scholarly journals The Distribution of Abcc6 in Normal Mouse Tissues Suggests Multiple Functions for this ABC Transporter

2003 ◽  
Vol 51 (7) ◽  
pp. 887-902 ◽  
Author(s):  
Konstanze Beck ◽  
Kimiko Hayashi ◽  
Brian Nishiguchi ◽  
Olivier Le Saux ◽  
Masando Hayashi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Epithelial Cells ◽  
Connective Tissue ◽  
Tissue Distribution ◽  
Cellular Localization ◽  
Immunohistochemical Analysis ◽  
Pseudoxanthoma Elasticum ◽  
Rnase Protection ◽  
Mouse Tissues ◽  
Extracellular Matrix Components

We have studied the tissue distribution of Abcc6, a member of the ABC transmembrane transporter subfamily C, in normal C57BL/6 mice. RNase protection assays revealed that although almost all tissues studied contained detectable levels of the mRNA encoding Abcc6, the highest levels of Abcc6 mRNA were found in the liver. In situ hybridization (ISH) demonstrated abundant Abcc6 mRNA in epithelial cells from a variety of tissues, including hepatic parenchymal cells, bile duct epithelia, kidney proximal tubules, mucosa and gland cells of the stomach, intestine, and colon, squamous epithelium of the tongue, corneal epithelium of the eye, keratinocytes of the skin, and tracheal and bronchial epithelium. Furthermore, we detected Abcc6 mRNA in arterial endothelial cells, smooth muscle cells of the aorta and myocardium, in circulating leukocytes, lymphocytes in the thymus and lymph nodes, and in neurons of the brain, spinal cord, and the specialized neurons of the retina. Immunohistochemical analysis using a polyclonal Abcc6 rabbit antibody confirmed the tissue distribution of Abcc6 suggested by our ISH studies and revealed the cellular localization of Abcc6 in the basolateral plasma membrane in the epithelial cells of proximal convoluted tubules in the kidney. Although the function of Abcc6 is unknown, mutations in the human ABCC6 gene result in a heritable disorder of connective tissue called pseudoxanthoma elasticum (PXE). Our results demonstrating the presence of Abcc6 in epithelial and endothelial cells in a variety of tissues, including those tissues affected in PXE patients, suggest a possible role for Abcc6 in the normal assembly of extracellular matrix components. However, the presence of Abcc6 in neurons and leukocytes, two cell populations not associated with connective tissue, also suggests a more complex multifunctional role for Abcc6.

scholarly journals Claudin-4 Undergoes Age-Dependent Change in Cellular Localization on Pig Jejunal Villous Epithelial Cells, Independent of Bacterial Colonization

2015 ◽  
Vol 2015 ◽  
pp. 1-14 ◽  
Author(s):  
J. Alex Pasternak ◽  
Coral Kent-Dennis ◽  
Andrew G. Van Kessel ◽  
Heather L. Wilson
Keyword(s):  
Epithelial Cells ◽  
Cellular Localization ◽  
Bacterial Colonization ◽  
Immunohistochemical Analysis ◽  
Commensal Microbiota ◽  
Newborn Piglets ◽  
Dependent Change ◽  
Surface Localization ◽  
Protective Strategies ◽  
Gnotobiotic Piglets

Newborn piglets are immunologically naïve and must receive passive immunity via colostrum within 24 hours to survive. Mechanisms by which the newborn piglet gut facilitates uptake of colostral cells, antibodies, and proteins may include FcRn and pIgR receptor-mediated endocytosis and paracellular transport between tight junctions (TJs). In the present study, FcRn gene (FCGRT) was minimally expressed in 6-week-old gut and newborn jejunum but it was expressed at significantly higher levels in the ileum of newborn piglets. pIgR was highly expressed in the jejunum and ileum of 6-week-old animals but only minimally in neonatal gut. Immunohistochemical analysis showed that Claudin-5 localized to blood vessel endothelial cells. Claudin-4 was strongly localized to the apical aspect of jejunal epithelial cells for the first 2 days of life after which it was redistributed to the lateral surface between adjacent enterocytes. Claudin-4 was localized to ileal lateral surfaces within 24 hours after birth indicating regional and temporal differences. Tissue from gnotobiotic piglets showed that commensal microbiota did not influence Claudin-4 surface localization on jejunal or ileal enterocytes. Regulation of TJs by Claudin-4 surface localization requires further investigation. Understanding the factors that regulate gut barrier maturation may yield protective strategies against infectious diseases.

scholarly journals Expression of Human Group II Phospholipase A2 in Transgenic Mice

1997 ◽  
Vol 45 (8) ◽  
pp. 1109-1119 ◽  
Author(s):  
Timo J. Nevalainen ◽  
V. Jukka O. Laine ◽  
David S. Grass
Keyword(s):  
In Situ Hybridization ◽  
Epithelial Cells ◽  
Urinary Bladder ◽  
Connective Tissue ◽  
Transgenic Mice ◽  
Phospholipase A ◽  
Human Group ◽  
Mouse Tissues ◽  
Group Ii

Group II phospholipase A2 (PLA2) has been proposed to play an important role in inflammation and defense against bacterial infection. We investigated tissues of transgenic mice expressing the human group II PLA2 gene by immunohistochemistry using rabbit anti-human group II PLA2 antibodies, and by in situ hybridization by probing with human group II PLA2 mRNA anti-sense (test) and sense (control) riboprobes. By immunohis-tochemistry, human group II PLA2 was found in various mouse tissues and cell types including hepatocytes, proximal tubule cells of the kidney, epithelial cells of the renal pelvis, urinary bladder and ureter, granulosa cells of Graafian follicles, aortic intima and media, cartilage, epiphyseal bone, bronchial epithelial cells, and connective tissue cells in the dermis. By in situ hybridization, group II PLA2 mRNA was localized in hepatocytes, epidermal cells, dermal cells, connective tissue fibroblasts, epithelial and smooth muscle cells of the urinary bladder, and cells of Bowman's capsule. These results show that human group II PLA2 is expressed in large amounts in hepatocytes and many extrahepatic tissues of the transgenic mice. These animals provide a useful new tool for studies on the metabolism, in vivo effects, and physiological and pathological roles of phospholipase A2. (J Histochem Cytochem 45:1109–1119, 1997)

scholarly journals Differential localization of mRNAs of collagen types I and II in chick fibroblasts, chondrocytes, and corneal cells by in situ hybridization using cDNA probes.

1986 ◽  
Vol 102 (6) ◽  
pp. 2302-2309 ◽  
Author(s):  
M Hayashi ◽  
Y Ninomiya ◽  
J Parsons ◽  
K Hayashi ◽  
B R Olsen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
In Situ Hybridization ◽  
Epithelial Cells ◽  
Type Ii Collagen ◽  
Type I ◽  
Type Ii ◽  
Collagen Types ◽  
Paraffin Sections ◽  
Extracellular Matrix Components

We have employed a highly specific in situ hybridization protocol that allows differential detection of mRNAs of collagen types I and II in paraffin sections from chick embryo tissues. All probes were cDNA restriction fragments encoding portions of the C-propeptide region of the pro alpha-chain, and some of the fragments also encoded the 3'-untranslated region of mRNAs of either type I or type II collagen. Smears of tendon fibroblasts and those of sternal chondrocytes from 17-d-old chick embryos as well as paraffin sections of 10-d-old whole embryos and of the cornea of 6.5-d-old embryos were hybridized with 3H-labeled probes for either type I or type II collagen mRNA. Autoradiographs revealed that the labeling was prominent in tendon fibroblasts with the type I collagen probe and in sternal chondrocytes with the type II collagen probe; that in the cartilage of sclera and limbs from 10-d-old embryos, the type I probe showed strong labeling of fibroblast sheets surrounding the cartilage and of a few chondrocytes in the cartilage, whereas the type II probe labeled chondrocytes intensely and only a few fibroblasts; and that in the cornea of 6.5-d-old embryos, the type I probe labeled the epithelial cells and fibroblasts in the stroma heavily, and the endothelial cells slightly, whereas the type II probe labeled almost exclusively the epithelial cells except for a slight labeling in the endothelial cells. These data indicate that embryonic tissues express these two collagen genes separately and/or simultaneously and offer new approaches to the study of the cellular regulation of extracellular matrix components.

scholarly journals Localization of Type 8 17β-hydroxysteroid Dehydrogenase mRNA in Mouse Tissues as Studied by In Situ Hybridization

2005 ◽  
Vol 53 (10) ◽  
pp. 1257-1271 ◽  
Author(s):  
Georges Pelletier ◽  
Van Luu-The ◽  
Songyun Li ◽  
Fernand Labrie
Keyword(s):  
In Situ Hybridization ◽  
Epithelial Cells ◽  
Stromal Cells ◽  
Cellular Localization ◽  
Pulmonary Arteries ◽  
Hydroxysteroid Dehydrogenase ◽  
Hybridization Signal ◽  
Mouse Tissues ◽  
Sites Of Action

The enzyme type 8 17β-hydroxysteroid dehydrogenase (17β-HSD) selectively catalyzes the conversion of estradiol (E2) to estrone (E1). To obtain detailed information on the sites of action of type 8 17β-HSD, we have studied the cellular localization of type 8 17β-HSD mRNA in mouse tissues using in situ hybridization. In the ovary, hybridization signal was detected in granulosa cells of growing follicles and luteal cells. In the uterus, type 8 17β-HSD mRNA was found in the epithelial (luminal and glandular) and stromal cells. In the female mammary gland, the enzyme mRNA was seen in ductal epithelial cells and stromal cells. In the testis, hybridization signal was observed in the seminiferous tubule. In the prostate, type 8 17β-HSD was detected in the epithelial cells of the acini and stromal cells. In the clitoral and preputial glands, labeling was detected in the epithelial cells of acini and small ducts. The three lobes of the pituitary gland were labeled. In the adrenal gland, hybridization signal was observed in the three zones of the cortex, the medulla being unlabeled. In the kidney, the enzyme mRNA was found to be expressed in the epithelial cells of proximal convoluted tubules. In the liver, all the hepatocytes exhibited a positive signal. In the lung, type 8 17β-HSD mRNA was detected in bronchial epithelial cells and walls of pulmonary arteries. The present data suggest that type 8 17β-HSD can exert its action to downregulate E2 levels in a large variety of tissues.

Expression and localization of aquaporins in rat gastrointestinal tract

1999 ◽  
Vol 276 (3) ◽  
pp. C621-C627 ◽  
Author(s):  
Yu Koyama ◽  
Tadashi Yamamoto ◽  
Tatsuo Tani ◽  
Kouei Nihei ◽  
Daisuke Kondo ◽  
...  
Keyword(s):  
Small Intestine ◽  
In Situ Hybridization ◽  
Gastrointestinal Tract ◽  
Epithelial Cells ◽  
Cellular Localization ◽  
Basolateral Membrane ◽  
Rnase Protection Assay ◽  
Rnase Protection ◽  
Basolateral Membranes

A family of water-selective channels, aquaporins (AQP), has been demonstrated in various organs and tissues. However, the localization and expression of the AQP family members in the gastrointestinal tract have not been entirely elucidated. This study aimed to demonstrate the expression and distribution of several types of the AQP family and to speculate on their role in water transport in the rat gastrointestinal tract. By RNase protection assay, expression of AQP1–5 and AQP8 was examined in various portions through the gastrointestinal tract. AQP1 and AQP3 mRNAs were diffusely expressed from esophagus to colon, and their expression was relatively intense in the small intestine and colon. In contrast, AQP4 mRNA was selectively expressed in the stomach and small intestine and AQP8 mRNA in the jejunum and colon. Immunohistochemistry and in situ hybridization demonstrated cellular localization of these AQP in these portions. AQP1 was localized on endothelial cells of lymphatic vessels in the submucosa and lamina propria throughout the gastrointestinal tract. AQP3 was detected on the circumferential plasma membranes of stratified squamous epithelial cells in the esophagus and basolateral membranes of cardiac gland epithelia in the lower stomach and of surface columnar epithelia in the colon. However, AQP3 was not apparently detected in the small intestine. AQP4 was present on the basolateral membrane of the parietal cells in the lower stomach and selectively in the basolateral membranes of deep intestinal gland cells in the small intestine. AQP8 mRNA expression was demonstrated in the absorptive columnar epithelial cells of the jejunum and colon by in situ hybridization. These findings may indicate that water crosses the epithelial layer through these water channels, suggesting a possible role of the transcellular route for water intake or outlet in the gastrointestinal tract.

scholarly journals Endothelial cells are an important source of BDNF in rat skeletal muscle

2022 ◽  
Vol 12 (1) ◽  
Author(s):  
Marina Cefis ◽  
Remi Chaney ◽  
Aurore Quirié ◽  
Clélia Santini ◽  
Christine Marie ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Endothelial Cells ◽  
Cellular Localization ◽  
Immunohistochemical Analysis ◽  
Receptor Expression ◽  
Type I ◽  
Type Ii ◽  
Rat Skeletal Muscle ◽  
Bdnf Expression ◽  
Trkb Receptors

AbstractBDNF (brain-derived neurotrophic factor) is present in skeletal muscle, controlling muscular metabolism, strength and regeneration processes. However, there is no consensus on BDNF cellular source. Furthermore, while endothelial tissue expresses BDNF in large amount, whether endothelial cells inside muscle expressed BDNF has never been explored. The aim of the present study was to provide a comprehensive analysis of BDNF localization in rat skeletal muscle. Cellular localization of BDNF and activated Tropomyosin-related kinase B (TrkB) receptors was studied by immunohistochemical analysis on soleus (SOL) and gastrocnemius (GAS). BDNF and activated TrkB levels were also measured in muscle homogenates using Western blot analysis and/or Elisa tests. The results revealed BDNF immunostaining in all cell types examined with a prominent staining in endothelial cells and a stronger staining in type II than type I muscular fibers. Endothelial cells but not other cells displayed easily detectable activated TrkB receptor expression. Levels of BDNF and activated TrkB receptors were higher in SOL than GAS. In conclusion, endothelial cells are an important and still unexplored source of BDNF present in skeletal muscle. Endothelial BDNF expression likely explains why oxidative muscle exhibits higher BDNF levels than glycolytic muscle despite higher the BDNF expression by type II fibers.

Tracing CD34+ Stromal Fibroblasts in Palatal Mucosa and Periodontal Granulation Tissue as a Possible Cell Reservoir for Periodontal Regeneration

2015 ◽  
Vol 21 (4) ◽  
pp. 837-848 ◽  
Author(s):  
Alexandra Roman ◽  
Emőke Páll ◽  
Carmen M. Mihu ◽  
Adrian S. Petruţiu ◽  
Lucian Barbu-Tudoran ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Connective Tissue ◽  
Granulation Tissue ◽  
Smooth Muscle Actin ◽  
Periodontal Regeneration ◽  
Spatial Relationship ◽  
Immunohistochemical Analysis ◽  
Stromal Fibroblasts ◽  
Close Spatial Relationship ◽  
Systemic Factors

AbstractThe aim of the present research was to trace CD34+ stromal fibroblastic cells (CD34+ SFCs) in the palatal connective tissue harvested for muco-gingival surgical procedures and in granulation tissues from periodontal pockets using immunohistochemical and transmission electron microscopy. Immunohistochemical analysis targeted the presence of three antigens: CD31,α-smooth muscle actin (α-SMA), and CD34. In the palate, CD31 staining revealed a colored inner ring of the vessels representing the endothelium,α-SMA+ was located in the medial layer of the vasculature, and CD34 was intensely expressed by endothelial cells and artery adventitial cells (considered to be CD34+ SFCs). Granulation tissue showed the same pattern for CD31+ andα-SMA, but a different staining pattern for CD34. Ultrastructural examination of the palatal tissue highlighted perivascular cells with fibroblast-like characteristics and pericytes in close spatial relationship to endothelial cells. The ultrastructural evaluation of granulation tissue sections confirmed the presence of neovasculature and the inflammatory nature of this tissue. The present study traced the presence of CD34+ SFCs and of pericytes in the palatal connective tissue thus highlighting once more its intrinsic regenerative capabilities. The clinical and systemic factors triggering mobilization and influencing the fate of local CD34+SCFs and other progenitors are issues to be further investigated.

Factors Involved In the Plasminogen Activation System in Human Breast Tumours

1994 ◽  
Vol 71 (05) ◽  
pp. 684-691 ◽  
Author(s):  
László Damjanovich ◽  
Csaba Turzó ◽  
Róza Ádány
Keyword(s):  
Epithelial Cells ◽  
Connective Tissue ◽  
Plasminogen Activators ◽  
Breast Tumour ◽  
Plasminogen Activation ◽  
Malignant Tumours ◽  
Plasminogen Activation System ◽  
Activation System ◽  
Malignant Breast ◽  
Pai 1

SummaryThe plasminogen activation system is a delicately balanced assembly of enzymes which seems to have primary influence on tumour progression. The conversion of plasminogen into serine protease plasmin with fibrinolytic activity depends on the actual balance between plasminogen activators (urokinase type; u-PA and tissue type; t-PA) and their inhibitors (type 1 and 2 plasminogen activator inhibitors; PAI-1 and PAI-2). The purpose of this study was to determine the exact histological localization of all the major factors involved in plasminogen activation, and activation inhibition (plasmin system) in benign and malignant breast tumour samples. Our results show that factors of the plasmin system are present both in benign and malignant tumours. Cancer cells strongly labelled for both u-PA and t-PA, but epithelial cells of fibroadenoma samples were also stained for plasminogen activators at least as intensively as tumour cells in cancerous tissues. In fibroadenomas, all the epithelial cells were labelled for PAM. Staining became sporadic in malignant tumours, cells located at the periphery of tumour cell clusters regularly did not show reaction for PAI-1. In the benign tumour samples the perialveolar connective tissue stroma contained a lot of PAI-1 positive cells, showing characteristics of fibroblasts; but their number was strongly decreased in the stroma of malignant tumours. These findings indicate that the higher level of u-PA antigen, detected in malignant breast tumour samples by biochemical techniques, does not necessarily indicate increased u-PA production by tumour cells but it might be owing to the increased number of cells producing u-PA as well. In malignant tumours PAI-1 seems to be decreased in the frontage of malignant cell invasion; i.e. malignant cells at the host/tumour interface do not express PAI-1 in morphologically detectable quantity and in the peritumoural connective tissue the number of fibroblasts containing PAI-1 is also decreased.

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