Phosphatase-Mediated Crosstalk Control of ERK and p38 MAPK Signaling in Corneal Epithelial Cells

Wang, Zheng; Yang, Hua; Tachado, Souvenir D.; Capó-Aponte, José E.; Bildin, Victor N.; Koziel, Henry; Reinach, Peter S.

doi:10.1167/iovs.06-0642

Cited by 77 publications

(78 citation statements)

References 25 publications

(25 reference statements)

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“…Thus, a phosphatase-mediated crosstalk may exist between protein prenylation and the MAPK pathway in the regulation of neuronal differentiation from mouse ES cells promoted by IBA. Moreover, there may be a negative feedback regulation of their phosphorylation [17,36] . Otherwise, ERK, p38, and JNK may be downstream targets of protein prenylation.…”

Section: Discussionmentioning

confidence: 99%

“…GGTase I is also associated with the mitogen-activated protein kinase (MAPK) pathway [10] . The MAPK pathway regulates cell survival, proliferation, differentiation and motility [14,15] , such as the case of differentiation of mouse ES cells [15][16][17] . In the MAPK pathway, sustained activation or phosphorylation of extracellular signal-regulated kinase (ERK) is a specific requirement for the neural lineage commitment [8] and is associated with neuritis formation and neuron survival during ES cells differentiation [16] .…”

Section: Introductionmentioning

confidence: 99%

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Promoting effects of isobavachin on neurogenesis of mouse embryonic stem cells were associated with protein prenylation

Wang

Kong

et al. 2011

Acta Pharmacol Sin

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Aim: Some small molecules can induce mouse embryonic stem (ES) cells to differentiate into neuronal cells. Here, we explored the effect of isobavachin (IBA), a compound with a prenyl group at position 8 of ring A, on promoting neuronal differentiation and the potential role of its protein prenylation. Methods: The hanging drop method was employed for embryonic body (EB) formation to mimic embryo development in vivo. The EBs were treated with IBA at a final concentration of 10 -7 mol/L from EB stage (d 4) to d 8+10. Geranylgeranyltransferase I inhibitor GGTI-298 was subsequently used to disrupt protein prenylation. Neuronal subtypes, including neurons and astrocytes, were observed by fluorescence microscopy. Gene and protein expression levels were detected using RT-PCR and Western blot analysis, respectively. Results: With IBA treatment, nestin was highly expressed in the neural progenitors generated from EBs (d 4, d 8+0). EBs then further differentiated into neurons (marked by β-tubulin III) and astrocytes (marked by GFAP), which were both up-regulated in a timedependent manner on d 8+5 and d 8+10. Co-treatment with GGTI-298 selectively abolished the IBA-induced neuronal differentiation. Moreover, in the MAPK pathway, p38 and JNK phosphorylation were down-regulated, while ERK phosphorylation was up-regulated after IBA treatment at different neuronal differentiation passages. Conclusion: IBA can facilitate mouse ES cells differentiating into neuronal cells. The mechanism involved protein prenylation and, subsequently, phos-ERK activation and the phos-p38 off pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Promoting effects of isobavachin on neurogenesis of mouse embryonic stem cells were associated with protein prenylation

Wang

Kong

et al. 2011

Acta Pharmacol Sin

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“…This superfamily includes three signaling pathways: extracellular signal-regulated kinase (ERK), p38 and stress-activated protein kinase/ c-Jun N-terminal kinase (SAPK/JNK). MAPK signaling control of linked responses can be modulated via crosstalk between each of these pathways through stimulation of protein phosphatase (PP) activity and expression (Hoefen and Berk, 2002;Wang et al, 2006). In RCEC, crosstalk between the p38 and ERK pathways modulates hepatocyte growth factor (HGF) and keratinocyte growth factor (KGF) control of migration (Sharma and Bazan, 2003).…”

Section: Introductionmentioning

confidence: 99%

“…It is attributable to MAPK-induced up-regulation of PPs (i.e. PP-2A and MAP kinase phosphatase-1) expression and activity (Wang et al, 2006). The timing of PP changes is initiated by changes in the phosphorylation status of each MAPK pathway.…”

Section: Introductionmentioning

confidence: 99%

Differential dependence of regulatory volume decrease behavior in rabbit corneal epithelial cells on MAPK superfamily activation

Pan¹,

Capó-Aponte²,

Zhang³

et al. 2007

Experimental Eye Research

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We characterized the dependence of hypotonicity-induced regulatory volume decrease (RVD) responses on mitogen-activated protein kinase (MAPK) pathway signaling in SV40-immortalized rabbit corneal epithelial cells (RCEC). Following calcein-AM loading, RVD was monitored using a microplate fluorescence reader. Western blot analysis determined MAPK activation. After 30 min, the RVD response restored the relative cell volume to nearly isotonic values, whereas it was inhibited when cells were bathed either in a Cl − -free solution or with the Cl − -channel inhibitors: 5-nitro-2-(3-phenylpropylamino) benzoic acid or niflumic acid. Similar declines occurred with either a high-K + (20 mM) supplemented solution or the K + channel inhibitor 4-aminopyridine. Activation of extracellular signal-regulated kinase (ERK), p38, and stress-activated protein kinase/c-Jun Nterminal kinase (SAPK/JNK) was time and tonicity-dependent. Stimulation of ERK and SAPK/JNK was maximized earlier than that of p38. Activation of ERK and SAPK/JNK was insensitive to Cl − and K + channel inhibitors, whereas inhibition with either PD98059 or SP600125, respectively, blocked RVD. However, inhibition of p38 with SB203580 had no effect on RVD. Suppression of RVD instead blocked p38 activation. Differences in the dependence of RVD activation on Erk1/2 and p38 signaling were validated in dominant negative (d/n) -Erk1 and d/n-p38 cells. Volumesensitive Cl − and K + channel activation contributes, in concert, to RVD in RCEC. Therefore, swelling-induced ERK and SAPK/JNK stimulation precedes Cl − and K + channel activation, whereas p38 activation occurs as a consequence of RVD.

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“…Cytokines that mediate increases in proliferation commonly induce a response through stimulation of the p44/42MAPK pathway, whereas those involved in increasing cell migration act mostly through the p38MAPK pathway. [10][11][12][13][14] One of the well-studied pathways in CEC is the epidermal growth factor (EGF) receptor-linked p44/42MAPK and p38MAPK signaling cascades. 6,7,9,12,13,[15][16][17][18] In these cells, EGF activates NKCC1 and K + channels and the inhibition of either of these mechanisms blocks the mitogenic response to this growth factor.…”

Section: Introductionmentioning

confidence: 99%

Potassium-Chloride Cotransporter Mediates Cell Cycle Progression and Proliferation of Human Corneal Epithelial Cells

Capó-Aponte

Wang²,

Akıncı³

et al. 2007

Cell Cycle

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Epidermal growth factor (EGF)-induced proliferation of corneal epithelial cells contributes to its renewal, which maintains the protective and refractive properties of the cornea. This study characterized in human corneal epithelial cells (HCEC) the role of the potassium-chloride cotransporter (KCC) in mediating (1) EGF-induced mitogen-activated protein kinase (MAPK) pathway activation; (2) increases in cell cycle progression; and (3) proliferation. The KCC inhibitor [(dihydroindenyl)oxy] alkanoic acid (DIOA) and KCC activator N-ethylmaleimide (NEM), suppressed and enhanced EGF-induced p44/42MAPK activation, respectively. Such selective modulation was mirrored by corresponding changes in cell proliferation and shifts in cell cycle distribution. DIOA induced a 20% increase in G 0 /G 1 -phase cell population, whereas NEM induced a 22% increase in the proportion of cells in the G 2 /M-phase and accelerated the transition from G 0 /G 1 -phase to the S-phase. Associated with these changes, KCC1 content in a plasma membrane enriched fraction increased by 300%. Alterations in regulatory volume capacity were associated with corresponding changes in both KCC1 membrane content and activity. These results indicate that EGF-induced increases in KCC1 activity and content modulate cell volume changes required for (1) activation of the p44/42MAPK signaling pathway, (2) cell cycle progression, and (3) increases in cell proliferation.

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Phosphatase-Mediated Crosstalk Control of ERK and p38 MAPK Signaling in Corneal Epithelial Cells

Abstract: EGF-induced changes in Erk1/2 and p38 phosphorylation status are dependent on PP-mediated crosstalk. This control modulates the magnitude of growth factor-induced increases in corneal epithelial cell migration.

Cited by 77 publications

References 25 publications

Promoting effects of isobavachin on neurogenesis of mouse embryonic stem cells were associated with protein prenylation

Promoting effects of isobavachin on neurogenesis of mouse embryonic stem cells were associated with protein prenylation

Differential dependence of regulatory volume decrease behavior in rabbit corneal epithelial cells on MAPK superfamily activation

Potassium-Chloride Cotransporter Mediates Cell Cycle Progression and Proliferation of Human Corneal Epithelial Cells

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