Dual-specificity MAP kinase phosphatases in health and disease

Seternes, Ole Morten; Kidger, Andrew M.; Keyse, Stephen M.

doi:10.1016/j.bbamcr.2018.09.002

Cited by 108 publications

(86 citation statements)

References 199 publications

(371 reference statements)

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“…DUSP5 is a nuclear protein, and it dephosphorylates the threonine/tyrosine residues of ERK1/2 to affect numerous cellular functions, which contributes to the pathogenesis in many diseases (Lake, Correa, & Muller, ; Mandl, Slack, & Keyse, ; Seternes, Kidger, & Keyse, ; Zhang et al, ). We previously reported that the myogenic response and autoregulation of cerebral and renal blood flow (CBF and RBF) are enhanced in Dusp5 KO rats (Fan et al, ; Zhang et al, ).…”

Section: Discussionmentioning

confidence: 99%

Influence of dual‐specificity protein phosphatase 5 on mechanical properties of rat cerebral and renal arterioles

Zhang

Liu

et al. 2020

Physiol Rep

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We recently reported that KO of Dual-specificity protein phosphatase 5 (Dusp5) enhances myogenic reactivity and blood flow autoregulation in the cerebral and renal circulations in association with increased levels of pPKC and pERK1/2 in the cerebral and renal arteries and arterioles. In the kidney, hypertension-related renal damage was significantly attenuated in Dusp5 KO rats. Elevations in pPKC and pERK1/2 promote calcium influx in VSMC and facilitate vasoconstriction.However, whether DUSP5 plays a role in altering the passive mechanical properties of cerebral and renal arterioles has never been investigated. In this study, we found that KO of Dusp5 did not alter body weights, kidney and brain weights, plasma glucose, and Hb A1C levels. The expression of pERK is higher in the nucleus of primary VSMC isolated from Dusp5 KO rats. Dusp5 KO rats exhibited eutrophic vascular hypotrophy with smaller intracerebral parenchymal arterioles and renal interlobular arterioles without changing the wall-to-lumen ratios. These arterioles from Dusp5 KO rats displayed higher myogenic tones, better distensibility, greater compliance, and less stiffness compared with arterioles from WT control rats. VSMC of Dusp5 KO rats exhibited a stronger contractile capability.These results demonstrate, for the first time, that DUSP5 contributes to the regulation of the passive mechanical properties of cerebral and renal arterioles and provide new insights into the role of DUSP5 in vascular function, cancer, stroke, and other cardiovascular diseases. K E Y W O R D Sdistensibility, Dusp5, elastic modulus, interlobular arterioles, parenchymal arterioles, vascular stiffness

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Section: Discussionmentioning

confidence: 99%

Influence of dual‐specificity protein phosphatase 5 on mechanical properties of rat cerebral and renal arterioles

Zhang

Liu

et al. 2020

Physiol Rep

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“…MKPs are classified into three subgroups: tyrosine-specific phosphatases, serine-threonine phosphatases or dual-specificity (threonine/tyrosine) phosphatases (DS-MKPs), which represent the best-characterized class [ 13 ]. Currently, at least ten main DS-MKPs have been identified [ 14 ]. Based on their subcellular localization, DS-MKPs are divided into type I, II and III.…”

Section: The Mapk Familymentioning

confidence: 99%

JNK3 as Therapeutic Target and Biomarker in Neurodegenerative and Neurodevelopmental Brain Diseases

Musi

Agrò

Santarella

et al. 2020

Cells

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The c-Jun N-terminal kinase 3 (JNK3) is the JNK isoform mainly expressed in the brain. It is the most responsive to many stress stimuli in the central nervous system from ischemia to Aβ oligomers toxicity. JNK3 activity is spatial and temporal organized by its scaffold protein, in particular JIP-1 and β-arrestin-2, which play a crucial role in regulating different cellular functions in different cellular districts. Extensive evidence has highlighted the possibility of exploiting these adaptors to interfere with JNK3 signaling in order to block its action. JNK plays a key role in the first neurodegenerative event, the perturbation of physiological synapse structure and function, known as synaptic dysfunction. Importantly, this is a common mechanism in many different brain pathologies. Synaptic dysfunction and spine loss have been reported to be pharmacologically reversible, opening new therapeutic directions in brain diseases. Being JNK3-detectable at the peripheral level, it could be used as a disease biomarker with the ultimate aim of allowing an early diagnosis of neurodegenerative and neurodevelopment diseases in a still prodromal phase.

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“…In this study, we found that MAPK pathways, particularly ERK1/2, were activated by FGF‐2 via FGFR‐1 and were associated with eotaxin‐1 production in ASCs. Proteins in the MAPK family mediate many cellular functions, including protein expression, proliferation, and apoptosis (Puddicombe and Davies, 2000; Seternes et al, 2019). ERK1/2, JNK, p38 MAPK, ERK3/4, and ERK5 play central roles in these cell responses.…”

Section: Discussionmentioning

confidence: 99%

Fibroblast growth factor‐2 and interleukin‐4 synergistically induce eotaxin‐1 expression in adipose tissue‐derived stromal cells

Hattori

2020

Cell Biology International

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The relationships between eosinophils and adipose tissues are involved in metabolic homeostasis. Eotaxin is a chemokine with potent effects on eosinophil migration. To clarify the mechanisms of eotaxin expression in adipose tissues, we examined the effects of fibroblast growth factor-2 (FGF-2) and interleukin-4 (IL-4) stimulation on eotaxin expression in adipose tissue-derived stromal cells (ASCs), a type of adipocyte progenitor, in vitro. ASCs expressed eotaxin-1 and did not express eotaxin-2 or -3. Eotaxin-1 expression was increased in a concentration-dependent manner following FGF-2 treatment. Additionally, ASCs expressed FGF receptor-1 (FGFR-1) and did not express FGFR-2, -3, or -4. Eotaxin-1 expression was inhibited in cells treated with the FGFR tyrosine kinase inhibitor and extracellular signal-regulated kinase (ERK) inhibitor U0126, even in the presence of FGF-2. Moreover, eotaxin-1 expression was synergistically enhanced by combined treatment with FGF-2 and IL-4 and inhibited in the presence of U0126. Eotaxin-1 expression induced by FGF-2 and IL-4 was involved in ERK activation via FGFR-1 in ASCs. Upregulation of eotaxin expression in adipose tissues could increase eosinophil migration, thereby inducing IL-4 secretion and activation of alternative macrophages and improving glucose homeostasis. These findings provide insights into the mechanisms through which eotaxin mediates metabolic homeostasis in adipose tissues and eosinophils.

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Dual-specificity MAP kinase phosphatases in health and disease

Cited by 108 publications

References 199 publications

Influence of dual‐specificity protein phosphatase 5 on mechanical properties of rat cerebral and renal arterioles

Influence of dual‐specificity protein phosphatase 5 on mechanical properties of rat cerebral and renal arterioles

JNK3 as Therapeutic Target and Biomarker in Neurodegenerative and Neurodevelopmental Brain Diseases

Fibroblast growth factor‐2 and interleukin‐4 synergistically induce eotaxin‐1 expression in adipose tissue‐derived stromal cells

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