β-catenin signaling

Lam, Anna; Gottardi, Cara J.

doi:10.1097/bor.0b013e32834b3309

Cited by 166 publications

(82 citation statements)

References 46 publications

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“…Potentiating endogenous Wnt/β-catenin signaling promoted skin wound healing [40], which was partially attributable to the elevated proliferation, migration and local invasion of fibroblasts [41]. Thus, the activity of wnt3a and β-catenin in Wnt/ β -catenin signaling may be important for TGF-β2 to production of COLI.…”

Section: Discussionmentioning

confidence: 99%

Adipose-derived stem cells cooperate with fractional carbon dioxide laser in antagonizing photoaging: a potential role of Wnt and β-catenin signaling

Wang

Liu³

et al. 2014

Cell Biosci

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BackgroundIt is well established that adipose-derived stem cells (ADSCs) produce and secrete cytokines/growth factors that antagonize UV-induced photoaging of skin. However, the exact molecular basis underlying the anti-photoaging effects exerted by ADSCs is not well understood, and whether ADSCs cooperate with fractional carbon dioxide (CO2) laser to facilitate photoaging skin healing process has not been explored. Here, we investigated the impacts of ADSCs on photoaging in a photoaging animal model, its associated mechanisms, and its functional cooperation with fractional CO2 laser in treatment of photoaging skin.ResultsWe showed that ADSCs improved dermal thickness and activated the proliferation of dermal fibroblast. We further demonstrated that the combined treatment of ADSCs and fractional CO2 laser, the latter which is often used to resurface skin and treat wrinkles, had more beneficial effects on the photoaging skin compared with each individual treatment. In our prepared HDF photoaging model, flow cytometry showed that, after adipose derived stem cells conditioned medium (ADSC-CM) co-cultured HDF photoaging model, the cell proliferation rate is higher than UVB irradiation induced HDF modeling (p < 0.05). Additionally, the expressions of β-catenin and Wnt3a, which were up-regulated after the transplantation of ADSCs alone or in combination with fractional CO2 laser treatment. And the expression of wnt3a and β-catenin has the positive correlation with photoaging related protein TGF-β2 and COLI. We also verified these protein expressions in tissue level. In addition, after injected SFRP2 into ADSC-CM co-cultured HDF photoaging model, wnt3a inhibitor, compared with un-intervened group, wnt3a, β-catenin protein level significantly decreased.ConclusionBoth ADSCs and fractional CO2 laser improved photoaging skin at least partially via targeting dermal fibroblast activity which was increased in photoaging skin. The combinatorial use of ADSCs and fractional CO2 laser synergistically improved the healing process of photoaging skin. Thus, we provide a strong rationale for a combined use of ADSCs and fractional CO2 laser in treatment of photoaging skin in clinic in the future. Moreover, we provided evidence that the Wnt/β-catenin signaling pathway may contribute to the activation of dermal fibroblast by the transplantation of ADSCs in both vitro and vivo experiment.

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Section: Discussionmentioning

confidence: 99%

Adipose-derived stem cells cooperate with fractional carbon dioxide laser in antagonizing photoaging: a potential role of Wnt and β-catenin signaling

Wang

Liu³

et al. 2014

Cell Biosci

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“…65–67 The role of Wnt/β-catenin signaling in fibro-proliferative disorders was initially supported by strong correlations between β-catenin mutations and aggressive fibromatosis in human desmoids tumors. 68,69 Consistently, forced activation of β-catenin employing a mutant that resists ubiquitination-dependent degradation, is sufficient to drive exuberant collagen synthesis and fibrosis.…”

Section: β-Catenin Dependent Mechanismmentioning

confidence: 99%

The GSK-3 Family as Therapeutic Target for Myocardial Diseases

Lal

Ahmad

Woodgett

et al. 2015

Circulation Research

184

154

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GSK-3 is one of the very few signaling molecules that regulate a truly astonishing number of critical intracellular signaling pathways. It has been implicated in a number of diseases including heart failure, bipolar disorder, diabetes, Alzheimer’s disease, aging, inflammation and cancer. Furthermore, a recent clinical trial has validated the feasibility of targeting GSK-3 with small molecule inhibitors for human diseases. In the current review we will focus on its expanding role in the heart, concentrating primarily on recent studies that have employed cardiomyocyte- and fibroblast-specific conditional gene deletion in mouse models. We will highlight the role of the GSK-3 isoforms in various pathological conditions including myocardial aging, ischemic injury, myocardial fibrosis and cardiomyocyte proliferation. We will discuss our recent findings that deletion of GSK-3α specifically in cardiomyocytes attenuates ventricular remodeling and cardiac dysfunction post-MI by limiting scar expansion and promoting cardiomyocyte proliferation. The recent emergence of GSK-3β as a regulator of myocardial fibrosis will also be discussed. We will review our very recent findings that specific deletion of GSK-3β in cardiac fibroblasts leads to fibrogenesis, left ventricular dysfunction and excessive scarring in the ischemic heart. Finally, we will examine the underlying mechanisms that drive the aberrant myocardial fibrosis in the models in which GSK-3β is specifically deleted in cardiac fibroblasts. We will summarize these recent results and offer explanations, whenever possible, and hypotheses when not. For these studies we will rely heavily on our models and those of others to reconcile some of the apparent inconsistencies in the literature.

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“…Not only do cells exhibit different genetic expression profiles as they transition into the adult scar-forming phenotype, developmental stage and tissue of origin dramatically impact how fibroblasts respond to Wnt signaling (Lam and Gottardi, 2011). For example, Carre et al elucidated differences between mouse embryonic (E16.5) fibroblasts and postnatal (P1) fibroblasts following stimulation with Wnt-3a.…”

Section: Recent Advances In Scarless Wound Healing Researchmentioning

confidence: 99%

Scarless wound healing: finding the right cells and signals

et al. 2016

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From the moment we are born, every injury to the skin has the potential to form a scar, many of which can impair form and/or function. As such, scar management constitutes a billion-dollar industry. Yet effectively promoting scarless wound healing remains an elusive goal. The complex interactions of wound healing contribute to our inability to recapitulate scarless wound repair as it occurs in nature, such as in fetal skin and oral mucosa. However, many new advances have occurred over recent years, some of which have translated scientific findings from bench to bedside. In vivo lineage tracing has helped establish a variety of novel cellular culprits that may act as key drivers of the fibrotic response. These newly characterized cell populations present further targets for therapeutic intervention, some of which have already demonstrated promising results in animal models. Here, we discuss several recent studies that identify exciting approaches to diminishing scar formation (Fig. 1). Particular attention will also be paid to the canonical Wnt/β-catenin signaling pathway, which plays an important role in both embryogenesis and tissue repair. New insights into the differential effects of Wnt signaling on heterogeneous fibroblast and keratinocyte populations within the skin further demonstrate methods by which wound healing can be redirected to a more fetal, scarless phenotype.

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β-catenin signaling

Cited by 166 publications

References 46 publications

Adipose-derived stem cells cooperate with fractional carbon dioxide laser in antagonizing photoaging: a potential role of Wnt and β-catenin signaling

Adipose-derived stem cells cooperate with fractional carbon dioxide laser in antagonizing photoaging: a potential role of Wnt and β-catenin signaling

The GSK-3 Family as Therapeutic Target for Myocardial Diseases

Scarless wound healing: finding the right cells and signals

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