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  1. Book ; Online ; E-Book: Laboratory guide to the tight junction

    Hou, Jianghui

    2020  

    Author's details Jianghui Hou
    Keywords Tight junctions (Cell biology)
    Language English
    Size 1 online resource
    Publisher Academic Press
    Publishing place London
    Document type Book ; Online ; E-Book
    Note Includes index.
    Remark Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
    ISBN 0-12-818647-X ; 978-0-12-818647-3
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Book ; Online ; E-Book: The paracellular channel

    Hou, Jianghui

    biology, physiology, and disease

    2019  

    Abstract: The Paracellular Channel: Biology, Physiology and Disease serves as the first volume to offer a cohesive and unifying picture of the critical functions of paracellular channels (tight junctions) in different tissues. This new class of ion channel ... ...

    Author's details Jianghui Hou
    Abstract The Paracellular Channel: Biology, Physiology and Disease serves as the first volume to offer a cohesive and unifying picture of the critical functions of paracellular channels (tight junctions) in different tissues. This new class of ion channel utilizes a completely different mechanism to create ion passage pathways across the cell junction. This volume outlines common principles that govern the organization and regulation of these diverse cellular structures, describes the methodology of study, and highlights the pathophysiologic consequence of abnormal structure and functions of the paracellular channels in human diseases. Coverage includes biochemical, biophysical, structural, physiologic analyses of the paracellular channel, and new technologies for recording and characterization
    Keywords Tight Junction Proteins / physiology ; Tight Junctions / physiology
    Subject code 571.6
    Language English
    Size 1 Online-Ressource (xvii, 230 Seiten), Illustrationen
    Publisher Academic Press, an imprint of Elsevier
    Publishing place London
    Publishing country Great Britain
    Document type Book ; Online ; E-Book
    Remark Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
    HBZ-ID HT019973740
    ISBN 978-0-12-814636-1 ; 9780128146354 ; 0-12-814636-2 ; 0128146354
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  3. Article ; Online: Lack of expression of miR-29a/b1 impairs bladder function in male mice

    Zunyi Wang / Robert Spitz / Chad Vezina / Jianghui Hou / Dale E. Bjorling

    Disease Models & Mechanisms, Vol 16, Iss

    2023  Volume 6

    Keywords mir-29a ; bladder fibrosis ; uroflow ; cystometry ; mice ; Medicine ; R ; Pathology ; RB1-214
    Language English
    Publishing date 2023-06-01T00:00:00Z
    Publisher The Company of Biologists
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article: The Impact of Urbanization on the Distribution of Spontaneous Herbaceous Plants in an Ancient City: A Pilot Case Study in Jingzhou, China.

    Hou, Shuwang / Tian, Changwei / Meng, Jianghui / Liu, Chunyan / Yao, Zhen

    Plants (Basel, Switzerland)

    2023  Volume 12, Issue 19

    Abstract: Spontaneous herbaceous plants (SHPs) play an essential role in urban biodiversity. Research on the diversity of SHPs has profound implications for the conservation of urban biodiversity and green space management in the process of urbanization. We ... ...

    Abstract Spontaneous herbaceous plants (SHPs) play an essential role in urban biodiversity. Research on the diversity of SHPs has profound implications for the conservation of urban biodiversity and green space management in the process of urbanization. We investigated the habitat, life form, and growth form of SHPs by combining samples and inspections in Jingzhou, in central southern China. Additionally, we chose three typical regions-Ji'nan, Gucheng, and Shashi-for the examination and comparison of biodiversity. The results showed that diverse habitats provided abundant living space for SHPs of different growth forms and life forms in Jingzhou. Water edges with higher humidity do not significantly support more SHP growth forms and life forms, except for pseudo-rosette, partial-rosette, and perennial plants. In addition, both wasteland and road gaps and slopes support significantly more SHP growth forms, including erect, tussock, and others. Wasteland supported the vast majority of species, both growth forms and life forms. In the diverse habitats, there are 352 plant species belonging to 70 families and 236 genera in Jingzhou (Ji'nan 184 species, Gucheng 157 species, and Shashi 127 species). Plant species diversity differed according to the level of management. The Ji'nan region had a large number of SHP species because of the less disruptive and milder management implemented in this region. SHPs show good performance and can provide wild landscape effects; therefore, they have the potential to be used in many urban landscaping applications. In the process of urbanization expansion, we should implement the concept of protection and coordinated development in new construction areas. Our study has important implications for the support of SHPs in urban areas.
    Language English
    Publishing date 2023-09-22
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2704341-1
    ISSN 2223-7747
    ISSN 2223-7747
    DOI 10.3390/plants12193353
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Claudins and mineral metabolism.

    Hou, Jianghui

    Current opinion in nephrology and hypertension

    2016  Volume 25, Issue 4, Page(s) 308–313

    Abstract: Purpose of review: The tight junction conductance made of the claudin-based paracellular channel is important in the regulation of calcium and magnesium reabsorption in the kidney. This review describes recent findings of the structure, the function, ... ...

    Abstract Purpose of review: The tight junction conductance made of the claudin-based paracellular channel is important in the regulation of calcium and magnesium reabsorption in the kidney. This review describes recent findings of the structure, the function, and the physiologic regulation of claudin-14, claudin-16, and claudin-19 channels that through protein interactions confer calcium and magnesium permeability to the tight junction.
    Recent findings: Mutations in two tight junction genes - claudin-16 and claudin-19 - cause the inherited renal disorder familial hypomagnesemia with hypercalciuria and nephrocalcinosis. A recent genome-wide association study has identified claudin-14 as a major risk gene of hypercalciuric nephrolithiasis. The crystal structure of claudin-19 has recently been resolved allowing the reconstruction of a claudin assembly model from cis-dimers made of claudin-16 and claudin-19 interaction. MicroRNAs have been identified as novel regulators of the claudin-14 gene. The microRNA-claudin-14 operon is directly regulated by the Ca sensing receptor gene in response to hypercalcemia.
    Summary: The paracellular pathway in the kidney is particularly important for mineral metabolism. Three claudin proteins - claudin-14, claudin-16, and claudin-19 - contribute to the structure and function of this paracellular pathway. Genetic mutations and gene expression changes in these claudins may lead to alteration of the paracellular permeability to calcium and magnesium, ultimately affecting renal mineral metabolism.
    MeSH term(s) Calcium/metabolism ; Claudins/genetics ; Claudins/metabolism ; Genome-Wide Association Study ; Humans ; Hypercalciuria/genetics ; Hypercalciuria/metabolism ; Kidney/metabolism ; Magnesium/metabolism ; MicroRNAs/metabolism ; Nephrocalcinosis/genetics ; Nephrocalcinosis/metabolism ; Nephrolithiasis/genetics ; Nephrolithiasis/metabolism ; Receptors, Calcium-Sensing/metabolism ; Renal Tubular Transport, Inborn Errors/genetics ; Renal Tubular Transport, Inborn Errors/metabolism ; Tight Junctions/metabolism
    Chemical Substances CLDN19 protein, human ; Claudins ; MicroRNAs ; Receptors, Calcium-Sensing ; claudin 16 ; Magnesium (I38ZP9992A) ; Calcium (SY7Q814VUP) ; claudin 14 (W7WL5ZNY9I)
    Language English
    Publishing date 2016-05-14
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1151092-4
    ISSN 1473-6543 ; 1535-3842 ; 1062-4813 ; 1062-4821
    ISSN (online) 1473-6543 ; 1535-3842
    ISSN 1062-4813 ; 1062-4821
    DOI 10.1097/MNH.0000000000000239
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3686: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (2.OG)
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  6. Article ; Online: Paracellular transport in the collecting duct.

    Hou, Jianghui

    Current opinion in nephrology and hypertension

    2016  Volume 25, Issue 5, Page(s) 424–428

    Abstract: Purpose of review: The paracellular pathway through the tight junction provides an important route for chloride reabsorption in the collecting duct of the kidney. This review describes recent findings of how defects in paracellular chloride permeation ... ...

    Abstract Purpose of review: The paracellular pathway through the tight junction provides an important route for chloride reabsorption in the collecting duct of the kidney. This review describes recent findings of how defects in paracellular chloride permeation pathway may cause kidney diseases and how such a pathway may be regulated to maintain normal chloride homeostasis.
    Recent findings: The tight junction in the collecting duct expresses two important claudin genes - claudin-4 and claudin-8. Transgenic knockout of either claudin gene causes hypotension, hypochloremia, and metabolic alkalosis in experimental animals. The claudin-4 mediated chloride permeability can be regulated by a protease endogenously expressed by the collecting duct cell - channel-activating protease 1. Channel-activating protease 1 regulates the intercellular interaction of claudin-4 and its membrane stability. Kelch-like 3, previously identified as a causal gene for Gordon's syndrome, also known as pseudohypoaldosteronism II, directly interacts with claudin-8 and regulates its ubiquitination and degradation. The dominant pseudohypoaldosteronism-II mutation (R528H) in Kelch-like 3 abolishes claudin-8 binding, ubiquitination, and degradation.
    Summary: The paracellular chloride permeation pathway in the kidney is an important but understudied area in nephrology. It plays vital roles in renal salt handling and regulation of extracellular fluid volume and blood pressure. Two claudin proteins, claudin-4 and claudin-8, contribute to the function of this paracellular pathway. Deletion of either claudin protein from the collecting duct causes renal chloride reabsorption defects and low blood pressure. Claudins can be regulated on posttranslational levels by several mechanisms involving protease and ubiquitin ligase. Deregulation of claudins may cause human hypertension as exemplified in the Gordon's syndrome.
    MeSH term(s) Animals ; Blood Pressure ; Carrier Proteins ; Chlorides/metabolism ; Claudin-4/genetics ; Claudin-4/metabolism ; Claudins/genetics ; Humans ; Kidney Diseases/etiology ; Kidney Diseases/metabolism ; Kidney Tubules, Collecting/enzymology ; Kidney Tubules, Collecting/metabolism ; Permeability ; Pseudohypoaldosteronism/metabolism ; Renal Reabsorption ; Serine Endopeptidases/metabolism ; Tight Junctions/metabolism
    Chemical Substances Carrier Proteins ; Chlorides ; Claudin-4 ; Claudins ; KLHL3 protein, human ; Serine Endopeptidases (EC 3.4.21.-) ; prostasin (EC 3.4.21.-) ; claudin 8 (HJ6C19SU7L)
    Language English
    Publishing date 2016-08-01
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1151092-4
    ISSN 1473-6543 ; 1535-3842 ; 1062-4813 ; 1062-4821
    ISSN (online) 1473-6543 ; 1535-3842
    ISSN 1062-4813 ; 1062-4821
    DOI 10.1097/MNH.0000000000000253
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 3686: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  7. Article: Effect of Sun exposure-induced ferroptosis mechanisms on pathology and potential biological processes of primary melanoma by microarray data analysis.

    Gao, Yakun / Hou, Qiang / Guo, Rong / Ying, Jianghui / Xiong, Jiachao / Jiang, Hua

    Frontiers in genetics

    2022  Volume 13, Page(s) 998792

    Abstract: Objectives: ...

    Abstract Objectives:
    Language English
    Publishing date 2022-09-26
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2606823-0
    ISSN 1664-8021
    ISSN 1664-8021
    DOI 10.3389/fgene.2022.998792
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Lack of expression of miR-29a/b1 impairs bladder function in male mice.

    Wang, Zunyi / Spitz, Robert / Vezina, Chad / Hou, Jianghui / Bjorling, Dale E

    Disease models & mechanisms

    2023  Volume 16, Issue 6

    Abstract: Lower urinary tract symptoms (LUTS) refer to various urological diseases, and incomplete bladder emptying is common among affected patients. The etiology of LUTS is largely unknown, and investigations of LUTS suggest that bladder fibrosis contributes to ... ...

    Abstract Lower urinary tract symptoms (LUTS) refer to various urological diseases, and incomplete bladder emptying is common among affected patients. The etiology of LUTS is largely unknown, and investigations of LUTS suggest that bladder fibrosis contributes to pathogenesis of LUTS. MicroRNAs (miRNAs) are short (∼22 nucleotides), non-coding RNAs that repress target gene expression by a combination of mRNA degradation and translation inhibition. The miR-29 family is best known for its anti-fibrotic role in various organs. miR-29 was decreased in bladders of patients with outlet obstruction and a rat model of bladder outlet obstruction, suggesting that miR-29 may contribute to impaired bladder function subsequent to tissue fibrosis. We characterized bladder function in male mice lacking expression of Mir29a and Mir29b-1 (miR-29a/b1). Lack of miR-29a/b1 resulted in severe urinary retention, increased voiding duration and reduced flow rate, and these mice failed to void or voided irregularly during anesthetized cytometry. Collagens and elastin were increased in bladders of mice lacking miR-29a/b1. These findings reveal an important role for miR-29 in bladder homeostasis and suggest the therapeutic potential of miR-29 to improve symptoms in patients with LUTS.
    MeSH term(s) Mice ; Male ; Rats ; Animals ; Urinary Bladder/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Fibrosis ; Collagen
    Chemical Substances MicroRNAs ; Collagen (9007-34-5) ; MIRN29 microRNA, mouse
    Language English
    Publishing date 2023-06-07
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2451104-3
    ISSN 1754-8411 ; 1754-8403
    ISSN (online) 1754-8411
    ISSN 1754-8403
    DOI 10.1242/dmm.050054
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: The kidney tight junction (Review).

    Hou, Jianghui

    International journal of molecular medicine

    2014  Volume 34, Issue 6, Page(s) 1451–1457

    Abstract: The tight junction is an important subcellular organelle which plays a vital role in epithelial barrier function. Claudin, as the integral membrane component of tight junctions, creates a paracellular transport pathway for various ions to be reabsorbed ... ...

    Abstract The tight junction is an important subcellular organelle which plays a vital role in epithelial barrier function. Claudin, as the integral membrane component of tight junctions, creates a paracellular transport pathway for various ions to be reabsorbed by the kidneys. This review summarizes advances in claudin structure, function and pathophysiology in kidney diseases. Different claudin species confer selective paracellular permeability to each of three major renal tubular segments: the proximal tubule, the thick ascending limb of Henle's loop and the distal nephron. Defects in claudin function can cause a wide spectrum of kidney diseases, such as hypomagnesemia, hypercalciuria, kidney stones and hypertension. Studies using transgenic mouse models with claudin mutations have recapitulated several of these renal disease phenotypes and have elucidated the underlying biological mechanisms. Modern recording approaches based upon scanning ion conductance microscopy may resolve the biophysical nature of claudin transport function and provide novel insight into tight junction architecture.
    MeSH term(s) Animals ; Biological Transport ; Claudins/chemistry ; Claudins/metabolism ; Crystallography, X-Ray ; Humans ; Junctional Adhesion Molecules/chemistry ; Junctional Adhesion Molecules/metabolism ; Kidney/cytology ; Kidney/metabolism ; Models, Biological ; Tight Junction Proteins/metabolism ; Tight Junctions/metabolism
    Chemical Substances Claudins ; Junctional Adhesion Molecules ; Tight Junction Proteins
    Language English
    Publishing date 2014-10-01
    Publishing country Greece
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1444428-8
    ISSN 1791-244X ; 1107-3756
    ISSN (online) 1791-244X
    ISSN 1107-3756
    DOI 10.3892/ijmm.2014.1955
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 4942: Show issues Location:
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  10. Article ; Online: Denervation Affected Skin Wound Healing in a Modified Rat Model.

    Lu, Lu / Liu, Dandan / Ying, Jianghui / Yao, Zuochao / Hou, Qiang / Wang, Hui / Qi, Fazhi / Luan, Wenjie / Jiang, Hua

    The international journal of lower extremity wounds

    2022  , Page(s) 15347346221090758

    Abstract: ... ...

    Abstract Introduction
    Language English
    Publishing date 2022-03-28
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2171119-7
    ISSN 1552-6941 ; 1534-7346
    ISSN (online) 1552-6941
    ISSN 1534-7346
    DOI 10.1177/15347346221090758
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    Zs.A 6003: Show issues Location:
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