Bradykinin increased the permeability of BTB via NOS/NO/ZONAB-mediating down-regulation of claudin-5 and occludin

Li, Libo; Liu, Xiao-bai; Ma, Jun; Liu, Yunhui; Li, Zhiqing; Ma, Teng; Zhao, Xihe; Xi, Zhuo; Xue, Yixue

doi:10.1016/j.bbrc.2015.06.082

Cited by 26 publications

(19 citation statements)

References 21 publications

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“…In addition, the siZONAB transfection experiment confirmed that knockdown of ZONAB expression promoted the transdifferentiation and inhibited the proliferation of AECs. In the AECs, ZONAB inhibited transdifferentiation and promoted proliferation, which is consistent with the function of ZONAB in renal tubular epithelium (22), retina (34,36,37), cornea (39), intestine (40), liver (35), mammary gland (18) and brain (41,42), which is likely to be similar in lung tissue.…”

Section: Discussionsupporting

confidence: 76%

Decreased ZONAB expression promotes excessive transdifferentiation of alveolar epithelial cells in hyperoxia-induced bronchopulmonary dysplasia

Hou

Shi

et al. 2018

Int J Mol Med

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Previous studies by our group have confirmed excessive transdifferentiation of alveolar epithelial cells (AECs) in a hyperoxia‑induced bronchopulmonary dysplasia (BPD) model, but the underlying mechanism have remained elusive. The transcription factor zonula occludens 1‑associated nucleic acid binding protein (ZONAB) has the biological functions of inhibition of epithelial cell differentiation and promotion of epithelial cell proliferation. The aim of the present study was to explore the regulatory effect of ZONAB on the transdifferentiation and proliferation of AECs in a model of hyperoxia‑induced lung injury. Newborn Wistar rats were randomly allocated to a model group (inhalation of 85% O2) or a control group (inhalation of normal air), and ZONAB expression in lung tissues was detected at different time‑points. Type II AECs (AEC II) isolated from normal newborn rats were primarily cultured under an atmosphere of 85 or 21% O2, and ZONAB expression in the cells was examined. The primary cells were further transfected with ZONAB plasmid or small interfering (si)RNA and then exposed to hyperoxia, and the indicators for transdifferentiation and proliferation were measured. The present study indicated that ZONAB expression in AEC II of the BPD rats was significantly decreased from 7 days of exposure to hyperoxia onwards. In the AEC II isolated from normal neonatal rats, ZONAB expression in the model group was also reduced compared with that in the control group. After transfection with the plasmid pCMV6‑ZONAB, the expression of aquaporin 5 (type I alveolar epithelial cell marker) decreased and the expression of surfactant protein C (AEC II marker), proliferating‑cell nuclear antigen and cyclin D1 increased, which was opposite to the effects of ZONAB siRNA. Transfection with pCMV6‑ZONAB also alleviated excessive transdifferentiation and inhibited proliferation of AEC II induced by hyperoxia treatment. These results suggest that ZONAB expression in AEC II decreases under hyperoxia conditions, which promotes transdifferentiation and inhibits proliferation of AECs. This may, at least in part, be the underlying mechanism of lung epithelial injury in the hyperoxia-induced BPD model.

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Section: Discussionsupporting

confidence: 76%

Decreased ZONAB expression promotes excessive transdifferentiation of alveolar epithelial cells in hyperoxia-induced bronchopulmonary dysplasia

Hou

Shi

et al. 2018

Int J Mol Med

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“…Manipulation of other junctional transmembrane proteins, such as BVES, regulates ZONAB activation via a GEF-H1/RhoA-stimulated mechanism 140,148 . In endothelial cells of the blood-tumour-barrier, bradykinin-induced activation of nitric oxide synthesis induces increased permeability and ZONAB activation, leading to repression of claudin-5 and occludin promoters 149 . The group of dual localization proteins associated with tight junctions also includes junctional adaptors such as ZO-2, which travels to the nucleus at low cell density and interacts with several transcription factors including c-Myc, AP-1 and YAP, regulators of cell proliferation 44 .…”

Section: Signalling From Tight Junctionsmentioning

confidence: 99%

Tight junctions: from simple barriers to multifunctional molecular gates

Zihni

Mills

Matter

et al. 2016

Nat Rev Mol Cell Biol

1,085

925

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Main body of text: 5983 words 2Epithelia and endothelia separate different tissue compartments and protect multicellular organisms form the outside world. This requires the formation of tight junctions, selective gates that control paracellular diffusion of ions and solutes. Tight junctions also form the border between the apical and basolateral plasma membrane domains and are linked to the machinery that controls apicobasal polarization. Additionally, signalling networks that guide diverse cell behaviours and functions are connected to tight junctions, transmitting information to and from the cytoskeleton, nucleus and different cell adhesion complexes. Here, we discuss recent advances in our understanding of the molecular architecture and cellular functions of tight junctions.Microscopists in the 19 th century described the paracellular space between neighbouring cells within an epithelial sheet to be sealed by a "terminal bar", a structure later resolved by electron microscopy into a composite of distinct cell-cell junctions that is now called the epithelial junctional complex and is formed by tight junctions, adherens junctions and desmosomes 1,2 . As the former two junctions are more tightly associated and often reside at the apical end of the lateral membrane, they are often referred to as the apical junctional complex (however, in endothelia, tight junctions and adherens junctions can be intercalated) (Fig. 1). Tight junctions are essential for barrier formation, and their primary physiological role is to function as paracellular gates that restrict diffusion on the basis of size and charge. Selective paracellular diffusion is an essential process for the maintenance of homoeostasis in organs and tissues. Tight junctions have long been the most enigmatic of all adhesion complexes and eluded a detailed molecular and functional analysis due to their complex architecture. Recent years have witnessed the identification of a large array of components associated with tight junctions implicating these junctions in an unexpected range of different functions, thereby challenging the traditional model, in which tight junctions are considered a simple diffusion barrier formed by a rigid molecular complex. In line with these various functions, mutations in genes encoding tight junction proteins have been linked to a range of inherited human diseases. Additionally, tight junction components are known to be targeted by a number of pathogenic bacteria and viruses, which hijack tight junction proteins to enter and infect cells, or target junctional signalling mechanisms to cross tissue barriers. Although tight junctions are a vertebrate junction, many of their components and functions are evolutionarily conserved (Box 1).The main purpose of this review is to examine the recent advances in the unravelling of the molecular architecture of tight junctions and understanding their functions. We will discuss recent exciting insights into how tight junctions function as signalling platforms that guide cell behaviour and differen...

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“…Furthermore, it is known that NO can damage the junctional complex present in the endothelial cells of the CNS. The down-regulation of claudin-5 and occludin in the BBB promotes the translocation of ZONAB to the nucleus, allowing its interaction with the promoters for the TJ proteins and inhibits their production, which results in an increase in the barrier permeability (Liu et al 2015). It is possible that in PAM, the production of NO induced by the presence of amoebae could alter the permeability of the BBB and facilitates the migration of the leucocytes during the infection.…”

Section: Discussionmentioning

confidence: 99%

An In Vitro Model of the Blood–Brain Barrier: Naegleria fowleri Affects the Tight Junction Proteins and Activates the Microvascular Endothelial Cells

Coronado-Velázquez

Betanzos

Serrano-Luna

et al. 2018

J Eukaryotic Microbiology

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Naegleria fowleri causes a fatal disease known as primary amoebic meningoencephalitis. This condition is characterized by an acute inflammation that originates from the free passage of peripheral blood cells to the central nervous system through the alteration of the blood-brain barrier. In this work, we established models of the infection in rats and in a primary culture of endothelial cells from rat brains with the aim of evaluating the activation and the alterations of these cells by N. fowleri. We proved that the rat develops the infection similar to the mouse model. We also found that amoebic cysteine proteases produced by the trophozoites and the conditioned medium induced cytopathic effect in the endothelial cells. In addition, N. fowleri can decrease the transendothelial electrical resistance by triggering the destabilization of the tight junction proteins claudin-5, occludin, and ZO-1 in a time-dependent manner. Furthermore, N. fowleri induced the expression of VCAM-1 and ICAM-1 and the production of IL-8, IL-1β, TNF-α, and IL-6 as well as nitric oxide. We conclude that N. fowleri damaged the blood-brain barrier model by disrupting the intercellular junctions and induced the presence of inflammatory mediators by allowing the access of inflammatory cells to the olfactory bulbs.

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Bradykinin increased the permeability of BTB via NOS/NO/ZONAB-mediating down-regulation of claudin-5 and occludin

Cited by 26 publications

References 21 publications

Decreased ZONAB expression promotes excessive transdifferentiation of alveolar epithelial cells in hyperoxia-induced bronchopulmonary dysplasia

Decreased ZONAB expression promotes excessive transdifferentiation of alveolar epithelial cells in hyperoxia-induced bronchopulmonary dysplasia

Tight junctions: from simple barriers to multifunctional molecular gates

An In Vitro Model of the Blood–Brain Barrier: Naegleria fowleri Affects the Tight Junction Proteins and Activates the Microvascular Endothelial Cells

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