Transdifferentiation of tadpole pancreatic acinar cells to duct cells mediated by Notch and stromelysin-3

Mukhi, Sandeep; Brown, Donald D.

doi:10.1016/j.ydbio.2010.12.020

Cited by 15 publications

(8 citation statements)

References 40 publications

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“…Metalloproteinases obviously play important role in the migration of mesodermal cells and their transdifferentiation. ECM and different MMP are known to play significant role in cell transformation of vertebrates [75], [76], [77], [78]. The studies of this process in E. fraudatrix could clarify the natural mechanisms of transdifferentiation and the roles of ECM remodeling and proteases in this process.…”

Section: Discussionmentioning

confidence: 98%

Proteases from the Regenerating Gut of the Holothurian Eupentacta fraudatrix

Lamash

Dolmatov

2013

PLoS ONE

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Four proteases with molecular masses of 132, 58, 53, and 47 kDa were detected in the digestive system of the holothurian Eupentacta fraudatrix. These proteases displayed the gelatinase activity and characteristics of zinc metalloproteinases. The 58 kDa protease had similar protease inhibitor sensitivity to that of mammalian matrix metalloproteinases. Zymographic assay revealed different lytic activities of all four proteases during intestine regeneration in the holothurian. The 132 kDa protease showed the highest activity at the first stage. During morphogenesis (stages 2–4 of regeneration), the highest activity was measured for the 53 and 58 kDa proteases. Inhibition of protease activity exerts a marked effect on regeneration, which was dependent on the time when 1,10-phenanthroline injections commenced. When metalloproteinases were inhibited at the second stage of regeneration, the restoration rates were decreased. However, such an effect proved to be reversible, and when inhibition ceased, the previous rate of regeneration was recovered. When protease activity is inhibited at the first stage, regeneration is completely abolished, and the animals die, suggesting that early activation of the proteases is crucial for triggering the regenerative process in holothurians. The role of the detected proteases in the regeneration processes of holothurians is discussed.

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Section: Discussionmentioning

confidence: 98%

Proteases from the Regenerating Gut of the Holothurian Eupentacta fraudatrix

Lamash

Dolmatov

2013

PLoS ONE

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“…There were no differences between the CPZþN and CPZþPBS groups at the eighth week, which reached 20,396.96 AE 2047.39 and 19,747.35 AE 1682.11 mm, respectively (Figure 1(d) and (e)). However, the total distance traveled of mice in the CPZþPTU group was only 15,803.98 AE 1241.49 mm, shorter than that of the CPZþN group (20,396.96 AE 2047.39 mm) (P < 0.05) (Figure 1(d) and (e)). Conversely, the total distance traveled by mice in the CPZþT3 group was 21,167.86 AE 1646.75 mm, longer than that of the CPZþPBS group (19,747.35 AE 1682.11) (P < 0.05) (Figure 1(d) and (e)).…”

Section: Th Stimulates the Recovery Of Body Weight And Behaviors Impamentioning

confidence: 92%

“…16 TH is also necessary for arresting the cell cycle, 17,18 producing the myelin sheath 19 and transdifferentiation. 20 In addition to a role in the differentiation and maturation of oligodendrocytes via nuclear hormone receptors, TH also plays a role in the migration of OPCs in the subventricular zone (SVZ). [21][22][23] A recent study shows that the effect of TH on cortical remyelination alleviates CPZinduced demyelination.…”

Section: Introductionmentioning

confidence: 99%

Thyroid hormone alleviates demyelination induced by cuprizone through its role in remyelination during the remission period

Zhang

Zhan

et al. 2015

Exp Biol Med (Maywood)

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Multiple sclerosis (MS) is a disease induced by demyelination in the central nervous system, and the remission period of MS is crucial for remyelination. In addition, abnormal levels of thyroid hormone (TH) have been identified in MS. However, in the clinic, insufficient attention has been paid to the role of TH in the remission period. Indeed, TH not only functions in the development of the brain but also affects myelination. Therefore, it is necessary to observe the effect of TH on remyelination during this period. A model of demyelination induced by cuprizone (CPZ) was used to observe the function of TH in remyelination during the remission period of MS. Through weighing and behavioral tests, we found that TH improved the physical symptoms of mice impaired by CPZ. Supplementation of TH led to the repair of myelin as detected by immunohistochemistry and western blot. In addition, a sufficient TH supply resulted in an increase in myelinated axons without affecting myelin thickness and g ratio in the corpus callosum, as detected by electron microscopy. Double immunostaining with myelin basic protein and neurofilament 200 (NF200) showed that the CPZ-induced impairment of axons was alleviated by TH. Conversely, insufficient TH induced by 6-propyl-2-thiouracil resulted in the enlargement of mitochondria. Furthermore, we found that an adequate supply of TH promoted the proliferation and differentiation of oligodendrocyte lineage cells by immunofluorescence, which was beneficial to remyelination. Further, we found that TH reduced the number of astrocytes without affecting microglia. Conclusively, it was shown that TH alleviated demyelination induced by CPZ by promoting the development of oligodendrocyte lineage cells and remyelination. The critical time for remyelination is the remission period of MS. TH plays a significant role in alleviating demyelination during the remission period in the clinical treatment of MS.

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“…Interestingly, in studies on the postnatal developing gut in the mouse or on various organs of amphibians during TH-dependent metamorphosis, TH signaling has been shown to control several components of the Notch pathway (Kress et al, 2009;Buchholz et al, 2007;Mukhi and Brown, 2011;Sun et al, 2013;Das et al, 2006). However, it is not clear whether this control results in Notch activation, and the mechanisms of such regulation and its biological significance have remained largely unknown.…”

Section: Introductionmentioning

confidence: 99%

The thyroid hormone nuclear receptor TRα1 controls the Notch signaling pathway and cell fate in murine intestine

et al. 2015

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Thyroid hormones control various aspects of gut development and homeostasis. The best-known example is in gastrointestinal tract remodeling during amphibian metamorphosis. It is well documented that these hormones act via the TR nuclear receptors, which are hormone-modulated transcription factors. Several studies have shown that thyroid hormones regulate the expression of several genes in the Notch signaling pathway, indicating a possible means by which they participate in the control of gut physiology. However, the mechanisms and biological significance of this control have remained unexplored. Using multiple in vivo and in vitro approaches, we show that thyroid hormones positively regulate Notch activity through the TRα1 receptor. From a molecular point of view, TRα1 indirectly controls Notch1, Dll1, Dll4 and Hes1 expression but acts as a direct transcriptional regulator of the Jag1 gene by binding to a responsive element in the Jag1 promoter. Our findings show that the TRα1 nuclear receptor plays a key role in intestinal crypt progenitor/stem cell biology by controlling the Notch pathway and hence the balance between cell proliferation and cell differentiation.

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Transdifferentiation of tadpole pancreatic acinar cells to duct cells mediated by Notch and stromelysin-3

Cited by 15 publications

References 40 publications

Proteases from the Regenerating Gut of the Holothurian Eupentacta fraudatrix

Proteases from the Regenerating Gut of the Holothurian Eupentacta fraudatrix

Thyroid hormone alleviates demyelination induced by cuprizone through its role in remyelination during the remission period

The thyroid hormone nuclear receptor TRα1 controls the Notch signaling pathway and cell fate in murine intestine

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