scholarly journals Apelin signaling dependent endocardial protrusions promote cardiac trabeculation in zebrafish

2021 ◽  
Author(s):  
Jialing Qi ◽  
Annegret Rittershaus ◽  
Rashmi Priya ◽  
Shivani Mansingh ◽  
Didier Y.R. Stainier ◽  
...  
Keyword(s):  
Growth Factors ◽  
Cardiac Development ◽  
Close Contact ◽  
Erk Signaling ◽  
Zebrafish Embryos ◽  
Dynamic Membrane ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Membrane Protrusions ◽  
Apelin Receptor

AbstractDuring cardiac development, endocardial cells (EdCs) produce growth factors to promote myocardial morphogenesis and growth. In particular, EdCs produce Neuregulin which is required for ventricular cardiomyocytes (CMs) to seed the multicellular ridges known as trabeculae. Defects in Neuregulin signaling, or in endocardial sprouting towards CMs, cause hypotrabeculation. However, the mechanisms underlying endocardial sprouting remain largely unknown. Here, we first show by live imaging in zebrafish embryos that EdCs interact with CMs via dynamic membrane protrusions. After touching CMs, these protrusions remain in close contact with their target despite the vigorous cardiac contractions. Loss of the CM-derived peptide Apelin, or of the Apelin receptor, which is expressed in EdCs, leads to reduced endocardial sprouting and hypotrabeculation. Mechanistically, Neuregulin signaling requires endocardial protrusions to activate extracellular signal-regulated kinase (Erk) signaling in CMs and trigger their delamination. Altogether, these data show that Apelin signaling dependent endocardial protrusions modulate CM behavior during trabeculation.

Role of extracellular signal-regulated kinase (ERK) signaling in nucleotide excision repair and genotoxicity in response to As(III) and Pb(II)

2008 ◽  
Vol 80 (12) ◽  
pp. 2735-2750
Author(s):  
Ju-Pi Li ◽  
Chun-Yu Wang ◽  
Yen-An Tang ◽  
Yun-Wei Lin ◽  
Jia-Ling Yang
Keyword(s):  
Signaling Pathways ◽  
Nucleotide Excision Repair ◽  
Mammalian Cells ◽  
Excision Repair ◽  
Erk Signaling ◽  
Erk Activation ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Nucleotide Excision

Arsenic and lead can induce genetic injuries and epigenetic signaling pathways in cultured mammalian cells. To test whether signaling pathways affect the extent of genetic injuries, we explored the impacts of extracellular signal-regulated kinase 1 and 2 (ERK) on nucleotide excision repair (NER), cytotoxicity, and genotoxicity following sodium arsenite [As(III)] and lead acetate [Pb(II)]. Sustained ERK activation was observed in human cells exposed to As(III) and Pb(II). As(III) inhibited the cellular NER synthesis capability; conversely, Pb(II) stimulated it. ERK activation contributed to the As(III)-induced NER inhibition and micronucleus formation. In contrast, this signal was required for inducing cellular NER activity and preventing mutagenesis following Pb(II). ERK activation by Pb(II) was dependent on protein kinase C (PKCα) that also exhibited anti-mutagenicity. Enforced expression of ERK signaling markedly elevated the cellular NER activity, which was suppressed by As(III). Nonetheless, ERK activation could counteract the cytotoxicity caused by these two metals. Together, the results indicate that pro-survival ERK signaling exhibits dual and opposing impacts on NER process following As(III) and Pb(II) exposures. The findings also suggest that ERK is an important epigenetic signaling in the determination of metal genotoxicity.

scholarly journals Role of Phosphoinositide 3-Kinase and Endocytosis in Nerve Growth Factor-Induced Extracellular Signal-Regulated Kinase Activation via Ras and Rap1

2000 ◽  
Vol 20 (21) ◽  
pp. 8069-8083 ◽  
Author(s):  
Randall D. York ◽  
Derek C. Molliver ◽  
Savraj S. Grewal ◽  
Paula E. Stenberg ◽  
Edwin W. McCleskey ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Map Kinase ◽  
Pc12 Cells ◽  
Erk Signaling ◽  
Nerve Growth ◽  
Erk Activation ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Phosphoinositide 3 Kinase

ABSTRACT Neurotrophins promote multiple actions on neuronal cells including cell survival and differentiation. The best-studied neurotrophin, nerve growth factor (NGF), is a major survival factor in sympathetic and sensory neurons and promotes differentiation in a well-studied model system, PC12 cells. To mediate these actions, NGF binds to the TrkA receptor to trigger intracellular signaling cascades. Two kinases whose activities mediate these processes include the mitogen-activated protein (MAP) kinase (or extracellular signal-regulated kinase [ERK]) and phosphoinositide 3-kinase (PI3-K). To examine potential interactions between the ERK and PI3-K pathways, we studied the requirement of PI3-K for NGF activation of the ERK signaling cascade in dorsal root ganglion cells and PC12 cells. We show that PI3-K is required for TrkA internalization and participates in NGF signaling to ERKs via distinct actions on the small G proteins Ras and Rap1. In PC12 cells, NGF activates Ras and Rap1 to elicit the rapid and sustained activation of ERKs respectively. We show here that Rap1 activation requires both TrkA internalization and PI3-K, whereas Ras activation requires neither TrkA internalization nor PI3-K. Both inhibitors of PI3-K and inhibitors of endocytosis prevent GTP loading of Rap1 and block sustained ERK activation by NGF. PI3-K and endocytosis may also regulate ERK signaling at a second site downstream of Ras, since both rapid ERK activation and the Ras-dependent activation of the MAP kinase kinase kinase B-Raf are blocked by inhibition of either PI3-K or endocytosis. The results of this study suggest that PI3-K may be required for the signals initiated by TrkA internalization and demonstrate that specific endocytic events may distinguish ERK signaling via Rap1 and Ras.

scholarly journals Targeting extracellular signal-regulated kinase (ERK) signaling has therapeutic implications for inflammatory osteolysis

Bone ◽  
2010 ◽  
Vol 46 (3) ◽  
pp. 695-702 ◽  
Author(s):  
Sung Wook Seo ◽  
Daniel Lee ◽  
Hiroshi Minematsu ◽  
Abraham D. Kim ◽  
Mike Shin ◽  
...  
Keyword(s):  
Erk Signaling ◽  
Therapeutic Implications ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal

scholarly journals PERAN LATIHAN FISIK DALAM PENANGANAN OBESITAS: AKSI IRISIN PADA PROSES PENCOKELATAN

2021 ◽  
Vol 3 (1) ◽  
pp. 27
Author(s):  
Dewi Irawati Soeria Santoso ◽  
Imelda Rosalyn Sianipar ◽  
Neng Tine Kartinah
Keyword(s):  
Treatment Approach ◽  
Public Health Problem ◽  
Mitogen Activated Protein Kinase ◽  
Erk Signaling ◽  
Brown Adipocyte ◽  
White Adipocyte ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Mitogen Activated Protein ◽  
Prevalence Of Obesity

In recent years, the prevalence of obesity continues to increase, leading to a public health problem. Therefore, the obesity problem needs serious attention and treatment approaches. Exercise is one of the treatment approach to combat obesity because exercise plays a role in beiging/browning process. Beiging is a differentiation process from white adipocyte to beige adipocyte, which has similar characteristics to brown adipocyte and is marked with an increase of UCP-1 expression. Irisin plays a role in increasing UCP-1 expression by activating p38 mitogen-activated protein kinase (MAPK) and extracellular-signal regulated kinase (ERK) signaling. Muscle contraction during exercise can activate PGC-1α, which leads to the synthesis of irisin. Exercise may increase irisin levels in skeletal muscle and consequently, play as a mediator of beiging process in adipose tissue.

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