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1.
J Cyst Fibros ; 6(6): 419-22, 2007 Nov 30.
Artigo em Inglês | MEDLINE | ID: mdl-17434346

RESUMO

CFTR was reported to regulate ENaC channel opening, decreasing ENaC activity in airways and increasing it in sweat ducts. We generated MDCK-I cell lines stably expressing tagged alphabetagammaENaC+CFTR or ENaC alone, and developed an assay to quantify cell-surface half-life of ENaC. Surprisingly, we found that co-expressed CFTR stabilizes ENaC at the plasma membrane, suggesting that CFTR regulates ENaC stability, not just opening.


Assuntos
Regulador de Condutância Transmembrana em Fibrose Cística/metabolismo , Canais Epiteliais de Sódio/metabolismo , Animais , Linhagem Celular , Membrana Celular , Regulador de Condutância Transmembrana em Fibrose Cística/genética , Cães , Canais Epiteliais de Sódio/genética , Humanos
2.
J Physiol ; 567(Pt 1): 21-6, 2005 Aug 15.
Artigo em Inglês | MEDLINE | ID: mdl-15890704

RESUMO

Regulation of renal proximal tubular reabsorption of phosphate (Pi) is one of the critical steps in Pi homeostasis. Experimental evidence suggests that this regulation is achieved mainly by controlling the apical expression of the Na+-dependent Pi cotransporter type IIa (NaPi-IIa) in proximal tubules. Only recently have we started to obtain information regarding the molecular mechanisms that control the apical expression of NaPi-IIa. The first critical observation was the finding that truncation of only its last three amino acid residues has a strong effect on apical expression. A second major finding was the observation that the last intracellular loop of NaPi-IIa contains sequence information that confers parathyroid hormone (PTH) sensitivity. The use of the above domains of the cotransporter in yeast two-hybrid (Y2H) screening allowed the identification of proteins interacting with NaPi-IIa. Biochemical and morphological, as well as functional, analyses have allowed us to obtain insights into the physiological roles of such interactions, although our present knowledge is still far from complete.


Assuntos
Túbulos Renais Proximais/metabolismo , Fosfatos/metabolismo , Simportadores/metabolismo , Animais , Humanos , Sódio/metabolismo , Proteínas Cotransportadoras de Sódio-Fosfato , Proteínas Cotransportadoras de Sódio-Fosfato Tipo IIa
3.
Proc Biol Sci ; 266(1423): 1077-83, 1999 May 22.
Artigo em Inglês | MEDLINE | ID: mdl-10380684

RESUMO

Experimental studies have highlighted the potential influence of contaminants on marine mammal immune function and anthropogenic contaminants are commonly believed to influence the development of diseases observed in the wild. However, estimates of the impact of contaminants on wild populations are constrained by uncertainty over natural variation in disease patterns under different environmental conditions. We used photographic techniques to compare levels of epidermal disease in ten coastal populations of bottlenose dolphins (Tursiops truncatus) exposed to a wide range of natural and anthropogenic conditions. Epidermal lesions were common in all populations (affecting > 60% of individuals), but both the prevalence and severity of 15 lesion categories varied between populations. No relationships were found between epidermal disease and contaminant levels across the four populations for which toxicological data were available. In contrast, there were highly significant linear relationships with oceanographic variables. In particular, populations from areas of low water temperature and low salinity exhibited higher lesion prevalence and severity. Such conditions may impact on epidermal integrity or produce more general physiological stress, potentially making animals more vulnerable to natural infections or anthropogenic factors. These results show that variations in natural environmental factors must be accounted for when investigating the importance of anthropogenic impacts on disease in wild marine mammals.


Assuntos
Golfinhos , Dermatopatias/veterinária , Animais , Exposição Ambiental/efeitos adversos , Prevalência , Dermatopatias/epidemiologia , Dermatopatias/etiologia , Dermatopatias/fisiopatologia
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