scholarly journals A Locomotor Disorder Clinically Similar to Spastic Paresis in an Adult Friesian Bull

1980 ◽  
Vol 17 (3) ◽  
pp. 305-315 ◽  
Author(s):  
R. Bradley ◽  
W.V.S. Wueratne
Keyword(s):  
Skeletal Muscles ◽  
Hind Limb ◽  
Type I ◽  
Type Ii ◽  
Hind Limbs ◽  
Type Ii Cell ◽  
Spastic Paresis ◽  
Flexor Digitorum ◽  
I Cells ◽  
Severe Type

A 5-year-old Friesian stud bull developed a progressive locomotor disorder on return to stud after a period of rest. He had defects in conformation exacerbated by poor condition. The hind limbs were excessively straight. When he stood or moved, the Achilles tendons and their associated muscles were rigid. The disorder clinically resembled spastic paresis of calves. Necropsy showed a degenerative arthropathy in all hind limb joints below the hip. Lesions were also in tendons and skeletal muscles. The M. flexor digitorum superficialis had severe type II cell atrophy with many ring. lobulated and moth-eaten type I cells.

Fine-Structural Changes in a Lepidopteran Nervous System During Metamorphosis

1974 ◽  
Vol 14 (2) ◽  
pp. 369-387
Author(s):  
BARBARA J. McLAUGHLIN
Keyword(s):  
Tight Junctions ◽  
Manduca Sexta ◽  
Structural Changes ◽  
Cell Layer ◽  
Adult Emergence ◽  
Cell Junctions ◽  
Type I ◽  
Type Ii ◽  
Type Ii Cell ◽  
I Cells

The fine structure of the metamorphosing abdominal nerve cord of Manduca sexta has been studied. In fifth instar larvae, the connectives are ensheathed by a complex, thickened neural lamella. The underlying perineurium at this stage consists of 2 layers. The outer layer consists of interdigitating type I cells which are attached to the overlying neural lamella by hemidesmosomes, and to each other by occasional gap and tight junctions which persist throughout development. They are attached by desmosomes to a thin underlying type II cell layer, which is joined by gap and tight junctions and which has desmosomal attachments with the underlying glial membranes. The larval axons are surrounded by multiple glial wrappings containing bundles of microtubules. During the first week after larval-pupal ecdysis, the neural lamella degenerates and is phagocytosed by invading haemocytes. The underlying perineurial I cells gradually become hypertrophied and vacuolated. At the same time the type II layer, which does not increase in size, appears to be composed of either one or two cells which form a continuous ‘bracelet’ around each connective. The cellular bracelet is joined at one or two places by extensive gap, tight and septate junctions, and gap junctions are also seen along its perineurial I and glial borders. The underlying axons are embedded in vast amounts of glial cytoplasm containing relatively few microtubules. During the second week after larval-pupal ecdysis, the neural lamella is reformed and the perineurium flattens again. Type I and II cell junctions remain as described in earlier stages. Before adult emergence, the axons are again wrapped by glial cells rich in microtubules.

Type II epithelial cells are critical target for hyperoxia-mediated impairment of postnatal lung development

2006 ◽  
Vol 291 (5) ◽  
pp. L1101-L1111 ◽  
Author(s):  
Min Yee ◽  
Peter F. Vitiello ◽  
Jason M. Roper ◽  
Rhonda J. Staversky ◽  
Terry W. Wright ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cells ◽  
Lung Development ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Newborn Mice ◽  
Type I Cells ◽  
Type Ii Cell ◽  
I Cells

Type II epithelial cells are essential for lung development and remodeling, as they are precursors for type I cells and can produce vascular mitogens. Although type II cell proliferation takes place after hyperoxia, it is unclear why alveolar remodeling occurs normally in adults whereas it is permanently disrupted in newborns. Using a line of transgenic mice whose type II cells could be identified by their expression of enhanced green fluorescent protein and endogenous expression of surfactant proteins, we investigated the age-dependent effects of hyperoxia on type II cell proliferation and alveolar repair. In adult mice, type II cell proliferation was low during room air and hyperoxia exposure but increased during recovery in room air and then declined to control levels by day 7. Eight weeks later, type II cell number and alveolar compliance were indistinguishable from those in room air controls. In newborn mice, type II cell proliferation markedly increased between birth and postnatal day 7 before declining by postnatal day 14. Exposure to hyperoxia between postnatal days 1 and 4 inhibited type II cell proliferation, which resumed during recovery and was aberrantly elevated on postnatal day 14. Eight weeks later, recovered mice had 70% fewer type II cells and 30% increased lung compliance compared with control animals. Recovered mice also had higher levels of T1α, a protein expressed by type I cells, with minimal changes detected in genes expressed by vascular cells. These data suggest that perinatal hyperoxia adversely affects alveolar development by disrupting the proper timing of type II cell proliferation and differentiation into type I cells.

Expression ofN-deacetylase/sulfotransferase and 3-O-sulfotransferase in rat alveolar type II cells

2000 ◽  
Vol 279 (2) ◽  
pp. L292-L301 ◽  
Author(s):  
Zhong-Yuan Li ◽  
Kazunori Hirayoshi ◽  
Yasuhiro Suzuki
Keyword(s):  
Heparan Sulfate ◽  
Protein A ◽  
Sodium Chlorate ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Type I Cells ◽  
Type Ii Cell ◽  
I Cells

Basal laminae beneath alveolar type I cells are suggested to contain highly sulfated heparan sulfate-containing proteoglycans (PGs), and cultured type II cells accumulate highly sulfated matrices. To characterize the regulation of PG synthesis during the transition from type II cells to type I cells, we examined mRNA expression of N-deacetylase/sulfotransferase (NST) and 3- O-sulfotransferase (3-OST), two enzymes specific for heparan sulfate synthesis. We found that both freshly isolated and cultured type II cells expressed NST and 3-OST as shown by in situ hybridization. Expression of surfactant-associated protein A, B, and C mRNAs, determined by semiquantitative PCR, decreased during culture. Expression of type I cell marker T1α mRNA increased except in cells cultured on an Engelbrecht-Holm-Swarm gel. Expression of NST was dependent on cell density and matrix and was intense in conditions where cells spread fully, whereas 3-OST expression was unchanged in the conditions examined. The PG sulfation inhibitor sodium chlorate significantly inhibited cultured type II cell spreading, and this inhibition was reversed by sodium sulfate. These results suggest that highly sulfated PGs modified by NST are necessary for the spreading of cells during transdifferentiation of type II cells to mature type I cells.

[Ca2+]i oscillations regulate type II cell exocytosis in the pulmonary alveolus

2000 ◽  
Vol 279 (1) ◽  
pp. L5-L13 ◽  
Author(s):  
Yugo Ashino ◽  
Xiaoyou Ying ◽  
Leland G. Dobbs ◽  
Jahar Bhattacharya
Keyword(s):  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Cells ◽  
Lung Inflation ◽  
Type I Cells ◽  
Lung Expansion ◽  
Type Ii Cell ◽  
I Cells

Pulmonary surfactant, a critical determinant of alveolar stability, is secreted by alveolar type II cells by exocytosis of lamellar bodies (LBs). To determine exocytosis mechanisms in situ, we imaged single alveolar cells from the isolated blood-perfused rat lung. We quantified cytosolic Ca2+ concentration ([Ca2+]i) by the fura 2 method and LB exocytosis as the loss of cell fluorescence of LysoTracker Green. We identified alveolar cell type by immunofluorescence in situ. A 15-s lung expansion induced synchronous [Ca2+]i oscillations in all alveolar cells and LB exocytosis in type II cells. The exocytosis rate correlated with the frequency of [Ca2+]i oscillations. Fluorescence of the lipidophilic dye FM1-43 indicated multiple exocytosis sites per cell. Intracellular Ca2+ chelation and gap junctional inhibition each blocked [Ca2+]i oscillations and exocytosis in type II cells. We demonstrated the feasibility of real-time quantifications in alveolar cells in situ. We conclude that in lung expansion, type II cell exocytosis is modulated by the frequency of intercellularly communicated [Ca2+]i oscillations that are likely to be initiated in type I cells. Thus during lung inflation, type I cells may act as alveolar mechanotransducers that regulate type II cell secretion.

scholarly journals Expanding Role of Dopaminergic Inhibition in Hypercapnic Responses of Cultured Rat Carotid Body Cells: Involvement of Type II Glial Cells

2020 ◽  
Vol 21 (15) ◽  
pp. 5434 ◽  
Author(s):  
Erin M. Leonard ◽  
Colin A. Nurse
Keyword(s):  
Carotid Body ◽  
Cell Function ◽  
Atp Release ◽  
Purinergic Signalling ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Type I Cells ◽  
Type Ii Cell ◽  
I Cells

Dopamine (DA) is a well-studied neurochemical in the mammalian carotid body (CB), a chemosensory organ involved in O2 and CO2/H+ homeostasis. DA released from receptor (type I) cells during chemostimulation is predominantly inhibitory, acting via pre- and post-synaptic dopamine D2 receptors (D2R) on type I cells and afferent (petrosal) terminals respectively. By contrast, co-released ATP is excitatory at postsynaptic P2X2/3R, though paracrine P2Y2R activation of neighboring glial-like type II cells may boost further ATP release. Here, we tested the hypothesis that DA may also inhibit type II cell function. When applied alone, DA (10 μM) had negligible effects on basal [Ca2+]i in isolated rat type II cells. However, DA strongly inhibited [Ca2+]i elevations (Δ[Ca2+]i) evoked by the P2Y2R agonist UTP (100 μM), an effect opposed by the D2/3R antagonist, sulpiride (1–10 μM). As expected, acute hypercapnia (10% CO2; pH 7.4), or high K+ (30 mM) caused Δ[Ca2+]i in type I cells. However, these stimuli sometimes triggered a secondary, delayed Δ[Ca2+]i in nearby type II cells, attributable to crosstalk involving ATP-P2Y2R interactions. Interestingly sulpiride, or DA store-depletion using reserpine, potentiated both the frequency and magnitude of the secondary Δ[Ca2+]i in type II cells. In functional CB-petrosal neuron cocultures, sulpiride potentiated hypercapnia-induced Δ[Ca2+]i in type I cells, type II cells, and petrosal neurons. Moreover, stimulation of type II cells with UTP could directly evoke Δ[Ca2+]i in nearby petrosal neurons. Thus, dopaminergic inhibition of purinergic signalling in type II cells may help control the integrated sensory output of the CB during hypercapnia.

Anatomical arrangement of hypercapnia-activated cells in the superficial ventral medulla of rats

2002 ◽  
Vol 93 (2) ◽  
pp. 427-439 ◽  
Author(s):  
Yasumasa Okada ◽  
Zibin Chen ◽  
Wuhan Jiang ◽  
Shun-Ichi Kuwana ◽  
Frederic L. Eldridge
Keyword(s):  
Anatomical Structure ◽  
Type I ◽  
Type Ii ◽  
Type I Cells ◽  
Ventral Medulla ◽  
Surface Vessels ◽  
Type Ii Cell ◽  
Anatomical Arrangement ◽  
I Cells ◽  
Surface Vessel

The anatomical structure of central respiratory chemoreceptors in the superficial ventral medulla of rats was studied by using hypercapnia-induced c- foslabeling to identify cells directly stimulated by extracellular pH or Pco 2. The distribution of c- fos-positive cells was found to be predominantly perivascular to surface vessels. In the superficial ventral medullary midline, parapyramidal, and ventrolateral regions where c- fos-positive cells were concentrated, we found a common, characteristic, anatomical architecture. The medullary surface showed an indentation covered by a surface vessel, and the marginal glial layer was thickened. We classified c- fos-positive cells into two types. One (type I cell) was small, was located inside the marginal glial layer and close to the medullary surface, and surrounded fine vessels. The other (type II cell) was large and located dorsal to the marginal glial layer. c- fos Expression under synaptic blockade suggested that type I cells are intrinsically chemosensitive. The chemosensitivity of surface cells (possible type I cells) surrounding vessels was confirmed electrophysiologically in slice preparations. We suggest that this characteristic anatomical structure may be the central chemoreceptor.

Sulfation of extracellular matrices modifies responses of alveolar type II cells to fibroblast growth factors

1996 ◽  
Vol 271 (5) ◽  
pp. L688-L697 ◽  
Author(s):  
P. L. Sannes ◽  
J. Khosla ◽  
P. W. Cheng
Keyword(s):  
Growth Factors ◽  
Biological Significance ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Fibroblast Growth ◽  
Alveolar Type Ii Cells ◽  
Proliferation And Differentiation ◽  
Type Ii Cell

The pulmonary alveolar basement membrane (BM) associated with alveolar type II cells has been shown to be significantly less sulfated than that of type I cells. To examine the biological significance of this observation, we measured the incorporation of 5-bromodeoxyuridine (BrdU) as an indicator of DNA synthesis in isolated rat type II cells cultured for 72-120 h on substrata that were naturally sulfated, not sulfated, or chemically desulfated in serum-free, hormonally defined media, with and without selected growth factors. The percentage of cells incorporating BrdU was significantly elevated by desulfated chondroitin sulfate in the presence of fibroblast growth factor-2 (FGF-2 or basic FGF) and depressed by heparin in the presence of either FGF-1 or acidic FGF or FGF-2. This depressive effect was lost by removing sulfate from the heparin. Some responses were dependent on the period of time in culture and concentration and molecular weight of the substrata. These observations support the notion that sulfation per se of certain components of BM is a key determinant of type II cell responses to select growth factors that may define patterns of proliferation and differentiation.

scholarly journals Type I interferon promotes alveolar epithelial type II cell survival during pulmonary Streptococcus pneumoniae infection and sterile lung injury in mice

2016 ◽  
Vol 46 (9) ◽  
pp. 2175-2186 ◽  
Author(s):  
Barbara B. Maier ◽  
Anastasiya Hladik ◽  
Karin Lakovits ◽  
Ana Korosec ◽  
Rui Martins ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
Lung Injury ◽  
Cell Survival ◽  
Type I Interferon ◽  
Type I ◽  
Type Ii ◽  
Alveolar Epithelial ◽  
Type Ii Cell
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