Developmental roles of epithelial and interstitial cell lineages in hydra: analysis of chimeras

1978 ◽  
Vol 32 (1) ◽  
pp. 233-247
Author(s):  
B.A. Marcum ◽  
R.D. Campbell
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Interstitial Cell ◽  
Interstitial Cells ◽  
Considerable Influence ◽  
Cell Lineages

Chimeric hydra were prepared by recombining epithelial and interstitial cells between 3 strains of hydra of different sizes (maxi, normal, and mini strains). The resulting chimeras generally resembled the epithelial cell parent more than the interstitial cell parent in size, budding rate, tentacle number, and form. This suggests that epithelial cells normally exert considerable influence over hydra morphogenesis. However, the chimeras show some differences ascribable to interstitial cell origin. Furthermore, the 3 original strains, when deprived of interstitial cells, lose their distinguishing size differences. Thus both epithelial and interstitial cells (or interstitial cell derivatives) mutually participate in hydra's development.

Genetic analysis of developmental mechanisms in hydra. V. Cell lineage and development of chimera hydra

1978 ◽  
Vol 32 (1) ◽  
pp. 215-232
Author(s):  
T. Sugiyama ◽  
T. Fujisawa
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Interstitial Cell ◽  
Cell Lineage ◽  
Interstitial Cells ◽  
Nerve Cells ◽  
Polyp Size ◽  
Primary Determinant ◽  
One Year ◽  
Almost All

Chimeric hydra were produced by making use of a strain (nf-1) which lacks interstitial cells, nerve cells and nematocytes. This strain arises by spontaneous loss of interstitial cells from its parental strain (sf-1) (Sugiyama & Fujisawa, 1978). Reintroduction of interstitial cells from other strains into nf-1 leads to the creation of chimeric strains that consisted of epithelial cells derived from strain sf-1 and interstitial cells and their derivatives (nerves and nematocytes) from other strains. In chimeras, interstitial or epithelial cells apparently maintain very stable cell lineages; no indication was obtained that suggested interstitial cell differentiation into epithelial cells or dedifferentiation in the opposite direction during the long courses of chimera cultures (up to one year). Developmental characters of chimeras were examined and compared to those of the epithelial cell (sf-1) and the interstitial cell donors. Almost all of the chimera's characters examined (growth rate, budding rate, tentacle numbers, polyp size, regenerative capacity, etc.) closely resembled those of the epithelial cell donor, but not of the interstitial cell donors. This suggests that epithelial cells, rather than interstitial or nerve cells, are the primary determinant of most, if not all, of hydra developmental characters.

Genetic analysis of developmental mechanisms in hydra. VI. Cellular composition of chimera hydra

1979 ◽  
Vol 35 (1) ◽  
pp. 1-15
Author(s):  
T. Sugiyama ◽  
T. Fujisawa
Keyword(s):  
Epithelial Cell ◽  
Genetic Analysis ◽  
Interstitial Cell ◽  
Cell Types ◽  
Interstitial Cells ◽  
Cellular Composition ◽  
Feedback Mechanisms ◽  
Cell Lineages ◽  
Developmental Mechanisms ◽  
Homeostatic Mechanisms

The homeostatic mechanisms that maintain constant cellular ratios in hydra tissue were studied using mutant and chimeric hydra strains. Mutants having abnormal cellular compositions are isolated through sexual inbreeding of wild hydra, as described in previous papers of this series. Chimeric hydra are produced by making use of a strain (nf-I) which lacks interstitial cells, nerve cells and nematocytes in its tissue. Reintroduction of interstitial cells from other strains (both normal and mutant) into nf-I leads to creation of chimeric strains having epithelial cell lineages from one strain (nf-I) and interstitial cell lineages from others. Analyses and comparisons of the cellular compositions of all these strains revealed that the numbers of nerve or interstitial cells in the chimeras were very similar to (statistically significantly correlated with) those in their interstitial cell donors. Since chimeras and their interstitial cell donors share the same interstitial cell lineages, this suggests that interstitial cells or their derivatives (nerves and nematocytes) play major roles in determining the nerve and interstitial cell levels in the hydra tissue. It is suggested that some form of homeostatic feedback mechanisms are probably involved in regulating the levels of these cell types.

Development of Hydra lacking nerve and interstitial cells

1978 ◽  
Vol 29 (1) ◽  
pp. 17-33 ◽  
Author(s):  
B.A. Marcum ◽  
R.D. Campbell
Keyword(s):  
Epithelial Cells ◽  
Interstitial Cell ◽  
Normal Development ◽  
Colchicine Treatment ◽  
Interstitial Cells ◽  
Normal Numbers ◽  
Active Growth ◽  
Essentially Normal ◽  
Prolonged Culture ◽  
I Cells

Hydra attenuata were rendered free of interstitial cells (I cells) and interstitial cell derivatives by colchicine treatment. These hydra were then cloned and cultivated for 18 months and their developmental capacities were studied. Some experimental hydra possessed a few (about 1% of the normal numbers) interstitial cells and retained this low level during prolonged culture and active growth without the differentiation of I-cells into specialized cells. Other hydra were completely freed of interstitial cells by the colchicine treatment. Maceration and histological analyses showed that once a hydra is freed of all interstitial cells it does not recover them, nor do its buds contain interstitial cells. I cell-free hydra also lack nerve cells, nematocytes, gametes and endodermal gland cells, and the tissue consists only of ectodermal and endodermal epithelial cells. Hydra completely lacking interstitial cells grow, bud, exhibit tissue renewal patterns, regenerate and preserve polarity generally typical of normal hydra. I cell-free hypostomal tissue has inductive capacity, as does normal hypostomal tissue, when implanted in I cell-free or normal gastric tissue. Regenerating I cell-free tissue undergoes precocious determination as does normal tissue. Only in some quantitative aspects do I cell-free hydra develop abnormally. We conclude that hydra consisting only of epithelial cells are capable of essentially normal development.

Genetic analysis of developmental mechanisms in hydra

Development ◽  
1984 ◽  
Vol 80 (1) ◽  
pp. 155-173
Author(s):  
Jun Takano ◽  
Tsutomu Sugiyama
Keyword(s):  
Epithelial Cell ◽  
Interstitial Cell ◽  
Cell Lineage ◽  
Normal Strain ◽  
Polyp Size ◽  
Bud Formation ◽  
Cell Lineages ◽  
Large Polyp ◽  
Naturally Occurring ◽  
High Head

Chimaeric hydra strains were produced from a normal strain (105) and a naturally-occurring mutant strain (L4) which has a large polyp size, a low budding rate and a high head-inhibition potential. Various properties of the chimaeras were then examined and compared to those of the two parental strains. Hydra tissue consists of three cell lineages: the ectodermal epithelial, the endodermal epithelial and the interstitial cell lineages. Using the methods recently developed by Marcum & Campbell (1978b) and by Wanek & Campbell (1982), six chimaeric strains were produced which contained six different combinations of the three cell lineages from 105 and L4. Evidence obtained from the comparison of the chimaeras and their parental strains indicates that the ectodermal epithelial cell lineage in L4 is primarily responsible for the large polyp size and the low budding rate of this strain, whereas the endodermal epithelial cell lineage is largely, and the interstitial cell lineage is also partially, responsible for the high head-inhibition potential in L4. This suggests that the mechanisms determining the occurrence and location of bud formation and the mechanisms determining the inhibition potential levels are not related to each other (cf. Takano & Sugiyama, 1983; Bode & Bode, 1983). Evidence was also obtained which suggests that the levels of the head-activation and head-inhibition potentials in the chimaeras are determined independent of each other, apparently without the cross-catalytic relationship between them assumed in the Gierer-Meinhardt model (Gierer & Meinhardt, 1972; Meinhardt & Gierer, 1974).

Reactive oxygen species differently regulate renal tubular epithelial and interstitial cell proliferation after ischemia and reperfusion injury

2010 ◽  
Vol 298 (5) ◽  
pp. F1118-F1129 ◽  
Author(s):  
Jinu Kim ◽  
Kyong-Jin Jung ◽  
Kwon Moo Park
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cells ◽  
Interstitial Cell ◽  
Interstitial Cells ◽  
Ischemia And Reperfusion ◽  
Oxygen Species ◽  
Tubular Epithelial Cells ◽  
Cell Type ◽  
A Cell ◽  
Cell Type Specific

Reactive oxygen species (ROS) function as an inducer of cell death and survival or proliferative factor, in a cell-type-specific and concentration-dependent manner. All of these roles are critical to ischemia-induced renal functional impairment and progressive fibrotic changes in the kidney. In an effort to define the role of ROS in the proliferation of tubular epithelial cells and of interstitial cells in kidneys recovering after ischemia and reperfusion (I/R) injury, experimental mice were subjected to 30 min of bilateral kidney ischemia and administered with manganese(III) tetrakis(1-methyl-4-pyridyl) porphyrin (MnTMPyP), a superoxide dismutase mimetic, from 2 to 15 days after I/R for 14 days daily (earlier and longer) and from 8 to 15 days after I/R for 8 days daily (later and shorter). Cell proliferation was assessed via 5′-bromo-2′-deoxyuridine (BrdU) incorporation assays for 20 h before the harvest of kidneys. After I/R, the numbers of BrdU-incorporating cells increased both in the tubules and interstitium. MnTMPyP administration was shown to accelerate the proliferation of tubular epithelial cells, presenting tubule-specific marker proteins along tubular segments, whereas it attenuated the proliferation of interstitial cells, evidencing α-smooth muscle actin, fibroblast-specific protein-1, F4/80, and NADPH oxidase-2 proteins; these results indicated that ROS attenuates tubular cell regeneration, but accelerates interstitial cell proliferation. Earlier and longer MnTMPyP treatment more effectively inhibited tissue superoxide formation, the increment of interstitial cells, and the decrement of epithelial cells compared with later and shorter treatment. After I/R, apoptotic cells appeared principally in the tubular epithelial cells, but not in the interstitial cells, thereby indicating that ROS is harmful in tubule cells, but is not in interstitial cells. In conclusion, ROS generated after I/R injury in cell proliferation and death performs a cell-type-specific and concentration-dependent role, even within the same tissues, and timely intervention of ROS is crucial for effective therapies.

Electron Microscopic Study of the Epithelium of the Seminal Vesicle of Aging Rats

1974 ◽  
Vol 32 ◽  
pp. 138-139
Author(s):  
V. F. Allison ◽  
G. C. Fink ◽  
G. W. Cearley
Keyword(s):  
Cell Growth ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Seminal Vesicle ◽  
Seminal Vesicles ◽  
Epithelial Layer ◽  
Epithelial Hyperplasia ◽  
Electron Microscopic ◽  
Aging Rats ◽  
Pseudostratified Epithelium

It is well known that epithelial hyperplasia (benign hypertrophy) is common in the aging prostate of dogs and man. In contrast, little evidence is available for abnormal epithelial cell growth in seminal vesicles of aging animals. Recently, enlarged seminal vesicles were reported in senescent mice, however, that enlargement resulted from increased storage of secretion in the lumen and occurred concomitant to epithelial hypoplasia in that species.The present study is concerned with electron microscopic observations of changes occurring in the pseudostratified epithelium of the seminal vescles of aging rats. Special attention is given to certain non-epithelial cells which have entered the epithelial layer.

Intranuclear Crystals in Regenerating Canine Kidneys

1973 ◽  
Vol 31 ◽  
pp. 412-413
Author(s):  
D.G. Osborne ◽  
L.J. McCormack ◽  
M.O. Magnusson ◽  
W.S. Kiser
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Tubular Epithelial Cell ◽  
Tubular Epithelial Cells ◽  
Cell Nuclei ◽  
Crystalline Structures ◽  
Small Crystals ◽  
Membrane Bound

During a project in which regenerative changes were studied in autotransplanted canine kidneys, intranuclear crystals were seen in a small number of tubular epithelial cells. These crystalline structures were seen in the control specimens and also in regenerating specimens; the main differences being in size and number of them. The control specimens showed a few tubular epithelial cell nuclei almost completely occupied by large crystals that were not membrane bound. Subsequent follow-up biopsies of the same kidneys contained similar intranuclear crystals but of a much smaller size. Some of these nuclei contained several small crystals. The small crystals occurred at one week following transplantation and were seen even four weeks following transplantation. As time passed, the small crystals appeared to fuse to form larger crystals.

Redistribution and dysfunction of integrins in cultured renal epithelial cells exposed to oxidative stress

1993 ◽  
Vol 264 (1) ◽  
pp. F149-F157 ◽  
Author(s):  
J. Gailit ◽  
D. Colflesh ◽  
I. Rabiner ◽  
J. Simone ◽  
M. S. Goligorsky
Keyword(s):  
Oxidative Stress ◽  
Cell Adhesion ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Surface ◽  
Apical Cell ◽  
Flow Cytometric Analysis ◽  
Adhesion Properties ◽  
Renal Tubular Cells ◽  
Renal Tubular

Tubular obstruction by detached renal tubular epithelial cells is a major cause of oliguria in acute renal failure. Viable renal tubular cells can be recovered from urine of patients with acute tubular necrosis, suggesting a possible defect in cell adhesion to the basement membrane. To study this process of epithelial cell desquamation in vitro, we investigated the effect of nonlethal oxidative stress on the integrin adhesion receptors of the primate kidney epithelial cell line BS-C-1. Morphological and functional studies of cell adhesion properties included the following: interference reflection microscopy, intravital confocal microscopy and immunocytochemistry, flow cytometric analysis of integrin receptor abundance, and cell-matrix attachment assay. High levels of the integrin subunits alpha 3, alpha v, and beta 1 were detected on the cell surface by fluorescence-activated cell sorting (FACS) analysis, as well as lower levels of alpha 1, alpha 2, alpha 4, alpha 5, alpha 6, and beta 3. Exposure of BS-C-1 cells to nonlethal oxidative stress resulted in the disruption of focal contacts, disappearance of talin from the basal cell surface, and in the redistribution of integrin alpha 3-subunits from predominantly basal location to the apical cell surface. As measured in a quantitative cell attachment assay, oxidative stress decreased BS-C-1 cell adhesion to type IV collagen, laminin, fibronectin, and vitronectin. Defective adhesion was not associated with a loss of alpha 3-, alpha 4-, or alpha v-integrin subunits from the cell surface.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals c-Src inactivation reduces renal epithelial cell-matrix adhesion, proliferation, and cyst formation

2011 ◽  
Vol 301 (2) ◽  
pp. C522-C529 ◽  
Author(s):  
Justine Elliott ◽  
Nadezhda N. Zheleznova ◽  
Patricia D. Wilson
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Collecting Duct ◽  
Specific Inhibitor ◽  
Cell Phenotype ◽  
Epithelial Cell Proliferation ◽  
Matrix Adhesion ◽  
Cyst Lining

c-Src is a non-receptor tyrosine kinase whose activity is induced by phosphorylation at Y418 and translocation from the cytoplasm to the cell membrane. Increased activity of c-Src has been associated with cell proliferation, matrix adhesion, motility, and apoptosis in tumors. Immunohistochemistry suggested that activated (pY418)-Src activity is increased in cyst-lining autosomal dominant polycystic kidney disease (ADPKD) epithelial cells in human and mouse ADPKD. Western blot analysis showed that SKI-606 (Wyeth) is a specific inhibitor of pY418-Src without demonstrable effects on epidermal growth factor receptor or ErbB2 activity in renal epithelia. In vitro studies on mouse inner medullary collecting duct (mIMCD) cells and human ADPKD cyst-lining epithelial cells showed that SKI-606 inhibited epithelial cell proliferation over a 24-h time frame. In addition, SKI-606 treatment caused a striking statistically significant decrease in adhesion of mIMCD and human ADPKD to extracellular collagen matrix. Retained viability of unattached cells was consistent with a primary effect on epithelial cell anchorage dependence mediated by the loss of extracellular matrix (ECM)-attachment due to α2β1-integrin function. SKI-606-mediated attenuation of the human ADPKD hyperproliferative and hyper-ECM-adhesive epithelial cell phenotype in vitro was paralleled by retardation of the renal cystic phenotype of Pkd1 orthologous ADPKD heterozygous mice in vivo. This suggests that SKI-606 has dual effects on cystic epithelial cell proliferation and ECM adhesion and may have therapeutic potential for ADPKD patients.

scholarly journals A Dual Role for Oncostatin M Signaling in the Differentiation and Death of Mammary Epithelial Cells in Vivo

2008 ◽  
Vol 22 (12) ◽  
pp. 2677-2688 ◽  
Author(s):  
Paul G. Tiffen ◽  
Nader Omidvar ◽  
Nuria Marquez-Almuina ◽  
Dawn Croston ◽  
Christine J. Watson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Oncostatin M ◽  
Specific Gene ◽  
Mammary Involution

Abstract Recent studies in breast cancer cell lines have shown that oncostatin M (OSM) not only inhibits proliferation but also promotes cell detachment and enhances cell motility. In this study, we have looked at the role of OSM signaling in nontransformed mouse mammary epithelial cells in vitro using the KIM-2 mammary epithelial cell line and in vivo using OSM receptor (OSMR)-deficient mice. OSM and its receptor were up-regulated approximately 2 d after the onset of postlactational mammary regression, in response to leukemia inhibitory factor (LIF)-induced signal transducer and activator of transcription-3 (STAT3). This resulted in sustained STAT3 activity, increased epithelial apoptosis, and enhanced clearance of epithelial structures during the remodeling phase of mammary involution. Concurrently, OSM signaling precipitated the dephosphorylation of STAT5 and repressed expression of the milk protein genes β-casein and whey acidic protein (WAP). Similarly, during pregnancy, OSM signaling suppressed β-casein and WAP gene expression. In vitro, OSM but not LIF persistently down-regulated phosphorylated (p)-STAT5, even in the continued presence of prolactin. OSM also promoted the expression of metalloproteinases MMP3, MMP12, and MMP14, which, in vitro, were responsible for OSM-specific apoptosis. Thus, the sequential activation of IL-6-related cytokines during mammary involution culminates in an OSM-dependent repression of epithelial-specific gene expression and the potentiation of epithelial cell extinction mediated, at least in part, by the reciprocal regulation of p-STAT5 and p-STAT3.

Sign in / Sign up

Export Citation Format

Share Document