Compliance-induced adherens junction formation in epithelial cells and tissues is regulated by JNK

You, Hui; Padmashali, Roshan M.; Ranganathan, Aishwarya; Lei, Pedro; Girnius, Nomeda; Davis, Roger J.; Andreadis, Stelios T.

doi:10.1242/jcs.122903

Cited by 24 publications

(24 citation statements)

References 63 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For example, the rapid adherens junction disassembly of T84 and SK-CO15 cell monolayers was accompanied by JNK activation and prevented by JNK inhibition (Naydenov et al, 2009), similar to our observations in JNK-inhibited fetal ovaries. Here too, as we observed in the SP600125-treated ovaries, E-cadherin and β-catenin are upregulated when JNK function is disrupted (Lee et al, 2009;You et al, 2013). Furthermore, JNK activation has been associated with E-cadherin inactivation and cell polarity loss in Drosophila epithelial cells (Igaki et al, 2006).…”

Section: Discussionsupporting

confidence: 60%

JNK signaling regulates E-cadherin junctions in germline cysts and determines primordial follicle formation in mice

Niu¹,

Wang²,

Wang³

et al. 2016

Journal of Cell Science

View full text Add to dashboard Cite

Physiologically, the size of the primordial follicle pool determines the reproductive lifespan of female mammals, while its establishment largely depends on a process of germline cyst breakdown during the perinatal period. The mechanisms regulating this process are poorly understood. Here we demonstrate that c-Jun amino-terminal kinase (JNK) signaling is crucial for germline cyst breakdown and primordial follicle formation. JNK was specifically localized in oocytes and its activity increased as germline cyst breakdown progressed. Importantly, disruption of JNK signaling with a specific inhibitor (SP600125) or knockdown technology (Lenti-JNK-shRNAs) resulted in significantly suppressed cyst breakdown and primordial follicle formation in cultured mouse ovaries. Our results show that E-cadherin is intensely expressed in germline cysts, and that its decline is necessary for oocyte release from the cyst. However, inhibition of JNK signaling leads to aberrantly enhanced localization of E-cadherin at oocyte-oocyte contact sites. WNT4 expression is upregulated after SP600125 treatment. Additionally, similar to the effect of SP600125 treatment, WNT4 overexpression delays cyst breakdown and is accompanied by abnormal E-cadherin expression patterns. In conclusion, our results suggest that JNK signaling, which is inversely correlated with WNT4, plays an important role in perinatal germline cyst breakdown and primordial follicle formation by regulating E-cadherin junctions between oocytes in mouse ovaries.

show abstract

Section: Discussionsupporting

confidence: 60%

JNK signaling regulates E-cadherin junctions in germline cysts and determines primordial follicle formation in mice

Niu¹,

Wang²,

Wang³

et al. 2016

Journal of Cell Science

View full text Add to dashboard Cite

show abstract

“…Recently, our laboratory showed that substrate stiffness regulated AJ formation between epithelial cells in two-dimensional (2D) cultures and in three-dimensional (3D) epidermal tissues in vitro and in vivo by regulating the phosphorylation levels of the c-Janus N-terminal kinase (JNK) [51]. Rigid substrates led to JNK activation and AJ disassembly, while soft matrices suppressed JNK activity leading to AJ formation.…”

Section: Adherens Junctions: Signal Transduction and Mechanosensingmentioning

confidence: 99%

CDH2 and CDH11 act as regulators of stem cell fate decisions

2015

Self Cite

View full text Add to dashboard Cite

Accumulating evidence suggests that the mechanical and biochemical signals originating from cell-cell adhesion are critical for stem cell lineage specification. In this review, we focus on the role of cadherin mediated signaling in development and stem cell differentiation, with emphasis on two well-known cadherins, cadherin-2 (CDH2) (N-cadherin) and cadherin-11 (CDH11) (OB-cadherin). We summarize the existing knowledge regarding the role of CDH2 and CDH11 during development and differentiation in vivo and in vitro. We also discuss engineering strategies to control stem cell fate decisions by fine-tuning the extent of cell-cell adhesion through surface chemistry and microtopology. These studies may be greatly facilitated by novel strategies that enable monitoring of stem cell specification in real time. We expect that better understanding of how intercellular adhesion signaling affects lineage specification may impact biomaterial and scaffold design to control stem cell fate decisions in three-dimensional context with potential implications for tissue engineering and regenerative medicine.

show abstract

“… 37 It is well known that stiffness of substrates mediates the cross talk between cell-substrate and cell-cell adhesion 38 . Under low Ca 2+ concentration, epithelial cells prefer to stay as individual cells and adhere firmly on stiff substrate through integrin-mediated focal adhesion.…”

Section: Cell-cell Junction Formationmentioning

confidence: 99%

JNK is a novel regulator of intercellular adhesion

You¹,

Lei²,

Andreadis³

2013

Tissue Barriers

Self Cite

View full text Add to dashboard Cite

c-Jun N-terminal Kinase (JNK) is a family of protein kinases, which are activated by stress stimuli such as inflammation, heat stress and osmotic stress, and regulate diverse cellular processes including proliferation, survival and apoptosis. In this review, we focus on a recently discovered function of JNK as a regulator of intercellular adhesion. We summarize the existing knowledge regarding the role of JNK during the formation of cell-cell junctions. The potential mechanisms and implications for processes requiring dynamic formation and dissolution of cell-cell junctions including wound healing, migration, cancer metastasis and stem cell differentiation are also discussed.

show abstract

Compliance-induced adherens junction formation in epithelial cells and tissues is regulated by JNK

Cited by 24 publications

References 63 publications

JNK signaling regulates E-cadherin junctions in germline cysts and determines primordial follicle formation in mice

JNK signaling regulates E-cadherin junctions in germline cysts and determines primordial follicle formation in mice

CDH2 and CDH11 act as regulators of stem cell fate decisions

JNK is a novel regulator of intercellular adhesion

Contact Info

Product

Resources

About