scholarly journals From a syncytium to mononucleate cells and back: Yki and JNK in symphony

2019 ◽  
Vol 218 (11) ◽  
pp. 3531-3532
Author(s):  
Dhananjay Chaturvedi ◽  
K. VijayRaghavan
Keyword(s):  
Signaling Pathways ◽  
Cell Fate ◽  
Longitudinal Muscle ◽  
Single Cells ◽  
Jnk Signaling ◽  
Cell Biol ◽  
Drosophila Larvae ◽  
Ventral Longitudinal Muscle ◽  
Developmental Remodeling

Alary muscle syncytia in Drosophila larvae undergo a remarkable process of dedifferentiation into single cells that then fuse to become ventral longitudinal muscle in the adult. In this issue, Schaub et al. (2019. J. Cell Biol. https://doi.org/10.1083/jcb.201905048) identify the Hippo and JNK signaling pathways as key regulators of this process of developmental remodeling of cell fate.

Use of Flexible Materials with a Novel Pressure Driven Equibiaxial Cell Stretching Device for Mechanical Stimulation of Single Mammalian Cells

2003 ◽  
Vol 773 ◽  
Author(s):  
James D. Kubicek ◽  
Stephanie Brelsford ◽  
Philip R. LeDuc
Keyword(s):  
Cell Fate ◽  
Mechanical Stimulation ◽  
Mammalian Cells ◽  
Cellular Response ◽  
Single Cells ◽  
Complex Nature ◽  
Cellular Behavior ◽  
Cell Stretching ◽  
Stimulation Of ◽  
Pressure Driven

AbstractMechanical stimulation of single cells has been shown to affect cellular behavior from the molecular scale to ultimate cell fate including apoptosis and proliferation. In this, the ability to control the spatiotemporal application of force on cells through their extracellular matrix connections is critical to understand the cellular response of mechanotransduction. Here, we develop and utilize a novel pressure-driven equibiaxial cell stretching device (PECS) combined with an elastomeric material to control specifically the mechanical stimulation on single cells. Cells were cultured on silicone membranes coated with molecular matrices and then a uniform pressure was introduced to the opposite surface of the membrane to stretch single cells equibiaxially. This allowed us to apply mechanical deformation to investigate the complex nature of cell shape and structure. These results will enhance our knowledge of cellular and molecular function as well as provide insights into fields including biomechanics, tissue engineering, and drug discovery.

scholarly journals YAP and endothelin-1 signaling: an emerging alliance in cancer

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Piera Tocci ◽  
Giovanni Blandino ◽  
Anna Bagnato
Keyword(s):  
Signaling Pathways ◽  
Cell Fate ◽  
Therapeutic Option ◽  
Hippo Pathway ◽  
Signaling Network ◽  
Nuclear Accumulation ◽  
Binding Motif ◽  
Mutant P53 ◽  
Endothelin 1 ◽  
The Hippo Pathway

AbstractThe rational making the G protein-coupled receptors (GPCR) the centerpiece of targeted therapies is fueled by the awareness that GPCR-initiated signaling acts as pivotal driver of the early stages of progression in a broad landscape of human malignancies. The endothelin-1 (ET-1) receptors (ET-1R), known as ETA receptor (ETAR) and ETB receptor (ETBR) that belong to the GPCR superfamily, affect both cancer initiation and progression in a variety of cancer types. By the cross-talking with multiple signaling pathways mainly through the scaffold protein β-arrestin1 (β-arr1), ET-1R axis cooperates with an array of molecular determinants, including transcription factors and co-factors, strongly affecting tumor cell fate and behavior. In this scenario, recent findings shed light on the interplay between ET-1 and the Hippo pathway. In ETAR highly expressing tumors ET-1 axis induces the de-phosphorylation and nuclear accumulation of the Hippo pathway downstream effectors, the paralogous transcriptional cofactors Yes-associated protein (YAP) and Transcriptional coactivator with PDZ-binding motif (TAZ). Recent evidence have discovered that ET-1R/β-arr1 axis instigates a transcriptional interplay involving YAP and mutant p53 proteins, which share a common gene signature and cooperate in a oncogenic signaling network. Mechanistically, YAP and mutp53 are enrolled in nuclear complexes that turn on a highly selective YAP/mutp53-dependent transcriptional response. Notably, ET-1R blockade by the FDA approved dual ET-1 receptor antagonist macitentan interferes with ET-1R/YAP/mutp53 signaling interplay, through the simultaneous suppression of YAP and mutp53 functions, hampering metastasis and therapy resistance. Based on these evidences, we aim to review the recent findings linking the GPCR signaling, as for ET-1R, to YAP/TAZ signaling, underlining the clinical relevance of the blockade of such signaling network in the tumor and microenvironmental contexts. In particular, we debate the clinical implications regarding the use of dual ET-1R antagonists to blunt gain of function activity of mutant p53 proteins and thereby considering them as a potential therapeutic option for mutant p53 cancers. The identification of ET-1R/β-arr1-intertwined and bi-directional signaling pathways as targetable vulnerabilities, may open new therapeutic approaches able to disable the ET-1R-orchestrated YAP/mutp53 signaling network in both tumor and stromal cells and concurrently sensitizes to high-efficacy combined therapeutics.

scholarly journals Crosstalk between MUC1 and VEGF in angiogenesis and metastasis: a review highlighting roles of the MUC1 with an emphasis on metastatic and angiogenic signaling

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Farnaz Khodabakhsh ◽  
Parnaz Merikhian ◽  
Mohammad Reza Eisavand ◽  
Leila Farahmand
Keyword(s):  
Tumor Growth ◽  
Signaling Pathways ◽  
Cell Fate ◽  
Endothelial Cell Proliferation ◽  
Mucin 1 ◽  
Signaling Transduction ◽  
Growth And Survival ◽  
Angiogenic Proteins ◽  
Angiogenic Effect ◽  
And Migration

AbstractVEGF and its receptor family (VEGFR) members have unique signaling transduction system that play significant roles in most pathological processes, such as angiogenesis in tumor growth and metastasis. VEGF-VEGFR complex is a highly specific mitogen for endothelial cells and any de-regulation of the angiogenic balance implicates directly in endothelial cell proliferation and migration. Moreover, it has been shown that overexpressing Mucin 1 (MUC1) on the surface of many tumor cells resulting in upregulation of numerous signaling transduction cascades, such as growth and survival signaling pathways related to RTKs, loss of cell-cell and cell-matrix adhesion, and EMT. It promotes gene transcription of pro-angiogenic proteins such as HIF-1α during periods of oxygen scarcity (hypoxia) to enhance tumor growth and angiogenesis stimulation. In contrast, the cytoplasmic domain of MUC1 (MUC1-C) inhibits apoptosis, which in turn, impresses upon cell fate. Besides, it has been established that reduction in VEGF expression level correlated with silencing MUC1-C level indicating the anti-angiogenic effect of MUC1 downregulation. This review enumerates the role of MUC1-C oncoprotein and VEGF in angiogenesis and metastasis and describes several signaling pathways by which MUC1-C would mediate the pro-angiogenic activities of cancer cells.

scholarly journals Intravital microscopy imaging of kidney injury and regeneration

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yue Liu ◽  
Zongjin Li
Keyword(s):  
Cell Fate ◽  
Intravital Microscopy ◽  
Single Cells ◽  
Elevated Serum ◽  
Kidney Injury ◽  
Lineage Tracing ◽  
Tissue Slices ◽  
Microscopy Imaging ◽  
Two Photon Microscopy ◽  
Nitrogen Levels

AbstractAcute kidney injury (AKI) is a common clinical symptom, which is mainly manifested by elevated serum creatinine and blood urea nitrogen levels. When AKI is not repaired in time, the patient is prone to develop chronic kidney disease (CKD). The kidney is composed of more than 30 different cells, and its structure is complex. It is extremely challenging to understand the lineage relationships and cell fate of these cells in the process of kidney injury and regeneration. Since the 20th century, lineage tracing technology has provided an important mean for studying organ development, tissue damage repair, and the differentiation and fate of single cells. However, traditional lineage tracing methods rely on sacrificing animals to make tissue slices and then take snapshots with conventional imaging tools to obtain interesting information. This method cannot achieve dynamic and continuous monitoring of cell actions on living animals. As a kind of intravital microscopy (IVM), two-photon microscopy (TPM) has successfully solved the above problems. Because TPM has the ability to penetrate deep tissues and can achieve imaging at the single cell level, lineage tracing technology with TPM is gradually becoming popular. In this review, we provided the key technical elements of lineage tracing, and how to use intravital imaging technology to visualize and quantify the fate of renal cells.

Silibinin suppresses astroglial activation in a mouse model of acute Parkinson׳s disease by modulating the ERK and JNK signaling pathways

2015 ◽  
Vol 1627 ◽  
pp. 233-242 ◽  
Author(s):  
Yujeong Lee ◽  
Hye Jeong Chun ◽  
Kyung Moon Lee ◽  
Young-Suk Jung ◽  
Jaewon Lee
Keyword(s):  
Mouse Model ◽  
Signaling Pathways ◽  
Jnk Signaling ◽  
Astroglial Activation

scholarly journals Inhibition of H1N1 influenza virus by selenium nanoparticles loaded with zanamivir through p38 and JNK signaling pathways

RSC Advances ◽  
2017 ◽  
Vol 7 (56) ◽  
pp. 35290-35296 ◽  
Author(s):  
Zhengfang Lin ◽  
Yinghua Li ◽  
Min Guo ◽  
Misi Xiao ◽  
Changbing Wang ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Virus Infection ◽  
Signaling Pathways ◽  
Clinical Application ◽  
Influenza Virus Infection ◽  
Aqueous Solubility ◽  
H1n1 Influenza ◽  
Solubility Limit ◽  
H1n1 Influenza Virus ◽  
Jnk Signaling

Zanamivir is an effective drug for influenza virus infection, but strong molecular polarity and aqueous solubility limit its clinical application.

scholarly journals Chromatin Dynamics in Intestinal Epithelial Homeostasis: A Paradigm of Cell Fate Determination versus Cell Plasticity

2020 ◽  
Vol 16 (6) ◽  
pp. 1062-1080
Author(s):  
Jérémie Rispal ◽  
Fabrice Escaffit ◽  
Didier Trouche
Keyword(s):  
Signaling Pathways ◽  
Cell Fate ◽  
Chromatin Modification ◽  
Intestinal Cell ◽  
Intestinal Epithelial ◽  
Cell Plasticity ◽  
Chromatin Dynamics ◽  
Irritable Bowel ◽  
The Many

AbstractThe rapid renewal of intestinal epithelium is mediated by a pool of stem cells, located at the bottom of crypts, giving rise to highly proliferative progenitor cells, which in turn differentiate during their migration along the villus. The equilibrium between renewal and differentiation is critical for establishment and maintenance of tissue homeostasis, and is regulated by signaling pathways (Wnt, Notch, Bmp…) and specific transcription factors (TCF4, CDX2…). Such regulation controls intestinal cell identities by modulating the cellular transcriptome. Recently, chromatin modification and dynamics have been identified as major actors linking signaling pathways and transcriptional regulation in the control of intestinal homeostasis. In this review, we synthesize the many facets of chromatin dynamics involved in controlling intestinal cell fate, such as stemness maintenance, progenitor identity, lineage choice and commitment, and terminal differentiation. In addition, we present recent data underlying the fundamental role of chromatin dynamics in intestinal cell plasticity. Indeed, this plasticity, which includes dedifferentiation processes or the response to environmental cues (like microbiota’s presence or food ingestion), is central for the organ’s physiology. Finally, we discuss the role of chromatin dynamics in the appearance and treatment of diseases caused by deficiencies in the aforementioned mechanisms, such as gastrointestinal cancer, inflammatory bowel disease or irritable bowel syndrome.

Sign in / Sign up

Export Citation Format

Share Document