Tight junction modulation and its relationship to drug delivery☆

Salama, Noha N.; Eddington, Natalie D.; Fasano, Alessio

doi:10.1016/j.addr.2006.01.003

Cited by 303 publications

(101 citation statements)

References 89 publications

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“…2C) strongly indicates that ANG-I enters zebrafish in which it is converted to ANG-II. Rather than transcellularly, ANG may enter larvae via tight junctions (Salama et al 2006). The dosage of ANG used in this study was higher than in previous studies, in which isolated kidney segments were infused with ANG-II (1-100 nM; Houillier et al 1996, Rothenberger et al 2007; the requirement for higher levels in this study may reflect the reduced permeability of ANG into larval zebrafish.…”

Section: Discussioncontrasting

confidence: 38%

Angiotensin-II promotes Na+ uptake in larval zebrafish, Danio rerio, in acidic and ion-poor water

Kumai

Bernier

Perry

2013

Journal of Endocrinology

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The contribution of the renin-angiotensin system (RAS) to Na C uptake was investigated in larval zebrafish (Danio rerio). At 4 days post fertilization (dpf), the level of whole-body angiotensin-II (ANG-II) was significantly increased after 1-or 3-h exposure to acidic (pHZ4.0) or ion-poor water (20-fold dilution of Ottawa tapwater), suggesting rapid activation of the RAS. Long-term (24 h) treatment of 3 dpf larvae with ANG-I or ANG-II significantly increased Na C uptake which was accompanied by an increase in mRNA expression of the NaInduction of Na C uptake by exposure to ANG-I was blocked by simultaneously treating larvae with lisinopril (an angiotensin-converting enzyme inhibitor). Acute (2 h) exposure to acidic water or ion-poor water led to significant increase in Na C uptake which was partially blocked by the ANG-II receptor antagonist, telmisartan. Consistent with these data, translational knockdown of renin prevented the stimulation of Na C uptake following exposure to acidic or ion-poor water. The lack of any effects of pharmacological inhibition (using RU486), or knockdown of glucocorticoid receptors on the stimulation of Na C uptake during acute exposure to acidic or ion-poor environments, indicates that the acute effects of RAS occur independently of cortisol signaling. The results of this study demonstrate that the RAS is involved in Na C homeostasis in larval zebrafish. Key Words" angiotensin-II" cortisol " zebrafish " osmoregulation " ion-poor water " acidic water

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Section: Discussioncontrasting

confidence: 38%

Angiotensin-II promotes Na+ uptake in larval zebrafish, Danio rerio, in acidic and ion-poor water

Kumai

Bernier

Perry

2013

Journal of Endocrinology

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“…FD-4, a hydrophilic and high-molecular-weight drug, would permeate through a paracellular pathway by passive diffusion. 14 2 ). Corneal TEER in the present study is consistent with this report.…”

Section: Resultsmentioning

confidence: 99%

Electrophysiological Characterization of Tight Junctional Pathway of Rabbit Cornea Treated with Ophthalmic Ingredients

Nakamura

Yamada

Teshima

et al. 2007

Biological & Pharmaceutical Bulletin

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“…These include the use of influx transporters, blocking of efflux transporters, or receptor-mediated endocytosis (2). Alternative approaches aim to enhance paracellular permeation of drugs by loosening the TJ (3,4). This strategy has the advantage that it could improve the delivery of structurally unrelated drugs, and the drug itself does not have to be modified.…”

mentioning

confidence: 99%

Molecular Determinants of the Interaction between Clostridium perfringens Enterotoxin Fragments and Claudin-3

Winkler¹,

Gehring

Wenzel

et al. 2009

Journal of Biological Chemistry

106

144

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Tight junction modulation and its relationship to drug delivery☆

Cited by 303 publications

References 89 publications

Angiotensin-II promotes Na+ uptake in larval zebrafish, Danio rerio, in acidic and ion-poor water

Angiotensin-II promotes Na+ uptake in larval zebrafish, Danio rerio, in acidic and ion-poor water

Electrophysiological Characterization of Tight Junctional Pathway of Rabbit Cornea Treated with Ophthalmic Ingredients

Molecular Determinants of the Interaction between Clostridium perfringens Enterotoxin Fragments and Claudin-3

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