Nuclear Factor of Activated T Cells c1 Mediates p21-activated Kinase 1 Activation in the Modulation of Chemokine-induced Human Aortic Smooth Muscle Cell F-actin Stress Fiber Formation, Migration, and Proliferation and Injury-induced Vascular Wall Remodeling

Kundumani‐Sridharan, Venkatesh; Singh, Nikhlesh K.; Kumar, Sanjay; Gadepalli, Ravisekhar; Rao, Gadiparthi N.

doi:10.1074/jbc.m113.454082

Cited by 39 publications

(33 citation statements)

References 50 publications

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“…Furthermore, we found that MCP-1 up-regulates expression of telomerase and increases the proliferation potential of synovial MPCs (Harris et al, 2013). It is also interesting to note that p21 has been previously implicated as a negative regulator of telomerase, and that at least one group has suggested that a signaling pathway exists between MCP-1 and p21 (Kundumani-Sridharan et al, 2013). The link between MCP-1/CCL2 and p21 will require additional research to validate and uncover the signaling pathway mechanism.…”

Section: Discussionmentioning

confidence: 86%

Increased levels of p21(CIP1/WAF1) correlate with decreased chondrogenic differentiation potential in synovial membrane progenitor cells.

Masson

Hess

O’Brien

et al. 2015

Mechanisms of Ageing and Development

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Section: Discussionmentioning

confidence: 86%

Increased levels of p21(CIP1/WAF1) correlate with decreased chondrogenic differentiation potential in synovial membrane progenitor cells.

Masson

Hess

O’Brien

et al. 2015

Mechanisms of Ageing and Development

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“…The possible functional heterogeneity among NFAT isoforms may explain this apparent conflict between our VIVIT and adenoviral infection results. This, it can be argued that, while NFATc3 opposes NPC proliferation, VIVIT inhibits all NFAT isoforms including those previously shown to activate NPC proliferation in embryonic stem cells (Wong et al, ) and vessels (Kundumani‐Sridharan et al, ). Other authors have found NFAT inhibitory actions on cell growth similar to those obtained here with NFATc3 overexpression.…”

Section: Discussionmentioning

confidence: 96%

NFAT transcription factors regulate survival, proliferation, migration, and differentiation of neural precursor cells

Serrano-Pérez

Fernández

Neria

et al. 2015

Glia

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The study of factors that regulate the survival, proliferation, and differentiation of neural precursor cells (NPCs) is essential to understand neural development as well as brain regeneration. The Nuclear Factor of Activated T Cells (NFAT) is a family of transcription factors that can affect these processes besides playing key roles during development, such as stimulating axonal growth in neurons, maturation of immune system cells, heart valve formation, and differentiation of skeletal muscle and bone. Interestingly, NFAT signaling can also promote cell differentiation in adults, participating in tissue regeneration. The goal of the present study is to evaluate the expression of NFAT isoforms in NPCs, and to investigate its possible role in NPC survival, proliferation, migration, and differentiation. Our findings indicate that NFAT proteins are active not only in neurogenic brain regions such as hippocampus and subventricular zone (SVZ), but also in cultured NPCs. The inhibition of NFAT activation with the peptide VIVIT reduced neurosphere size and cell density in NPC cultures by decreasing proliferation and increasing cell death. VIVIT also decreased NPC migration and differentiation of astrocytes and neurons from NPCs. In addition, we identified NFATc3 as a predominant NFAT isoform in NPC cultures, finding that a constitutively-active form of NFATc3 expressed by adenoviral infection reduces NPC proliferation, stimulates migration, and is a potent inducer of NPC differentiation into astrocytes and neurons. In summary, our work uncovers active roles for NFAT signaling in NPC survival, proliferation and differentiation, and highlights its therapeutic potential for tissue regeneration.

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“…In various tissues, PAKs are activated by a wide range of stimuli[2,2,9,10,19–21,30,36,63–67] and a number of G-protein-coupled-receptors[26,68]. However, little is known of their ability to be activated by GI hormones/neurotransmitters or if so, the cellular signaling cascades involved.…”

Section: Discussionmentioning

confidence: 99%

“…PAK3 has a much more restricted expression, being predominantly expressed in the brain, although recent reports has identify it in enteroendocrine cells [17]. Studies demonstrate that PAKs play an important signaling role in various tissues for a wide range of cellular stimuli including bioactive lipids [18,19], oncogenes [20], chemokines [21], growth factors [22–29], cellular stress [9,10], radiation [30], and with activation of some G-protein-coupled receptors [26,31]. However, there is little information on the activation of Group-I-PAKs by gastrointestinal (GI) hormones/neurotransmitters and GI growth factors in normal GI tissues.…”

Section: Introductionmentioning

confidence: 99%

Gastrointestinal hormones/neurotransmitters and growth factors can activate P21 activated kinase 2 in pancreatic acinar cells by novel mechanisms

Nuche-Berenguer

Jensen

2015

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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P-21-activated kinases(PAKs) are serine/threonine kinases comprising six isoforms divided in two groups, group-I(PAK1-3)/group-II(PAK4-6) which play important roles in cell cytoskeletal dynamics, survival, secretion and proliferation and are activated by diverse stimuli. However, little is known about PAKs ability to be activated by gastrointestinal(GI) hormones/neurotransmitters/growth-factors. We used rat pancreatic acini to explore the ability of GI- hormones/neurotransmitters/growth-factors to activate Group-I-PAKs and the signaling cascades involved. Only PAK2 was present in acini. PAK2 was activated by some pancreatic growth-factors[EGF, PDGF, bFGF], by secretagogues activating phospholipase-C(PLC) [CCK, carbachol, bombesin] and by post-receptor stimulants activating PKC[TPA], but not agents only mobilizing cellular calcium or increasing cyclic AMP. CCK-activation of PAK2 required both high- and low-affinity-CCK1-receptor-state activation. It was partially reduced by PKC- or Src-inhibition, but not with PI3K-inhibitors(wortmannin, LY294002) or thapsigargin. IPA-3, which prevents PAK2 binding to small-GTPases partially inhibited PAK2-activation, as well as reduced CCK-induced ERK1/2 activation and amylase release induced by CCK or bombesin. This study demonstrates pancreatic acini, possess only one Group-I-PAK, PAK2. CCK and other GI-hormones/neurotransmitters/growth-factors activate PAK2 via small GTPases(CDC42/Rac1), PKC and SFK but not cytosolic calcium or PI3K. CCK-activation of PAK2 showed several novel features being dependent on both receptor-activation states, having PLC-and PKC-dependent/independent components and small-GTPase-dependent/independent components. These results show PAK2 is important in signaling cascades activated by numerous pancreatic stimuli which mediate their various physiological/pathophysiological responses and thus could be a promising target for the development of therapies in some pancreatic disorders such as pancreatitis.

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Nuclear Factor of Activated T Cells c1 Mediates p21-activated Kinase 1 Activation in the Modulation of Chemokine-induced Human Aortic Smooth Muscle Cell F-actin Stress Fiber Formation, Migration, and Proliferation and Injury-induced Vascular Wall Remodeling

Cited by 39 publications

References 50 publications

Increased levels of p21(CIP1/WAF1) correlate with decreased chondrogenic differentiation potential in synovial membrane progenitor cells.

Increased levels of p21(CIP1/WAF1) correlate with decreased chondrogenic differentiation potential in synovial membrane progenitor cells.

NFAT transcription factors regulate survival, proliferation, migration, and differentiation of neural precursor cells

Gastrointestinal hormones/neurotransmitters and growth factors can activate P21 activated kinase 2 in pancreatic acinar cells by novel mechanisms

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