Epithelium formation in the Drosophila midgut depends on the interaction of endoderm and mesoderm

Development ◽  
1994 ◽  
Vol 120 (3) ◽  
pp. 579-590 ◽  
Author(s):  
U. Tepass ◽  
V. Hartenstein
Keyword(s):  
Epithelial Cells ◽  
Direct Contact ◽  
Mesenchymal Cells ◽  
Midgut Epithelium ◽  
Wild Type ◽  
Larval Midgut ◽  
Visceral Mesoderm ◽  
Epithelial Sheet ◽  
Endodermal Cells ◽  
Mesenchymal Epithelial Transition

The reorganization of mesenchymal cells into an epithelial sheet is a widely used morphogenetic process in metazoans. An example of such a process is the formation of the Drosophila larval midgut epithelium that develops through a mesenchymal-epithelial transition from endodermal midgut precursors. We have studied this process in wild type and a number of mutants that show defects in midgut epithelium formation. Our results indicate that the visceral mesoderm serves as a basal substratum to which endodermal cells have to establish direct contact in order to form an epithelium. Furthermore, we have analyzed the midgut phenotype of embryos mutant for the gene shotgun, and the results suggest that shotgun directs adhesion between midgut epithelial cells, which is independent from the adhesion between endoderm and visceral mesoderm.

Neurulation and the cortical tractor model for epithelial folding

Development ◽  
1986 ◽  
Vol 96 (1) ◽  
pp. 19-49
Author(s):  
Antone G. Jacobson ◽  
George F. Oster ◽  
Garrett M. Odell ◽  
Louis Y. Cheng
Keyword(s):  
Epithelial Cells ◽  
Computer Simulations ◽  
Dynamic Structure ◽  
Mesenchymal Cells ◽  
Epithelial Morphogenesis ◽  
Apical Region ◽  
New Model ◽  
Epithelial Sheet ◽  
Epithelial Sheets ◽  
Placode Formation

We present here a new model for epithelial morphogenesis, which we call the ‘cortical tractor model’. This model assumes that the motile activities of epithelial cells are similar to those of mesenchymal cells, with the added constraint that the cells in an epithelial sheet remain attached at their apical circumference. In particular, we assert that there is a time-averaged motion of cortical cytoplasm which flows from the basal and lateral surfaces to the apical region. This cortical flow carries with it membrane and adhesive structures that are inserted basally and resorbed apically. Thus the apical seal that characterizes epithelial sheets is a dynamic structure: it is continuously created by the cortical flow which piles up components near where they are recycled in the apical region. By use of mechanical analyses and computer simulations we demonstrate that the cortical tractor motion can reproduce a variety of epithelial motions, including columnarization (placode formation), imagination and rolling. It also provides a mechanism for driving active cell rearrangements within an epithelial sheet, while maintaining the integrity of the apical seal. Active repacking of epithelial cells appears to drive a number of morphogenetic processes. Neurulation in amphibians provides an example of a process in which all four of the above morphogenetic movements appear to play a role. Here we reexamine the process of neurulation in amphibians in light of the cortical tractor model, and find that it provides an integrated view of this important morphogenetic process.

scholarly journals Expression of lysophosphatidic acid receptor 5 is necessary for the regulation of intestinal Na+/H+ exchanger 3 by lysophosphatidic acid in vivo

2018 ◽  
Vol 315 (4) ◽  
pp. G433-G442 ◽  
Author(s):  
Kayte A. Jenkin ◽  
Peijian He ◽  
C. Chris Yun
Keyword(s):  
Epithelial Cells ◽  
Lysophosphatidic Acid ◽  
Direct Evidence ◽  
Intestinal Epithelial Cells ◽  
Regulatory Role ◽  
Intestinal Epithelial ◽  
Fluid Absorption ◽  
Wild Type

Lysophosphatidic acid (LPA) is a bioactive lipid molecule, which regulates a broad range of pathophysiological processes. Recent studies have demonstrated that LPA modulates electrolyte flux in the intestine, and its potential as an antidiarrheal agent has been suggested. Of six LPA receptors, LPA5 is highly expressed in the intestine. Recent studies by our group have demonstrated activation of Na+/H+ exchanger 3 (NHE3) by LPA5. However, much of what has been elucidated was achieved using colonic cell lines that were transfected to express LPA5. In the current study, we engineered a mouse that lacks LPA5 in intestinal epithelial cells, Lpar5ΔIEC, and investigated the role of LPA5 in NHE3 regulation and fluid absorption in vivo. The intestine of Lpar5ΔIEC mice appeared morphologically normal, and the stool frequency and fecal water content were unchanged compared with wild-type mice. Basal rates of NHE3 activity and fluid absorption and total NHE3 expression were not changed in Lpar5ΔIEC mice. However, LPA did not activate NHE3 activity or fluid absorption in Lpar5ΔIEC mice, providing direct evidence for the regulatory role of LPA5. NHE3 activation involves trafficking of NHE3 from the terminal web to microvilli, and this mobilization of NHE3 by LPA was abolished in Lpar5ΔIEC mice. Dysregulation of NHE3 was specific to LPA, and insulin and cholera toxin were able to stimulate and inhibit NHE3, respectively, in both wild-type and Lpar5ΔIEC mice. The current study for the first time demonstrates the necessity of LPA5 in LPA-mediated stimulation of NHE3 in vivo. NEW & NOTEWORTHY This study is the first to assess the role of LPA5 in NHE3 regulation and fluid absorption in vivo using a mouse that lacks LPA5 in intestinal epithelial cells, Lpar5ΔIEC. Basal rates of NHE3 activity and fluid absorption, and total NHE3 expression were not changed in Lpar5ΔIEC mice. However, LPA did not activate NHE3 activity or fluid absorption in Lpar5ΔIEC mice, providing direct evidence for the regulatory role of LPA5.

scholarly journals Proximal tubule-specific overexpression of netrin-1 suppresses acute kidney injury-induced interstitial fibrosis and glomerulosclerosis through suppression of IL-6/STAT3 signaling

2013 ◽  
Vol 304 (8) ◽  
pp. F1054-F1065 ◽  
Author(s):  
Punithavathi Ranganathan ◽  
Calpurnia Jayakumar ◽  
Ganesan Ramesh
Keyword(s):  
Acute Kidney Injury ◽  
Epithelial Cells ◽  
Interstitial Fibrosis ◽  
Kidney Injury ◽  
Transgenic Animals ◽  
Acute Injury ◽  
Tubular Epithelial Cells ◽  
Wild Type ◽  
Proximal Tubular Epithelial Cells ◽  
Proximal Tubular

Acute kidney injury-induced organ fibrosis is recognized as a major risk factor for the development of chronic kidney disease, which remains one of the leading causes of death in the developed world. However, knowledge on molecules that may suppress the fibrogenic response after injury is lacking. In ischemic models of acute kidney injury, we demonstrate a new function of netrin-1 in regulating interstitial fibrosis. Acute injury was promptly followed by a rise in serum creatinine in both wild-type and netrin-1 transgenic animals. However, the wild-type showed a slow recovery of kidney function compared with netrin-1 transgenic animals and reached baseline by 3 wk. Histological examination showed increased infiltration of interstitial macrophages, extensive fibrosis, reduction of capillary density, and glomerulosclerosis. Collagen IV and α-smooth muscle actin expression was absent in sham-operated kidneys; however, their expression was significantly increased at 2 wk and peaked at 3 wk after reperfusion. These changes were reduced in the transgenic mouse kidney, which overexpresses netrin-1 in proximal tubular epithelial cells. Fibrosis was associated with increased expression of IL-6 and extensive and chronic activation of STAT3. Administration of IL-6 exacerbated fibrosis in vivo in wild-type, but not in netrin-1 transgenic mice kidney and increased collagen I expression and STAT3 activation in vitro in renal epithelial cells subjected to hypoxia-reoxygenation, which was suppressed by netrin-1. Our data suggest that proximal tubular epithelial cells may play a prominent role in interstitial fibrosis and that netrin-1 could be a useful therapeutic agent for treating kidney fibrosis.

scholarly journals TLR4 deficiency promotes autophagy during cigarette smoke-induced pulmonary emphysema

2012 ◽  
Vol 303 (9) ◽  
pp. L748-L757 ◽  
Author(s):  
Chang Hyeok An ◽  
Xiao Mei Wang ◽  
Hilaire C. Lam ◽  
Emeka Ifedigbo ◽  
George R. Washko ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Lung Disease ◽  
Pulmonary Emphysema ◽  
Obstructive Lung Disease ◽  
Caspase 3 ◽  
Chronic Obstructive Lung Disease ◽  
Chronic Obstructive ◽  
Tlr4 Expression ◽  
Wild Type ◽  
Deficient Mice

Toll-like receptors (TLRs) exert important nonimmune functions in lung homeostasis. TLR4 deficiency promotes pulmonary emphysema. We examined the role of TLR4 in regulating cigarette smoke (CS)-induced autophagy, apoptosis, and emphysema. Lung tissue was obtained from chronic obstructive lung disease (COPD) patients. C3H/HeJ ( Tlr4-mutated) mice and C57BL/10ScNJ ( Tlr4-deficient) mice and their respective control strains were exposed to chronic CS or air. Human or mouse epithelial cells (wild-type, Tlr4-knockdown, and Tlr4-deficient) were exposed to CS-extract (CSE). Samples were analyzed for TLR4 expression, and for autophagic or apoptotic proteins by Western blot analysis or confocal imaging. Chronic obstructive lung disease lung tissues and human pulmonary epithelial cells exposed to CSE displayed increased TLR4 expression, and increased autophagic [microtubule-associated protein-1 light-chain-3B (LC3B)] and apoptotic (cleaved caspase-3) markers. Beas-2B cells transfected with TLR4 siRNA displayed increased expression of LC3B relative to control cells, basally and after exposure to CSE. The basal and CSE-inducible expression of LC3B and cleaved caspase-3 were elevated in pulmonary alveolar type II cells from Tlr4-deficient mice. Wild-type mice subjected to chronic CS-exposure displayed airspace enlargement;, however, the Tlr4-mutated or Tlr4-deficient mice exhibited a marked increase in airspace relative to wild-type mice after CS-exposure. The Tlr4-mutated or Tlr4-deficient mice showed higher levels of LC3B under basal conditions and after CS exposure. The expression of cleaved caspase-3 was markedly increased in Tlr4-deficient mice exposed to CS. We describe a protective regulatory function of TLR4 against emphysematous changes of the lung in response to CS.

scholarly journals Tolerance of high levels of wild-type p53 in transformed epithelial cells dependent on auto-regulation by mdm-2

Oncogene ◽  
1997 ◽  
Vol 14 (15) ◽  
pp. 1859-1868 ◽  
Author(s):  
Jeremy P Blaydes ◽  
Véronique Gire ◽  
Janet M Rowson ◽  
David Wynford-Thomas
Keyword(s):  
Epithelial Cells ◽  
Wild Type ◽  
Wild Type P53

scholarly journals Pathology of Exfoliated Oropharyngeal Epithelial Cells Infected with Wild-Type Adenovirus

1972 ◽  
Vol 24 (3) ◽  
pp. 389-397 ◽  
Author(s):  
David P. McCormick ◽  
Quirino Galapon ◽  
Carl Berling
Keyword(s):  
Epithelial Cells ◽  
Wild Type

scholarly journals Increased Association of Deamidated αA-N101D with Lens Membrane of Transgenic αAN101D vs. Wild Type αA Mice: Potential Effects on Intracellular Ionic Imbalance and Membrane Disorganization

2020 ◽  
Author(s):  
Om Srivast ◽  
Kiran Srivast ◽  
Roy Joseph ◽  
Landon Wilson
Keyword(s):  
Epithelial Cells ◽  
Western Blot ◽  
Immunogold Labeling ◽  
Human Lens ◽  
Membrane Association ◽  
Related Protein ◽  
Wild Type ◽  
Age Related ◽  
Ionic Imbalance

Abstract We have generated two mouse models, in one by inserting the human lens αAN101D transgene in CRYαAN101D mice, and in the other by inserting human wild-type αA-transgene in CRYαAWT mice. The CRYαAN101D mice developed cortical cataract at about 7-months of age relative to CRYαAWT mice. The objective of the study was to determine the following relative changes in the lenses of CRYαAN101D- vs. CRYαAWT mice: age-related changes with specific emphasis on protein insolubilization, relative membrane-association of αAN101D vs. WTαA proteins, and changes in intracellular ionic imbalance and membrane organization. Methods: Lenses of varying ages from CRYαAWT and CRYαAN101D mice were compared for an age-related protein insolubilization. The relative lens membrane-association of the αAN101D- and WTαA proteins in the two types of mice was determined by immunohistochemical-, immunogold-labeling-, and western blot analyses. The relative levels of membrane-binding of recombinant αAN101D- and WTαA proteins was determined by an in vitro assay, and the levels of intracellular Ca2+ uptake and Na, K-ATPase mRNA were determined in the cultured epithelial cells from lenses of the two types of mice.Results: Compared to the lenses of CRYαAWT, the lenses of CRYαAN101D mice exhibited: (A) An increase in age-related protein insolubilization beginning at about 4-months of age. (B) A greater lens membrane-association of αAN101D- relative to WTαA protein during immunogold-labeling- and western blot analyses, including relatively a greater membrane swelling in the CRYαAN101D lenses. (C) During in vitro assay, the greater levels of binding αAN101D- relative to WTαA protein to membranes was observed. (D) The 75% lower level of Na, K-ATPase mRNA but 1.5X greater Ca2+ uptake were observed in cultured lens epithelial cells of CRYαAN101D- than those of CRYαAWT mice. Conclusions: The results show that an increased lens membrane association of αAN101D--relative WTαA protein in CRYαAN101D mice than CRYαAWT mice occurs, which causes intracellular ionic imbalance, and in turn, membrane swelling that potentially leads to cortical opacity.

Transforming growth factor-β2-mediated mesenchymal transition in lens epithelial cells is repressed in the absence of RAGE

2021 ◽  
Vol 478 (12) ◽  
pp. 2285-2296
Author(s):  
Mi-Hyun Nam ◽  
Mina B. Pantcheva ◽  
Johanna Rankenberg ◽  
Ram H. Nagaraj
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Knockout Mice ◽  
Transforming Growth Factor ◽  
Smooth Muscle Actin ◽  
Lens Epithelial Cells ◽  
Wild Type ◽  
Mesenchymal Transition ◽  
Smad Signaling ◽  
Transforming Growth Factor Β2

Transforming growth factor-β2 (TGFβ2)-mediated epithelial to mesenchymal transition (EMT) in lens epithelial cells (LECs) has been implicated in fibrosis associated with secondary cataracts. In this study, we investigated whether the receptor for advanced glycation end products (RAGE) plays a role in TGFβ2-mediated EMT in LECs. Unlike in the LECs from wild-type mice, TGFβ2 failed to elicit an EMT response in LECs from RAGE knockout mice. The lack of RAGE also diminished TGFβ2-mediated Smad signaling. In addition, treatment with TGFβ2 increased IL-6 levels in LECs from wild-type mice but not in those from RAGE knockout mice. Treatment of human LECs with the RAGE inhibitor FPS-ZM1 reduced TGFβ2-mediated Smad signaling and the EMT response. Unlike that in wild-type lenses, the removal of fiber cell tissue in RAGE knockout lenses did not result in elevated levels of α-smooth muscle actin (α-SMA), fibronectin (FN), and integrin β1 in capsule-adherent LECs. Taken together, these results suggest that TGFβ2 signaling is intricately linked to RAGE. Targeting RAGE could be explored as a therapeutic strategy against secondary cataracts.

Hydra regeneration from recombined ectodermal and endodermal tissue. II. Differential stability in the ectodermal and endodermal epithelial organization

1997 ◽  
Vol 110 (16) ◽  
pp. 1919-1934
Author(s):  
M. Murate ◽  
Y. Kishimoto ◽  
T. Sugiyama ◽  
T. Fujisawa ◽  
H. Takahashi-Iwanaga ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Structural Changes ◽  
Light And Electron Microscopy ◽  
Single Layer ◽  
Strong Interactions ◽  
High Plasticity ◽  
Spherical Structure ◽  
Epithelial Sheet ◽  
Differential Stability ◽  
Tissue Recombination

Hydra tissue consists of the ectodermal and the endodermal layers. When the two layers were separated by procaine treatment and then recombined, the ectodermal epithelial cells spread as a single cell layer over the endoderm as in epiboly in vertebrate embryogenesis, and the resultant spherical structure subsequently regenerated into a complete hydra. In this study, light and electron microscopy were used to examine the structural changes which took place in the cells and tissue during this epibolic ectodermal spreading process. Within a few hours after tissue recombination, the endoderm underwent dramatic changes; it lost its epithelial sheet organization, and turned into a mass of irregularly shaped cells without the apical-basal cell polarity initially present. In contrast, the ectoderm maintained its basic epithelial sheet organization as it spread over the endoderm. Later, the endodermal epithelial cells reorganized themselves into a single-layered epithelial sheet underneath the spreading ectodermal layer. The resultant spherical structure consisted of a single layer of ectodermal epithelial cells outside, a single layer of endodermal epithelial cells inside, and an empty cavity in the center as in normal hydra tissue. This structure regenerated into hydra in the following days. These and other observations demonstrate that the two-layered epithelial sheet organization is highly dynamic, and that its stability is maintained by strong interactions between the two layers in normal hydra. It is suggested that this dynamic nature of the hydra tissue, particularly the high plasticity of the endodermal epithelial sheet organization, may be an important element for the high regenerative capacity of this organism.

A transgenic model for studying development of the enteric nervous system in normal and aganglionic mice

Development ◽  
1992 ◽  
Vol 116 (1) ◽  
pp. 167-175 ◽  
Author(s):  
R.P. Kapur ◽  
C. Yost ◽  
R.D. Palmiter
Keyword(s):  
Transgene Expression ◽  
Mesenchymal Cells ◽  
Enteric Neurons ◽  
Renal Capsule ◽  
Wild Type ◽  
Enteric Ganglia ◽  
Dopamine Beta Hydroxylase ◽  
Transgenic Embryos ◽  
Beta Galactosidase ◽  
Intrinsic Neurons

The dopamine beta-hydroxylase promoter has been shown to direct expression of the reporter gene product, beta-galactosidase, to enteric neurons and putative embryonic neuroblasts in transgenic mice (Mercer et al., 1991; Kapur et al., 1991). In this paper, expression of the transgene, D beta H-nlacZ, in the gastrointestinal tract is characterized in more detail in wild-type mice and mice which are also homozygous for the lethal spotted allele (ls). Expression of the transgene in wild-type embryos was first detected in scattered mesenchymal cells in the proximal foregut on embryonic day 9.5, and progressed distally until embryonic day 13.5 when the entire length of the gut was colonized by such cells. Several observations suggest that the mesenchymal cells which express the transgene (MCET) are, in fact, enteric neuroblasts, probably derived from the vagal neural crest. (1) The presence of MCET in progressively more caudal portions of the embryonic gut correlated with the neurogenic potential of isolated gastrointestinal segments grafted under the renal capsule. (2) Mitotic activity of MCET was demonstrated by incorporation of [3H]thymidine in utero. (3) The migratory behavior of MCET and/or their precursors was revealed in anastomotic subcapsular grafts of gut from transgenic and non-transgenic embryos; enteric ganglia of the latter were populated by MCET from the former. (4) Enteric expression of the transgene postnatally was restricted to intrinsic neurons that coexpressed other phenotypic markers of neuronal differentiation. The pattern of transgene expression in ls/ls mice was identical to that seen in ls/+ and +/+ mice until embryonic day 12.5.(ABSTRACT TRUNCATED AT 250 WORDS)

Sign in / Sign up

Export Citation Format

Share Document