scholarly journals PHRED-1 is a divergent neurexin-1 homolog that organizes muscle fibers and patterns organs during regeneration

2017 ◽  
Author(s):  
Carolyn E. Adler ◽  
Alejandro Sánchez Alvarado
Keyword(s):  
Body Wall ◽  
Structural Integrity ◽  
Transmembrane Protein ◽  
Muscle Fibers ◽  
Cell Types ◽  
Bhlh Transcription Factor ◽  
Body Parts ◽  
Normal Muscle ◽  
Complex Process ◽  
Multiple Cell

AbstractRegeneration of body parts requires the replacement of multiple cell types. To dissect this complex process, we utilized planarian flatworms that are capable of regenerating any tissue after amputation. An RNAi screen for genes involved in regeneration of the pharynx identified a novel gene, Pharynx regeneration defective-1 (PHRED-1) as essential for normal pharynx regeneration. PHRED-1 is a predicted transmembrane protein containing EGF, Laminin G, and WD40 domains, is expressed in muscle, and has predicted homologs restricted to other lophotrochozoan species. Knockdown of PHRED-1 causes abnormal regeneration of muscle fibers in both the pharynx and body wall muscle. In addition to defects in muscle regeneration, knockdown of PHRED-1 or the bHLH transcription factor MyoD also causes defects in muscle and intestinal regeneration. Together, our data demonstrate that muscle plays a key role in restoring the structural integrity of closely associated organs, and in planarians it may form a scaffold that facilitates normal intestinal branching.Graphical AbstractHighlights-PHRED-1 is a predicted transmembrane protein that contains Laminin G, EGF and WD40 domains-PHRED-1 is required for normal muscle patterning during regeneration-phred-1 is expressed in muscle cells-Muscle forms an essential scaffold for regeneration

scholarly journals A Conserved LIM Protein That Affects Muscular Adherens Junction Integrity and Mechanosensory Function in Caenorhabditis elegans

1999 ◽  
Vol 144 (1) ◽  
pp. 45-57 ◽  
Author(s):  
Oliver Hobert ◽  
Donald G. Moerman ◽  
Kathleen A. Clark ◽  
Mary C. Beckerle ◽  
Gary Ruvkun
Keyword(s):  
Caenorhabditis Elegans ◽  
Body Wall ◽  
Structural Integrity ◽  
Adherens Junctions ◽  
Functional Characterization ◽  
Adherens Junction ◽  
Cell Types ◽  
Loss Of Function ◽  
Body Wall Muscles ◽  
Lim Proteins

We describe here the molecular and functional characterization of the Caenorhabditis elegans unc-97 gene, whose gene product constitutes a novel component of muscular adherens junctions. UNC-97 and homologues from several other species define the PINCH family, a family of LIM proteins whose modular composition of five LIM domains implicates them as potential adapter molecules. unc-97 expression is restricted to tissue types that attach to the hypodermis, specifically body wall muscles, vulval muscles, and mechanosensory neurons. In body wall muscles, the UNC-97 protein colocalizes with the β-integrin PAT-3 to the focal adhesion-like attachment sites of muscles. Partial and complete loss-of-function studies demonstrate that UNC-97 affects the structural integrity of the integrin containing muscle adherens junctions and contributes to the mechanosensory functions of touch neurons. The expression of a Drosophila homologue of unc-97 in two integrin containing cell types, muscles, and muscle-attached epidermal cells, suggests that unc-97 function in adherens junction assembly and stability has been conserved across phylogeny. In addition to its localization to adherens junctions UNC-97 can also be detected in the nucleus, suggesting multiple functions for this LIM domain protein.

scholarly journals Klotho inhibits neuronal senescence in human brain organoids

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Mohammed R. Shaker ◽  
Julio Aguado ◽  
Harman Kaur Chaggar ◽  
Ernst J. Wolvetang
Keyword(s):  
Human Brain ◽  
Cortical Neurons ◽  
Brain Aging ◽  
Transmembrane Protein ◽  
Cell Types ◽  
The Body ◽  
Aging Effects ◽  
Multiple Cell ◽  
Senescence Associated Genes

AbstractAging is a major risk factor for many neurodegenerative diseases. Klotho (KL) is a glycosylated transmembrane protein that is expressed in the choroid plexus and neurons of the brain. KL exerts potent anti-aging effects on multiple cell types in the body but its role in human brain cells remains largely unclear. Here we show that human cortical neurons, derived from human pluripotent stem cells in 2D cultures or in cortical organoids, develop the typical hallmarks of senescent cells when maintained in vitro for prolonged periods of time, and that moderate upregulation or repression of endogenous KL expression in cortical organoids inhibits and accelerates senescence, respectively. We further demonstrate that KL expression alters the expression of senescence-associated genes including, extracellular matrix genes, and proteoglycans, and can act in a paracrine fashion to inhibit neuronal senescence. In summary, our results establish an important role for KL in the regulation of human neuronal senescence and offer new mechanistic insight into its role in human brain aging.

scholarly journals Vascular Calcification in Chronic Kidney Disease: Diversity in the Vessel Wall

Biomedicines ◽  
2021 ◽  
Vol 9 (4) ◽  
pp. 404
Author(s):  
Prabhatchandra Dube ◽  
Armelle DeRiso ◽  
Mitra Patel ◽  
Dhanushya Battepati ◽  
Bella Khatib-Shahidi ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Molecular Mechanisms ◽  
Cell Types ◽  
Complex Process ◽  
Cardiovascular Morbidity And Mortality ◽  
Depth Analysis ◽  
Multiple Cell ◽  
Different Cell Types

Vascular calcification (VC) is one of the major causes of cardiovascular morbidity and mortality in patients with chronic kidney disease (CKD). VC is a complex process expressing similarity to bone metabolism in onset and progression. VC in CKD is promoted by various factors not limited to hyperphosphatemia, Ca/Pi imbalance, uremic toxins, chronic inflammation, oxidative stress, and activation of multiple signaling pathways in different cell types, including vascular smooth muscle cells (VSMCs), macrophages, and endothelial cells. In the current review, we provide an in-depth analysis of the various kinds of VC, the clinical significance and available therapies, significant contributions from multiple cell types, and the associated cellular and molecular mechanisms for the VC process in the setting of CKD. Thus, we seek to highlight the key factors and cell types driving the pathology of VC in CKD in order to assist in the identification of preventative, diagnostic, and therapeutic strategies for patients burdened with this disease.

Designing an Interchangeable Multi-Material Nozzle System for 3D Bioprinting Process

2021 ◽  
Author(s):  
Cartwright Nelson ◽  
Slesha Tuladhar ◽  
Md Ahasan Habib
Keyword(s):  
Rheological Properties ◽  
Structural Integrity ◽  
Three Dimensional ◽  
Cell Types ◽  
3D Bioprinting ◽  
Print Head ◽  
Functional Tissue ◽  
Multiple Cell ◽  
Continuous Deposition ◽  
Bio Material

Abstract Three-dimensional bioprinting is a rapidly growing field attempting to recreate functional tissues for medical and pharmaceutical purposes. Development of functional tissue requires deposition of multiple biomaterials encapsulating multiple cell types i.e. bio-ink necessitating switching ability between bio-inks. Existing systems use more than one print head to achieve this complex interchangeable deposition, which decreases efficiency, structural integrity, and accuracy. In this research, we developed a nozzle system capable of switching between multiple bio-inks with continuous deposition ensuring the minimum transition distance so that precise deposition transitioning can be achieved. Finally, the effect of rheological properties of different bio-material compositions on the transition distance is investigated by fabricating the sample scaffolds.

Adult-Fetal Fibroblast Interactions: Effects on Cell Migration and Implications for Cell Transplantation

2005 ◽  
Vol 14 (5) ◽  
pp. 331-337 ◽  
Author(s):  
Vlad C. Sandulache ◽  
Joseph E. Dohar ◽  
Patricia A. Hebda
Keyword(s):  
Wound Healing ◽  
Healing Process ◽  
Intrinsic Property ◽  
Cell Types ◽  
Wound Healing Process ◽  
Complex Process ◽  
Culture Model ◽  
Multiple Cell ◽  
Close Cooperation

Wound healing is a complex process involving close cooperation between multiple cell types. During wound healing, fibroblasts are primarily responsible for synthesis of the replacement extracellular matrix. Fibroblast therapy is under investigation in this and other laboratories for its potential use to modulate the final outcome of the wound-healing process. This study addresses the potential interactions between transplanted and host fibroblasts, using a two-dimensional mixed culture model. Our results show that fibroblasts of two different phenotypes, fetal and adult, exhibit different speeds of in vitro migration. These migration speeds are conserved in mixed cocultures, suggesting that the migratory response is an intrinsic property of the fibroblast rather than a response to juxtacrine or paracrine signals. These results have relevance for cell-based therapies in that they demonstrate that donor fibroblasts of a different phenotype may at least partially retain that phenotype in the host environment and in the presence of endogenous fibroblasts.

scholarly journals Angiogenesis in Inflammatory Bowel Disease

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Canan Alkim ◽  
Huseyin Alkim ◽  
Ali Riza Koksal ◽  
Salih Boga ◽  
Ilker Sen
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Cell Types ◽  
Research Area ◽  
Complex Process ◽  
Multiple Cell ◽  
Inflammatory Bowel ◽  
New Research ◽  
Chronic Intestinal Inflammation

Angiogenesis is an important component of pathogenesis of inflammatory bowel disease (IBD). Chronic inflammation and angiogenesis are two closely related processes. Chronic intestinal inflammation is dependent on angiogenesis and this angiogenesis is modulated by immune system in IBD. Angiogenesis is a very complex process which includes multiple cell types, growth factors, cytokines, adhesion molecules, and signal transduction. Lymphangiogenesis is a new research area in the pathogenesis of IBD. While angiogenesis supports inflammation via leukocyte migration, carrying oxygen and nutrients, on the other hand, it has a major role in wound healing. Angiogenic molecules look like perfect targets for the treatment of IBD, but they have risk for serious side effects because of their nature.

scholarly journals Multiple cell types contribute to the atherosclerotic lesion fibrous cap by PDGFRβ and bioenergetic mechanisms

2021 ◽  
Vol 3 (2) ◽  
pp. 166-181 ◽  
Author(s):  
Alexandra A. C. Newman ◽  
Vlad Serbulea ◽  
Richard A. Baylis ◽  
Laura S. Shankman ◽  
Xenia Bradley ◽  
...  
Keyword(s):  
Atherosclerotic Lesion ◽  
Cell Types ◽  
Fibrous Cap ◽  
Multiple Cell

scholarly journals MyD88 Is Not Required for Muscle Injury-Induced Endochondral Heterotopic Ossification in a Mouse Model of Fibrodysplasia Ossificans Progressiva

Biomedicines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 630
Author(s):  
Huili Lyu ◽  
Cody M. Elkins ◽  
Jessica L. Pierce ◽  
C. Henrique Serezani ◽  
Daniel S. Perrien
Keyword(s):  
Heterotopic Ossification ◽  
Muscle Injury ◽  
Cell Types ◽  
Fibrodysplasia Ossificans Progressiva ◽  
Inflammatory Signaling ◽  
Conditional Deletion ◽  
Pathway Crosstalk ◽  
Multiple Cell

Excess inflammation and canonical BMP receptor (BMPR) signaling are coinciding hallmarks of the early stages of injury-induced endochondral heterotopic ossification (EHO), especially in the rare genetic disease fibrodysplasia ossificans progressiva (FOP). Multiple inflammatory signaling pathways can synergistically enhance BMP-induced Smad1/5/8 activity in multiple cell types, suggesting the importance of pathway crosstalk in EHO and FOP. Toll-like receptors (TLRs) and IL-1 receptors mediate many of the earliest injury-induced inflammatory signals largely via MyD88-dependent pathways. Thus, the hypothesis that MyD88-dependent signaling is required for EHO was tested in vitro and in vivo using global or Pdgfrα-conditional deletion of MyD88 in FOP mice. As expected, IL-1β or LPS synergistically increased Activin A (ActA)-induced phosphorylation of Smad 1/5 in fibroadipoprogenitors (FAPs) expressing Alk2R206H. However, conditional deletion of MyD88 in Pdgfrα-positive cells of FOP mice did not significantly alter the amount of muscle injury-induced EHO. Even more surprisingly, injury-induced EHO was not significantly affected by global deletion of MyD88. These studies demonstrate that MyD88-dependent signaling is dispensable for injury-induced EHO in FOP mice.

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