scholarly journals Apoptosis is a generator of Wnt-dependent regeneration and homeostatic cell renewal in the ascidian Ciona

Biology Open ◽  
2021 ◽  
Vol 10 (4) ◽  
Author(s):  
William R. Jeffery ◽  
Špela Gorički
Keyword(s):  
Stem Cells ◽  
Wnt Signaling ◽  
Progenitor Cells ◽  
Adult Stem Cells ◽  
Cell Renewal ◽  
Body Parts ◽  
Wound Site ◽  
And Function ◽  
Canonical Wnt ◽  
Organ Replacement

ABSTRACT In the ascidian Ciona intestinalis, basal body parts regenerate distal structures but distal body parts do not replace basal structures. Regeneration involves the activity of adult stem cells in the branchial sac, which proliferate and produce migratory progenitor cells for tissue and organ replacement. Branchial sac-derived stem cells also replenish recycling cells lining the pharyngeal fissures during homeostatic growth. Apoptosis at injury sites occurs early during regeneration and continuously in the pharyngeal fissures during homeostatic growth. Caspase 1 inhibitor, caspase 3 inhibitor, or pan-caspase inhibitor Z-VAD-FMK treatment blocked apoptosis, prevented regeneration, and suppressed branchial sac growth and function. A pharmacological screen and siRNA-mediated gene knockdown indicated that regeneration requires canonical Wnt signaling. Wnt3a protein rescued both caspase-blocked regeneration and branchial sac growth. Inhibition of apoptosis did not affect branchial sac stem cell proliferation but prevented the survival of progenitor cells. After bisection across the mid-body, apoptosis occurred only in the regenerating basal fragments, although both fragments contained a part of the branchial sac, suggesting that apoptosis is unilateral at the wound site and the presence of branchial sac stem cells is insufficient for regeneration. The results suggest that apoptosis-dependent Wnt signaling mediates regeneration and homeostatic growth in Ciona.

scholarly journals Apoptosis is a generator of Wnt-dependent regeneration and homeostatic cell renewal in the ascidian Ciona

2020 ◽  
Author(s):  
William R. Jeffery ◽  
Spela Goricki
Keyword(s):  
Stem Cells ◽  
Wnt Signaling ◽  
Progenitor Cells ◽  
Adult Stem Cells ◽  
Cell Renewal ◽  
Body Parts ◽  
Transient Event ◽  
Wound Site ◽  
And Function ◽  
Canonical Wnt

AbstractBody regeneration is unilateral in the ascidian Ciona intestinalis: severed basal body parts can regenerate distal structures, such as the siphons and neural complex, but severed distal body parts do not replace basal structures. Regeneration involves the activity of adult stem cells in vasculature of the branchial sac, which are induced to proliferate and produce migratory progenitor cells for the replacement of missing tissues and organs. Branchial sac-derived stem cells also replenish continuously recycling cells lining the pharyngeal fissures during homeostatic growth. Apoptosis at injury sites is an early and transient event of regeneration and occurs continuously in the pharyngeal fissures during homeostatic growth. Treatment of amputated animals with caspase 1 inhibitor, caspase 3 inhibitor, or the pan-caspase inhibitor Z-VAD-FMK blocked apoptosis, prevented regeneration, and suppressed the growth and function of the branchial sac. A pharmacological screen and inhibitory siRNA treatments indicated that regeneration and homeostatic growth require canonical Wnt signaling. Furthermore, exogenously supplied recombinant Wnt3a protein rescued both caspase-blocked regeneration and normal branchial sac growth. As determined by EdU pulse-chase studies, inhibition of apoptosis did not affect branchial sac stem cell proliferation but instead prevented the survival of progenitor cells. After bisection across the mid-body, apoptosis at the injury site occurred in the regenerating basal fragments, but not in the non-regenerating distal fragments, although both fragments contain a large portion of the branchial sac, suggesting that apoptosis is unilateral at the wound site and the presence of branchial sac stem cells is insufficient for regeneration. The results show that apoptosis-dependent Wnt signaling mediates regeneration and homeostatic growth by promoting progenitor cell survival in Ciona.

scholarly journals Reciprocal interaction between mesenchymal stem cells and transit amplifying cells regulates tissue homeostasis

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Junjun Jing ◽  
Jifan Feng ◽  
Jingyuan Li ◽  
Hu Zhao ◽  
Thach-Vu Ho ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Wnt Signaling ◽  
Adult Stem Cells ◽  
Cell Types ◽  
Tissue Homeostasis ◽  
Canonical Wnt Signaling ◽  
Multiple Organs ◽  
Canonical Wnt

Interaction between adult stem cells and their progeny is critical for tissue homeostasis and regeneration. In multiple organs, mesenchymal stem cells (MSCs) give rise to transit amplifying cells (TACs), which then differentiate into different cell types. However, whether and how MSCs interact with TACs remains unknown. Using the adult mouse incisor as a model, we present in vivo evidence that TACs and MSCs have distinct genetic programs and engage in reciprocal signaling cross talk to maintain tissue homeostasis. Specifically, an IGF-WNT signaling cascade is involved in the feedforward from MSCs to TACs. TACs are regulated by tissue-autonomous canonical WNT signaling and can feedback to MSCs and regulate MSC maintenance via Wnt5a/Ror2-mediated non-canonical WNT signaling. Collectively, these findings highlight the importance of coordinated bidirectional signaling interaction between MSCs and TACs in instructing mesenchymal tissue homeostasis, and the mechanisms identified here have important implications for MSC–TAC interaction in other organs.

scholarly journals Effect of Wnt Signaling on the Differentiation of Islet β-Cells from Adipose-Derived Stem Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Hefei Wang ◽  
Yu Ren ◽  
Xiao Hu ◽  
Min Ma ◽  
Xiao Wang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Protein Expression ◽  
Wnt Signaling ◽  
Mrna Expression ◽  
Adult Stem Cells ◽  
Adipose Derived Stem Cells ◽  
Β Cells ◽  
Pancreatic Development ◽  
Mrna And Protein Expression ◽  
And Function

The Wnt signaling is critical for pancreatic development and islet function; however, its precise effects on the development and function of the β-cells remain controversial. Here we examined mRNA and protein expression of components of the Wnt signaling throughout the differentiation of islet β-cells from adipose-derived stem cells (ADSCs). After induction, ADSCs expressed markers of β-cells, including the insulin, PDX1, and glucagon genes, and the PDX1, CK19, nestin, insulin, and C-peptide proteins, indicating their successful differentiation. Compared with pancreatic adult stem cells (PASCs), the quantities of insulin, GLUT2, and Irs2 mRNA decreased, whereas Gcg, Gck, and Irs1 mRNA increased. Over time, during differentiation, insulin mRNA and protein expression increased, Gcg and Gck mRNA expression increased, Irs1 mRNA expression decreased and then increased, and Irs2 mRNA increased and then decreased (all P<0.05). The expression of Dvl-2, LRP5, and GSK3β mRNA as well as the Dvl-2, GSK3β, and p-GSK3β proteins also increased (P<0.05). Expression of TCF7L2 (6–10 d) and β-catenin mRNA as well as the β-catenin protein increased but not significantly (P>0.05). Our results indicate that the Wnt signaling is activated during ADSC differentiation into islet β-cells, but there was no obvious enrichment of nonphosphorylated β-catenin protein.

scholarly journals Wnt Signaling in Vascular Calcification

2021 ◽  
Vol 8 ◽  
Author(s):  
Kaylee Bundy ◽  
Jada Boone ◽  
C. LaShan Simpson
Keyword(s):  
Cardiovascular Disease ◽  
Wnt Signaling ◽  
Signaling Pathway ◽  
Vascular Calcification ◽  
Arterial Wall ◽  
Wnt Signaling Pathway ◽  
Phenotypic Switch ◽  
Wnt Ligands ◽  
And Function ◽  
Canonical Wnt

Cardiovascular disease is a worldwide epidemic and considered the leading cause of death globally. Due to its high mortality rates, it is imperative to study the underlying causes and mechanisms of the disease. Vascular calcification, or the buildup of hydroxyapatite within the arterial wall, is one of the greatest contributors to cardiovascular disease. Medial vascular calcification is a predictor of cardiovascular events such as, but not limited to, hypertension, stiffness, and even heart failure. Vascular smooth muscle cells (VSMCs), which line the arterial wall and function to maintain blood pressure, are hypothesized to undergo a phenotypic switch into bone-forming cells during calcification, mimicking the manner by which mesenchymal stem cells differentiate into osteoblast cells throughout osteogenesis. RunX2, a transcription factor necessary for osteoblast differentiation and a target gene of the Wnt signaling pathway, has also shown to be upregulated when calcification is present, implicating that the Wnt cascade may be a key player in the transdifferentiation of VSMCs. It is important to note that the phenotypic switch of VSMCs from a healthy, contractile state to a proliferative, synthetic state is necessary in response to the vascular injury surrounding calcification. The lingering question, however, is if VSMCs acquire this synthetic phenotype through the Wnt pathway, how and why does this signaling occur? This review seeks to highlight the potential role of the canonical Wnt signaling pathway within vascular calcification based on several studies and further discuss the Wnt ligands that specifically aid in VSMC transdifferentiation.

scholarly journals Canonical Wnt-signaling modulates the tempo of dendritic growth of adult-born hippocampal neurons

2020 ◽  
Author(s):  
Jana Heppt ◽  
Marie-Theres Wittmann ◽  
Jingzhong Zhang ◽  
Daniela Vogt-Weisenhorn ◽  
Nilima Prakash ◽  
...  
Keyword(s):  
Young Adult ◽  
Wnt Signaling ◽  
Progenitor Cells ◽  
Dendritic Growth ◽  
Functional Integration ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Canonical Wnt Signaling ◽  
Adult Born Neurons ◽  
Canonical Wnt

AbstractIn adult hippocampal neurogenesis neural stem/progenitor cells generate new dentate granule neurons that contribute to hippocampal plasticity. The establishment of a morphologically defined dendritic arbor is central to the functional integration of adult-born neurons. Here, we investigated the role of canonical Wnt/β-catenin-signaling in dendritogenesis of adult-born neurons. We show that canonical Wnt-signaling follows a biphasic pattern, with high activity in stem/progenitor cells, attenuation in early immature neurons, and re-activation during maturation, and demonstrate that the biphasic activity pattern is required for proper dendrite development. Increasing β-catenin-signaling in maturing neurons of young adult mice transiently accelerated dendritic growth, but eventually resulted in dendritic defects and excessive spine numbers. In middle-aged mice, in which protracted dendrite and spine development was paralleled by lower canonical Wnt-signaling activity, enhancement of β-catenin-signaling restored dendritic growth and spine formation to levels observed in young adult animals. Our data indicate that precise timing and strength of β-catenin-signaling is essential for the correct functional integration of adult-born neurons and suggest Wnt/β-catenin-signaling as a pathway to ameliorate deficits in adult neurogenesis during aging.

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