Tubular Elongation Research Articles

Occurrence of Microplastics in the Tissues of Nile Tilapia (Orechromis niloticus) from Zobe Dam, Katsina State, Nigeria

A study of the detection of microplastics on Oreochromis niloticus in Zobe Reservoir, Katsina State, Nigeria was carried out. Three fish sampling sites were used; the upstream (Tsawatsawa), midstream (Makera), and downstream (Garhi) were selected based on variation of anthropogenic activities. A total number of one hundred and forty-four (144) fish samples with a total weight (MTW) and total length (MTL) varied between 134.1 ±1.50 to 154.2± 3.41g and 17.5 ± 0.10– 22.1± 0.54 cm respectively, were collected and analysed for the presence of microplastics using standard protocols. Fourier Transform Infrared Spectrophotometer (FTIR) was used for the chemical characterization of microplastic composition examined in the fish species. The examination of microplastic occurrence in different sampled fish gills, liver, and kidney revealed the presence of Polystyrene, Polypropylene, Polyethylene terephthalate, Nylon, Polyester, and Polyvinyl chloride. Fish from all sampling sites revealed varying histopathological alterations ranging from lifting of epithelium thickening, distortion of the primary lamellae, and degeneration of secondary lamellae, blood congestion, and massive lamellae degeneration in the gill tissues. Liver tissues had hepatocyte hypertrophy, sinusoidal dilatation and cytoplasmic vacuolation, presence of lipid granules, cellular infiltration, cytoplasmic vacuolation, and haemorrhage. The kidney tissues were presented with Bowman’s capsules hyperplasia, tubular elongation, renal tubular epithelium shrinkage, hyperplasia, and cytoplasmic vacuolization of renal cells. The severity of the damage varies from site to site indicating that the water body is experiencing pollution at varying locations. Our findings provide important insights into the prevalence and distribution of microplastics in this particular environment.

Colossal C130 Fullertubes: Soluble [5,5] C130-D5h(1) Pristine Molecules with 70 Nanotube Carbons and Two 30-Atom Hemifullerene End-caps.

We report the seminal experimental isolation and DFT characterization of pristine [5,5] C130-D5h(1) fullertubes. This achievement represents the largest soluble carbon molecule obtained in its pristine form. The [5,5] C130 species is the highest aspect ratio fullertube purified to date and now surpasses the recent gigantic [5,5] C120-D5d(1). In contrast to C90, C100, and C120 fullertubes, the longer C130-D5h has more nanotubular carbons (70) than end-cap fullerenyl atoms (60). Starting from 39,393 possible C130 isolated pentagon rule (IPR) structures and after analyzing polarizability, retention time, and UV-vis spectra, these three layers of data remarkably predict a single candidate isomer and fullertube, [5,5] C130-D5h(1). This structural assignment is augmented by atomic resolution STEM data showing distinctive and tubular "pill-like" structures with diameters and aspect ratios consistent with [5,5] C130-D5h(1) fullertubes. The high selectivity of the aminopropanol reaction with spheroidal fullerenes permits facile separation and removal of fullertubes from soot extracts. Experimental analyses (HPLC retention time, UV-vis, and STEM) were synergistically used (with polarizability and DFT property calculations) to down select and confirm the C130 fullertube structure. Achieving the isolation of a new [5,5] C130-D5h fullertube opens the door to application development and fundamental studies of electron confinement, fluorescence, and metallic character for a fullertube series of molecules with systematic tubular elongation. This [5,5] fullertube family also invites comparative studies with single-walled carbon nanotubes (SWCNTs), nanohorns (SWCNHs), and fullerenes.

Anteater nose sign and reverse anteater nose sign: Are they specific for calcaneonavicular coalition?

The anteater nose sign has been described on imaging in the case of the calcaneonavicular coalition and is produced by a tubular elongation of the anterior calcaneal process that approaches or overlaps the navicular bone, resembling an anteater’s nose. Similarly, the reverse anteater sign refers to the posterior and lateral extension of the navicular bone, also seen in the case of the calcaneonavicular coalition. Originally described on lateral or oblique foot/ankle radiographs, this appearance is also observed in the case of magnetic resonance images (MRI) on sagittal sections. We describe a case of a talocalcaneal coalition, in which the MRI had a similar appearance, thereby confusing the imaging findings of the case, and discuss the key imaging features for the correct diagnosis. We also propose a new sign, “Opposing beak sign,” for this similar appearance in the case of a talo-calcaneal coalition, awareness of which as a distinct entity on sagittal MRI would help correct preoperative diagnosis and subsequent management.

Differential role of planar cell polarity gene Vangl2 in embryonic and adult mammalian kidneys.

Planar cell polarity (PCP) pathway is crucial for tissue morphogenesis. Mutations in PCP genes cause multi-organ anomalies including dysplastic kidneys. Defective PCP signaling was postulated to contribute to cystogenesis in polycystic kidney disease. This work was undertaken to elucidate the role of the key PCP gene, Vangl2, in embryonic and postnatal renal tubules and ascertain whether its loss contributes to cyst formation and defective tubular function in mature animals. We generated mice with ubiquitous and collecting duct-restricted excision of Vangl2. We analyzed renal tubules in mutant and control mice at embryonic day E17.5 and postnatal days P1, P7, P30, P90, 6- and 9-month old animals. The collecting duct functions were analyzed in young and adult mutant and control mice. Loss of Vangl2 leads to profound tubular dilatation and microcysts in embryonic kidneys. Mechanistically, these abnormalities are caused by defective convergent extension (larger tubular cross-sectional area) and apical constriction (cuboidal cell shape and a reduction of activated actomyosin at the luminal surface). However, the embryonic tubule defects were rapidly resolved by Vangl2-independent mechanisms after birth. Normal collecting duct architecture and functions were found in young and mature animals. During embryogenesis, Vangl2 controls tubular size via convergent extension and apical constriction. However, rapidly after birth, PCP-dependent control of tubular size is switched to a PCP-independent regulatory mechanism. We conclude that loss of the Vangl2 gene is dispensable for tubular elongation and maintenance postnatally. It does not lead to cyst formation and is unlikely to contribute to polycystic kidney disease.

Mitochondrial dysfunctions in leukoencephalopathy with brainstem and spinal cord involvement and lactate elevation (LBSL).

Several inherited human diseases have been linked to mitochondrial aminoacyl-tRNA synthetases (mtARSs). Leukoencephalopathy with brainstem and spinal cord involvement and lactate elevation (LBSL) is a leukodystrophy caused by mutations in the DARS2 gene which encodes mitochondrial aspartyl-tRNA synthetase. As mitochondrial ARSs are key components of the mitochondrial translation apparatus, we investigated the effects of DARS2 mutations on mitochondrial functions and mitochondrial morphology in an LBSL patient. In fibroblasts from the patient with LBSL, biosynthesis of respiratory chain complex proteins encoded by mitochondrial DNA was decreased, while those encoded by nuclear DNA were not. Cellular oxygen consumption rates and respiratory control ratio were decreased in the LBSL patient; in addition, fragmentation of mitochondria was increased, while their tubular elongation and interconnectivity were decreased. Taken together, these findings suggest that DARS2 mutations impair translations of mitochondrial DNA-encoded respiratory chain complex proteins, consequently causing dysfunction of cellular respiration and impediment of mitochondrial dynamics, which highlights the role of mtARSs in the maintenance of normal mitochondrial bioenergetics and dynamics.

Role of Core Planar Cell Polarity Vangl2 Gene in the Renal Tubule Development in Mice

Background: Polycystic kidney disease (PKD) is a common kidney disease that affects the development and maintenance of renal tubules, leads to cyst formation, and often progresses to end-stage kidney disease. It has been postulated that defective planar cell polarity (PCP) signaling contributes to initiation of cyst formation in PKD via controlling both convergent extension (CE, a process of directional cell movements) and oriented cell division (OCD, a process of directional cell divisions during tubular elongation post-natally). Indeed, mutations of the key PCP gene, Van Gogh-like 2 (Vangl2), lead to abnormal renal tubules in murine embryonic kidneys, correlating with the original postulate. Methods: In order to further understand the influence of the Vangl2 gene on renal morphogenesis and cystogenesis, control and Vangl2 mutant embryos—as well as post-natal Vangl2 mice with conditional excision of the Vangl2 gene in renal collecting tubules—were generated, then analyzed using immunostaining and fluorescence microscopy. Results: Our results show that Vangl2 plays a role in CE and apical constriction (AC) during embryonic stage of tubulogenesis. Compared to control animals, mutant Vangl2Δ/Δ and conditional Vangl2Δ/CD embryos displayed: i) a significant dilation in the diameter of renal tubules seen as an increased tubule cross-section area and a larger number of cells per cross-section; and ii) changes in cell shape indicative of defective AC. Surprisingly, post-natal mice showed virtually no difference in any of these aspects comparing to control mice, suggesting that other pathways may compensate for the lack of PCP signaling in maintenance of the tubule architecture. Limitations: a) The analysis of the renal tubules at the specific time points does not account for the dynamics of tubular movement and growth in real time; b) a mechanistic and morphological distinction between mice and humans may exist in the renal collecting duct tubules, pertaining to the Vangl2 gene’s influence in the PCP pathway; and c) the degree of mosaicism resulting from the gene excision by Cre-recombinase may correlate with the severity of the phenotype. Conclusion: We conclude that the PCP pathway is required for normal tubule development during embryogenesis. Our results, however, indicate that the cystogenesis seen in PKD postnatally may not be directly attributed to the disrupted PCP signaling, and requires the derangement of additional pathways.

Postnatal Developmental Changes of the Kidneys of the Albino Rat

Background: Being a highly immature organ at birth, the rat kidney is morphologically as fetal when compared with humans. Events that occur during fetal development might determine adult renal diseases. Aim of work: This study aimed to characterize the postnatal developmental changes of the kidneys in albino rats using light microscope from postnatal day (PND) 2 until PND 70. This may give references to pathologists when evaluating juvenile toxicology studies. Materials and Methods: Ten healthy pregnant albino rats were used in this study. Twenty-five of their offsprings were obtained and divided according to age into five groups of 5 pups each.Group A: studied at PND 2. Group B: studied at PND 10. Group C: studied at PND 20. Group D: studied at PND 30. Group E: studied at PND 70. Kidneys were removed, processed for light microscopic study and 5 mm thick paraffin sections were obtained and stained with hematoxylin and eosin stain. Results: Light microscopic examination of the renal cortex at PND 2 revealed subcapsular nephrogenic zone contained immature renal developmental stages, juxtamedullary zone contained formed glomeruli with medullary rays between the two zones. The renal cortex acquired maturation centrifugally with the superficial nephrons was the last to mature by PND 20. The papilla was the most mature region of the kidney and at PND2; it had the structural composition of the inner stripe of outer medulla. The papillary maturation involved a process of tubular elongation and increase in the interstitium until reaching adult structure by PND 20. At PND 2, the medulla was the most immature zone being formed of islets of tubular structures among abundant interstitium with high degree of undifferentiation. Its maturation involved tubular elongation and decrease of the interstitium with the outer medulla was the last to mature as late as PND 30. Consequently, the medulla remained immature for a relatively long postnatal period, in comparison to the other kidney regions. Conclusion: It was concluded that, rat kidney is immature at birth and kidney sub regions mature at different rates during postnatal development. The papilla was the first to mature (PND 20) followed by the cortex (PND 20) and finally the medulla (PND 30).

Coalición calcáneo-navicular asociada a pie plano rígido infantil. A propósito de un caso

Tarsal coalition (a congenital fibrous, cartilaginous or bony connection between two bones) often leads to a flatfoot deformity in children. Usually it presents with recurrent ankle sprains or insidious onset of a painful rigid flatfoot and movement limitation of midtarsal and subtalar joints. Clinical diagnosis is confirmed by X-rays, computed axial tomography and nuclear magnetic resonance. The anteater nose sign is caused by a tubular elongation of the anterior process of the calcaneus that approaches or overlaps the tarsal scaphoid (navicular) and resembles the nose of an anteater on a lateral foot or ankle radiograph. The treatment of this union is primarily symptomatic but if the pain persists must be surgical .

FGF8 coordinates tissue elongation and cell epithelialization during early kidney tubulogenesis.

When a tubular structure forms during early embryogenesis, tubular elongation and lumen formation (epithelialization) proceed simultaneously in a spatiotemporally coordinated manner. We here demonstrate, using the Wolffian duct (WD) of early chicken embryos, that this coordination is regulated by the expression of FGF8, which shifts posteriorly during body axis elongation. FGF8 acts as a chemoattractant on the leader cells of the elongating WD and prevents them from epithelialization, whereas static (‘rear’) cells that receive progressively less FGF8 undergo epithelialization to form a lumen. Thus, FGF8 acts as a binary switch that distinguishes tubular elongation from lumen formation. The posteriorly shifting FGF8 is also known to regulate somite segmentation, suggesting that multiple types of tissue morphogenesis are coordinately regulated by macroscopic changes in body growth.

Planar Cell Polarity Pathway in Kidney Development and Function

The evolutionarily conserved planar cell polarity (PCP) signaling pathway controls tissue polarity within the plane orthogonal to the apical-basal axis. PCP was originally discovered inDrosophila melanogasterwhere it is required for the establishment of a uniform pattern of cell structures and appendages. In vertebrates, including mammals, the PCP pathway has been adapted to control various morphogenetic processes that are critical for tissue and organ development. These include convergent extension (crucial for neural tube closure and cochlear duct development) and oriented cell division (needed for tubular elongation), ciliary tilting that enables directional fluid flow, and other processes. Recently, strong evidence has emerged to implicate the PCP pathway in vertebrate kidney development. In this review, we will describe the experimental data revealing the role of PCP signaling in nephrogenesis and kidney disease.

The contactin RIG-6 mediates neuronal and non-neuronal cell migration in Caenorhabditis elegans

Cell adhesion molecules of the Immunoglobulin Superfamily (IgCAMs) are key factors in nervous system formation. The contactin subgroup of IgCAMs consists of GPI-anchored glycoproteins implicated in axon outgrowth, guidance, fasciculation and neuronal differentiation. The mechanism by which contactins facilitate neuronal development is not understood. To gain insight into the function of contactins, we characterized RIG-6, the sole contactin of Caenorhabditis elegans. We show that the contactin RIG-6 is involved in excretory cell (EC) tubular elongation. We also show that RIG-6 mediates axon outgrowth and guidance along both the anterior–posterior and dorso-ventral axis, during C. elegans development. We find that optimal RIG-6 expression is critical for accurate mechanosensory neuron axon elongation and ventral nerve cord architecture. In addition, our data suggest that the cytoplasmic UNC-53/NAV2 proteins may contribute to relay signaling via contactins.

Functional interactions between Fat family cadherins in tissue morphogenesis and planar polarity

The atypical cadherin fat (ft) was originally discovered as a tumor suppressor in Drosophila and later shown to regulate a form of tissue patterning known as planar polarity. In mammals, four ft homologs have been identified (Fat1-4). Recently, we demonstrated that Fat4 plays a role in vertebrate planar polarity. Fat4 has the highest homology to ft, whereas other Fat family members are homologous to the second ft-like gene, ft2. Genetic studies in flies and mice imply significant functional differences between the two groups of Fat cadherins. Here, we demonstrate that Fat family proteins act both synergistically and antagonistically to influence multiple aspects of tissue morphogenesis. We find that Fat1 and Fat4 cooperate during mouse development to control renal tubular elongation, cochlear extension, cranial neural tube formation and patterning of outer hair cells in the cochlea. Similarly, Fat3 and Fat4 synergize to drive vertebral arch fusion at the dorsal midline during caudal vertebra morphogenesis. We provide evidence that these effects depend on conserved interactions with planar polarity signaling components. In flies, the transcriptional co-repressor Atrophin (Atro) physically interacts with Ft and acts as a component of Fat signaling for planar polarity. We find that the mammalian orthologs of atro, Atn1 and Atn2l, modulate Fat4 activity during vertebral arch fusion and renal tubular elongation, respectively. Moreover, Fat4 morphogenetic defects are enhanced by mutations in Vangl2, a 'core' planar cell polarity gene. These studies highlight the wide range and complexity of Fat activities and suggest that a Fat-Atrophin interaction is a conserved element of planar polarity signaling.

Ductal plates in hepatic ductular reactions. Hypothesis and implications. II. Ontogenic liver growth in childhood

This article discusses the processes of bile duct growth and new lobule formation in the liver during childhood in the light of the ductal plate (DP) hypothesis. Unlike in other organs in which tubular elongation and branching ends with the creation of the organ-specific terminal differentiation products, in the liver a steadily enlarging parenchymal mass needs to establish continuity of its canalicular network with the existing bile duct system. The hypothesis suggests that this occurs by DP formation, like in the embryonic liver, and further assumes that pathological ductular reactions (DRs) induced by cholestasis or hypoxia are amplified equivalents of similar mechanisms operating at low level during liver growth. The concept is confronted with data on porcine liver growth, since swine and non-swine liver growth is thought to be comparable. Relative bile acid load may be the driving force for establishment of new canaliculo-ductular connections, supported in zones of relative hypoxia by hypoxia-inducible factor 1 alpha secreted by hepatocytes. The latter mechanism is at the base for induction of appropriate vascular changes in selected sinusoids, resulting in the development of portal inlet venules and additional draining central veins. The process gives rise to the formation of new single lobules by formation of new portal tracts or to the transformation of single lobules in compound lobules by development of new vascular septa. The concept of postnatal DP formation is important in the elucidation of several unexplained findings in adult liver diseases.

What Drives Cyst Formation in PKD?

Polycystic kidney disease (PKD) is the most common genetic cause of chronic kidney disease, with an incidence of 1:400 to 1:1000.1 PKD is characterized by many large fluid-filled cysts in the kidney and often leads to end-stage renal failure. Intensive work from numerous international teams has succeeded in identifying three genes that account for almost all cases of PKD: polycystin-1 ( PC-1 ), polycystin-2 ( PC-2 ), and polycystic kidney and hepatic disease 1 ( Pkhd1 ).2–4 Autosomal dominant PKD is caused by mutations in PC-1 or PC-2. PC-1 encodes a protein with a large extracellular domain, 11 transmembrane domains, and a cytoplasmic tail . PC-2 encodes a transient receptor potential channel with six transmembrane domains that resembles PC-1. Autosomal recessive PKD is caused by mutations in Pkhd1, another protein with a large extracellular domain, a single transmembrane domain, and a cytoplasmic domain. Although the loci responsible for PKD are known, it is still poorly understood why mutations in PC-1 , PC-2 , and Pkhd1 result in cyst formation. Numerous models have been proposed to account for the development of cysts.1 Recent notions, which raise a great deal of interest, are that ciliary function and/or planar cell polarity (PCP) is disrupted during cyst formation. The primary cilium is an antenna-like structure that emerges from the apical surface of kidney epithelial cells, which has been found to be a key signaling center for many developmental pathways.5 A role for …

Preparation of monoclonal antibody against LRR-WSC domain of polycystin-1 and distribution of polycystin-1 in kidney tissues and kidney cell lines

目的 用杂交瘤技术制备抗多囊蛋白-1 LRR-WSC区单克隆抗体,检测多囊蛋白-1在肾组织和肾细胞株中的分布和定位.方法用多囊蛋白-1 LRR-WSC区融合蛋白PC1-e免疫BALB/c小鼠,将其脾细胞与骨髓瘤细胞株SP2/0进行细胞融合,间接酶联免疫吸附试验(ELISA)筛选出阳性克隆,有限稀释法将杂交瘤细胞株单克隆化,间接ELISA法和免疫印迹法(WB)鉴定抗体的特异性.用制备的抗多囊蛋白-1 LRR-WSC区单克隆抗体,免疫组织化学和免疫细胞化学法检测多囊蛋白-1在不同肾组织和肾细胞株中的分布.结果细胞融合后经筛选和克隆得到的杂交瘤细胞株经WB分析表明,该细胞株分泌的单克隆抗体能特异地与多囊蛋白-1 LRR-WSC区结合.免疫组织化学显示,多囊蛋白-1主要分布于正常肾组织的远端肾小管和集合管,在胎肾囊肿组织中表达于近端肾小管,在人常染色体显性多囊肾病(ADPKD)肾囊肿组织中,表达于囊肿衬里上皮细胞,同时在ADPKD肾囊肿衬里上皮细胞系和猪近端肾小管细胞株(LLC-PK1)中也发现了多囊蛋白-1的表达.结论本实验成功制备了抗多囊蛋白-1 LRR-WSC区的单克隆抗体,该抗体对深入研究ADPKD的发病机制具有重要意义.多囊蛋白-1在肾组织中的表达模式对肾小管的形态发生、维持肾小管结构的完整性非常重要。

Amylin as a growth factor during fetal and postnatal development of the rat kidney

We have previously reported that amylin has mitogenic actions on tubular epithelial cells isolated from mature rat kidney and cultured in vitro. In experiments using in situ hybridization, we have demonstrated that amylin mRNA can be detected transiently in rat metanephros from embryo day 17 (E17) to postnatal day 3 (PN3). These transcripts are localized in the sub-nephrogenic zone. RT-PCR was performed using oligonucleotide primers for rat amylin and mRNA extracted from fetal body (E19), PN1 and PN5 metanephroi, and adult rat kidney. These results corroborate the finding, using in situ hybridization, that there is a window of expression of rat amylin in the developing kidney in the perinatal period. During this period tubular elongation is evident and amylin peptide, detected by immunohistochemical staining, is found associated with developing tubules. Some of these tubules also express a brush border glycoprotein, detected by immunohistochemical staining. Amylin acts as a mitogen with primary cultures of proximal tubular epithelial cells from PN4 renal cortex. An amylin antagonist inhibited this mitogenic action suggesting that this was mediated by amylin receptors as previously described. We suggest that amylin peptide is biosynthesized in the developing proximal tubules, acts in an autocrine fashion to promote the proliferation and differentiation of brush border epithelial cells and hence plays an important role as a growth factor in the development of the kidney.

Effects of glucose on migration, proliferation and tube formation by vascular endothelial cells

In order to elucidate the association between hyperglycemia and the vascular complications of diabetes, the effects of high glucose concentrations on the migration, proliferation and tube formation of bovine carotid artery endothelial cells were investigated. Cells treated with 16.7 and 33.3 mM glucose for 6 days showed 1.69- and 1.75-fold increase in serum-induced migration compared with cells treated with 5.6 mM glucose (p less than 0.05). The effect of glucose on cell proliferation was affected by serum concentration. When this was below 0.5%, a high glucose concentration stimulated cell growth to a maximum of 1.73 times that at a serum concentration of 0.05% (p less than 0.01) whereas at a serum concentration of 10%, growth was inhibited (p less than 0.05). Tube formation was studied by culturing the cells between two layers of collagen gel. Ultrastructurally, tubular structures were composed of one to several endothelial cells containing pinocytotic vesicles and cytoplasmic projections, and linked by junctional complexes. A basal lamina-like structure surrounded the abluminal surface. Treatment of the cells with 16.7 and 27.8 mM glucose for 4 days stimulated tubular elongation 1.85 and 1.71 times, respectively (p less than 0.01). Other osmogenic molecules such as mannitol and sucrose did not affect tube formation. These data imply that high glucose concentrations mimicking diabetic hyperglycemia may not inhibit the repair of endothelial injury and could act as a stimulator of neovascularization.

EARLY HISTOGENESIS OF THE ADULT LEAVES OF DARLINGTONIA CALIFORNICA (SARRACENIACEAE) AND ITS BEARING ON THE NATURE OF EPIASCIDIATE FOLIAR APPENDAGES

In order to assess the validity of various interpretations of tubular leaves of angiosperms, a histogenetic study of the ontogeny of adult leaves of Darlingtonia californica was undertaken. The adult leaf of Darlingtonia is characterized by a sheathing leaf base, an elongate ascidium, an overarching hood, and two “fishtail” appendages which arise near the leaf apex. A keellike growth, with two rows of alternate vascular bundles, traverses the tube from base to mouth. Ontogenetic studies show that the primordium arises by a monopodial rather than a sympodial mode of growth as previously reported. After the formation of a small, erect primordium, a restricted adaxial meristem is initiated that expands both adaxially and upwards. This “querzone” serves, in effect, to congenitally combine the two primordial margins during its extension. Growth and maturation of the subjacent portions cause tubular elongation in the leaf. Primordial apical divisions are later replaced by more general intercalary growth with acropetal and centrifugal maturation. The hood and fishtails are established early in ontogeny by adaxial growth of the primordial apex and subsequent activation of juxtaposed localized meristems. Comparative morphology has established that the epiascidiate leaf is a foliar appendage that undergoes certain specific morphogenetic modifications. It has a structural relationship to ensiform appendages of Acacia and Acorus as well as to peltate foliar organs. The early ontogeny of Darlingtonia leaves is considered to be homologous with other epiascidiate foliar organs, including some supposedly primitive carpels.