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. 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.

Regulation of interstitial cell differentiation in Hydra attenuata. I. Homeostatic control of interstitial cell population size

1976 ◽  
Vol 20 (1) ◽  
pp. 29-46 ◽  
Author(s):  
H.R. Bode ◽  
K.M. Flick ◽  
G.S. Smith
Keyword(s):  
Cell Differentiation ◽  
Epithelial Cells ◽  
Population Size ◽  
Cell Population ◽  
Interstitial Cell ◽  
Normal Population ◽  
Cell Types ◽  
Hydra Attenuata ◽  
I Cells ◽  
Continuous Labelling

Mechanisms regulating the population size of the multipotent interstitial cell (i-cell) in Hydra attenuata were investigated. Treatment of animals with 3 cycles of a regime of 24 h in 10-2 M hydroxyurea (HU) alternated with 12 h in culture medium selectively killed 95–99% of the i-cells, but had little effect on the epithelial cells. The i-cell population recovered to the normal i-cell:epithelial cell ratio of I:I within 35 days. Continuous labelling experiments with [3H]thymidine indicate that the recovery of the i-cell population is not due to a change in the length of the cell cycle of either the epithelial cells or the interstitial cells. In control animals 60% of the i-cell population undergo division daily while 40% undergo differentiation. Quantification of the cell types of HU-treated animals indicates that a greater fraction of the i-cells were dividing and fewer differentiating into nematocytes during the first 2 weeks of the recovery after HU treatment. Therefore, the mechanism for recovery involves a shift of the 60:40 division:differentiation ratio of i-cells towards a higher fraction in division until the normal population size of the i-cells is regained. This homeostatic mechanism represents one of the influences affecting i-cell differentiation.

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.

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.

scholarly journals Immunolocalization of Sonic Hedgehog (Shh) in Developing Mouse Lung

2001 ◽  
Vol 49 (12) ◽  
pp. 1593-1603 ◽  
Author(s):  
Leigh-Anne D. Miller ◽  
Susan E. Wert ◽  
Jeffrey A. Whitsett
Keyword(s):  
Epithelial Cells ◽  
Sonic Hedgehog ◽  
Normal Development ◽  
Clara Cell ◽  
Mouse Lung ◽  
Lung Hypoplasia ◽  
Hepatocyte Nuclear Factor ◽  
Clara Cells ◽  
Lung Morphogenesis ◽  
Conducting Airways

Expression of sonic hedgehog (Shh) is required for normal development of the lung during embryogenesis. Loss of Shh expression in mice results in tracheoesophageal fistula, lung hypoplasia, and abnormal lung lobulation. To determine whether Shh may play a role later in lung morphogenesis, immunostaining for Shh was performed in mouse lung from embryonic day (E) 10.5 to postnatal day (PD) 24. Shh was detected in the distal epithelium of the developing mouse lung from E10.5 to E16.5. From E16.5 until PD15, Shh was present in epithelial cells in both the peripheral and conducting airways. Although all cells of the developing epithelium uniformly expressed Shh at E10.5, Shh expression was restricted to subsets of epithelial cells by E16.5. Between E16.5 and PD15, non-uniform Shh staining of epithelial cells was observed in the conducting airways in a pattern consistent with the distribution of non-ciliated bronchiolar cells (i.e., Clara cells) and the Clara cell marker CCSP. Shh did not co-localize with hepatocyte nuclear factor/forkhead homologue-4 (HFH-4), β-tubulin, or with the presence of cilia. These results support the concept that Shh plays a distinct regulatory role in the lung later in morphogenesis, when it may influence formation or cytodifferentiation of the conducting airways.

Interstitial cells of Cajal and telocytes in the gut: twins, related or simply neighbor cells?

2016 ◽  
Vol 7 (2) ◽  
pp. 93-102 ◽  
Author(s):  
Maria Giuliana Vannucchi ◽  
Chiara Traini
Keyword(s):  
Interstitial Cells Of Cajal ◽  
Alimentary Tract ◽  
Interstitial Cell ◽  
Plasma Cells ◽  
Interstitial Cells ◽  
Local Response ◽  
Inflammatory Stimuli ◽  
Pace Maker ◽  
Unique Cell ◽  
Cells Of Cajal

AbstractIn the interstitium of the connective tissue several types of cells occur. The fibroblasts, responsible for matrix formation, the mast cells, involved in local response to inflammatory stimuli, resident macrophages, plasma cells, lymphocytes, granulocytes and monocytes, all engaged in immunity responses. Recently, another type of interstitial cell, found in all organs so far examined, has been added to the previous ones, the telocytes (TC). In the gut, in addition to the cells listed above, there are also the interstitial cells of Cajal (ICC), a peculiar type of cell exclusively detected in the alimentary tract with multiple functions including pace-maker activity. The possibility that TC and ICC could correspond to a unique cell type, where the former would represent an ICC variant outside the gut, was initially considered, however, further studies have clearly shown that ICC and TC are two distinct types of cells. In the gut, while the features and the roles of the ICC are established, part of the scientific community is still disputing these ‘new’ interstitial cells to which several names such as fibroblast-like cells (FLCs), interstitial Cajal-like cells or, most recently, PDGFRα+ cells have been attributed. This review will detail the main features and roles of the TC and ICC with the aim to establish their relationships and hopefully define the identity of the TC in the gut.

Tentacular and oral-disc regeneration in the sea anemone, Aiptasia diaphana

Development ◽  
1971 ◽  
Vol 26 (2) ◽  
pp. 253-270
Author(s):  
Irwin I. Singer
Keyword(s):  
Electron Microscopy ◽  
Cell Proliferation ◽  
Cellular Proliferation ◽  
Interstitial Cell ◽  
Interstitial Cells ◽  
Thymidine Uptake ◽  
Cell Distribution ◽  
Oral Disc ◽  
Cellular Division ◽  
Disc Regeneration

Autoradiography with [3H]thymidine and electron microscopy were used to determine (a) the patterns of cellular division exhibited by intact anemones, (b) if measurable increases in cellular proliferation accompany oral-disc regeneration, (c) whether interstitial cells are present in Aiptasia, and (d) if these cells could be responsible for the latter proliferative patterns. An oral-aboral gradient in cellular proliferation was exhibited by the epidermis of uncut anemones, with the highest levels in the tentacles. Wound healing did not require cell proliferation and did not immediately stimulatecellular division which was associated with subsequent morphogenetic events. Indices of presumptive oral-disc [3H]thymidine uptake into nuclei increased tenfold with the outgrowth of the new tentacles. This increase occurred in the epidermis, while only small amounts of gastrodermal proliferation were detected. It is hypothesized that the epidermis contributes new cells to the expanding gastrodermis during tentacle budding. Most of the [3H]thymidine-labeled nuclei were localized in the basal portions of the epidermis of intact anemones and 1- to 2-day-old regenerates; very few gastrodermal nuclei accumulated the label. Nests of interstitial cells and transforming interstitial cells were localized in the exact epidermal regions where nuclear labeling took place, suggesting that the proliferative patterns of intact and regenerating Aiptasia are a function of their interstitial cell distribution.

scholarly journals Renomedullary Interstitial Cell Endothelin A Receptors Regulate BP and Renal Function

2020 ◽  
Vol 31 (7) ◽  
pp. 1555-1568
Author(s):  
Chunyan Hu ◽  
Jayalakshmi Lakshmipathi ◽  
Deborah Stuart ◽  
Janos Peti-Peterdi ◽  
Georgina Gyarmati ◽  
...  
Keyword(s):  
Renal Function ◽  
Knockout Mice ◽  
Interstitial Cell ◽  
Collecting Duct ◽  
Interstitial Cells ◽  
Water Excretion ◽  
Endothelin 1 ◽  
Enhanced Production ◽  
Endothelin A Receptor ◽  
Endothelin A

BackgroundThe physiologic role of renomedullary interstitial cells, which are uniquely and abundantly found in the renal inner medulla, is largely unknown. Endothelin A receptors regulate multiple aspects of renomedullary interstitial cell function in vitro.MethodsTo assess the effect of targeting renomedullary interstitial cell endothelin A receptors in vivo, we generated a mouse knockout model with inducible disruption of renomedullary interstitial cell endothelin A receptors at 3 months of age.ResultsBP and renal function were similar between endothelin A receptor knockout and control mice during normal and reduced sodium or water intake. In contrast, on a high-salt diet, compared with control mice, the knockout mice had reduced BP; increased urinary sodium, potassium, water, and endothelin-1 excretion; increased urinary nitrite/nitrate excretion associated with increased noncollecting duct nitric oxide synthase-1 expression; increased PGE2 excretion associated with increased collecting duct cyclooxygenase-1 expression; and reduced inner medullary epithelial sodium channel expression. Water-loaded endothelin A receptor knockout mice, compared with control mice, had markedly enhanced urine volume and reduced urine osmolality associated with increased urinary endothelin-1 and PGE2 excretion, increased cyclooxygenase-2 protein expression, and decreased inner medullary aquaporin-2 protein content. No evidence of endothelin-1–induced renomedullary interstitial cell contraction was observed.ConclusionsDisruption of renomedullary interstitial cell endothelin A receptors reduces BP and increases salt and water excretion associated with enhanced production of intrinsic renal natriuretic and diuretic factors. These studies indicate that renomedullary interstitial cells can modulate BP and renal function under physiologic conditions.

scholarly journals Transitional human alveolar type II epithelial cells suppress extracellular matrix and growth factor gene expression in lung fibroblasts

2019 ◽  
Vol 317 (2) ◽  
pp. L283-L294 ◽  
Author(s):  
Kelly A. Correll ◽  
Karen E. Edeen ◽  
Rachel L. Zemans ◽  
Elizabeth F. Redente ◽  
Karina A. Serban ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Surfactant Protein ◽  
Lung Fibroblasts ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
I Cells

Epithelial-fibroblast interactions are thought to be very important in the adult lung in response to injury, but the specifics of these interactions are not well defined. We developed coculture systems to define the interactions of adult human alveolar epithelial cells with lung fibroblasts. Alveolar type II cells cultured on floating collagen gels reduced the expression of type 1 collagen (COL1A1) and α-smooth muscle actin (ACTA2) in fibroblasts. They also reduced fibroblast expression of hepatocyte growth factor (HGF), fibroblast growth factor 7 (FGF7, KGF), and FGF10. When type II cells were cultured at an air-liquid interface to maintain high levels of surfactant protein expression, this inhibitory activity was lost. When type II cells were cultured on collagen-coated tissue culture wells to reduce surfactant protein expression further and increase the expression of some type I cell markers, the epithelial cells suppressed transforming growth factor-β (TGF-β)-stimulated ACTA2 and connective tissue growth factor (CTGF) expression in lung fibroblasts. Our results suggest that transitional alveolar type II cells and likely type I cells but not fully differentiated type II cells inhibit matrix and growth factor expression in fibroblasts. These cells express markers of both type II cells and type I cells. This is probably a normal homeostatic mechanism to inhibit the fibrotic response in the resolution phase of wound healing. Defining how transitional type II cells convert activated fibroblasts into a quiescent state and inhibit the effects of TGF-β may provide another approach to limiting the development of fibrosis after alveolar injury.

Immunolocalisation of androgen receptor to interstitial cells in fetal rat testes and to mesenchymal and epithelial cells of associated ducts

1995 ◽  
Vol 147 (2) ◽  
pp. 285-293 ◽  
Author(s):  
G Majdic ◽  
M R Millar ◽  
P T K Saunders
Keyword(s):  
Androgen Receptor ◽  
Epithelial Cells ◽  
Leydig Cells ◽  
Interstitial Cells ◽  
Mesenchymal Cells ◽  
Wolffian Duct ◽  
Nuclear Staining ◽  
Mullerian Duct ◽  
Fetal Rat ◽  
Fetal Leydig Cells

Abstract Androgens are required for the development of male internal and external genitalia. Androgen action is mediated by an intracellular receptor which acts as a transcription factor following activation by ligand binding. The aim of the present study was to define the time of appearance of androgen receptor (AR) in the male fetal rat gonad using immunohistochemistry. Intact fetuses (days 13·5–16·5) or testicular tissue (days 16·5–20·5 and days 3–7 postnatal) were fixed in Bouins' solution and processed into paraffin wax. On day 16·5 nuclear AR were present in mesenchymal cells surrounding the Wolffian duct but those around the Mullerian duct were receptor negative. During the following day (17–18) the abundance of nuclear staining increased, becoming detectable in the epithelial cells of the Wolffian ducts. Within the testis some nuclear staining was apparent at day 17 but was confined to interstitial cells surrounding the seminiferous cords. As development of the testis proceeded the abundance of nuclear AR in peritubular and elongated mesenchymal cells increased. AR were not detected in fetal Leydig cells expressing 3β-hydroxysteroid dehydrogenase nor in the ovaries or associated ducts of female fetuses at the same ages. In conclusion, in the rat we have found AR expression detectable by immunohistochemistry in mesonephric mesenchyme to be confined to that underlying the Wolffian ducts and to be absent from the area around the degenerating Mullerian duct. On and after day 17 of gestation AR is present in Wolffian duct epithelial cell nuclei and within the testis it is confined to peritubular and interstitial cells which may have migrated from the mesonephros. Fetal Leydig cells were receptor negative. Within the seminiferous cords AR in Sertoli cells remained low until after birth and some perinuclear staining was detected in cells thought to be gonocytes. We believe this to be the first report of immunolocalisation of AR to fetal testicular interstitial cells. Journal of Endocrinology (1995) 147, 285–293

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