment with the S. japonica extracts. miR-181a knockdown confirmed that keratinocyte differentiation was regulated by increased miR-181a expression upon treatment with the S. japonica extracts or troxerutin.

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Effects of the Selective Protein Kinase C Inhibitor, Ro 31-7549, on the Proliferation of Cultured Mouse Epidermal Keratinocytes

Cited by 30 publications

References 23 publications

Signal transduction in keratinocytes

Signal transduction in keratinocytes

Sustained phospholipase D activation is associated with keratinocyte differentiation

Sophora japonica extracts accelerates keratinocyte differentiation through miR-181a

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