Connexins 43 and 26 Are Differentially Increased after Rat Bladder Outlet Obstruction

Haefliger, Jacques‐Antoine; Tissières, Pierre; Tawadros, Thomas; Formenton, Andrea; Bény, Jean‐Louis; Nicod, Pascal; Frey, Peter; Meda, Paolo

doi:10.1006/excr.2001.5465

Cited by 83 publications

(70 citation statements)

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“…In vitro, spontaneous contractions were inhibited by heptanol, which is known to block gap junctions. 42 A more acute model of obstruction, that is, one lasting for 7-9 hr, 43 also demonstrated an increase in Cx43 mRNA expression in detrusor smooth muscle. However, recent studies using laser caption microdissection microscopy found that human detrusor myocytes expressed Cx45 rather than Cx43, whereas in biopsies of detrusor muscle cells, both Cxs were demonstrated.…”

Section: Intercellular Communicationmentioning

confidence: 96%

Detrusor myocyte activity and afferent signaling

Andersson

2009

Neurourology and Urodynamics

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Aims: To discuss (1) mechanisms involved in the generation and control of myocyte contractions and consequent afferent nerve activity and (2) these mechanisms as targets for drugs aimed for treatment of overactive bladder (OAB) symptoms and detrusor overactivity (DO). Methods: Literature review of myocyte activation, bladder afferent nerves, mediators in the bladder, and translational aspects of the findings. Results: During bladder filling, there is normally no parasympathetic outflow from the spinal cord. Despite this, the bladder develops tone during filling and also exhibits non-synchronized local contractions and relaxations that are caused by a basal myogenic mechanical activity that may be reinforced by release of, for example, acetylcholine from non-neuronal and/or neuronal sources or local mediators, such as prostaglandins and endothelins. It is suggested that these spontaneous contractions are able to generate activity in afferent nerves (''afferent noise'') that may contribute to DO and OAB. Conclusions: Spontaneous bladder myocyte contractions and factors that are able to modulate them, as well as the consequent afferent nerve activity, may be targets for drugs meant for treatment of OAB/DO. Neurourol.

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Section: Intercellular Communicationmentioning

confidence: 96%

Detrusor myocyte activity and afferent signaling

Andersson

2009

Neurourology and Urodynamics

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“…For the in situ hybridization of the renin transcript, kidneys were cryostat-sectioned at 12 mm thickness. Sections were fixed 10 minutes with 4% paraformaldehyde in PBS, rinsed in diethyl pyrocarbonate, and hybridized as previously described (23,72) with a probe corresponding to the same fragment used for Northern blot analysis of renin (32). Briefly, hybridization with digoxigenin-labeled antisense riboprobes was carried out for 40 hours at 58°C in 5× SSC and 50% formamide.…”

Section: Figurementioning

confidence: 99%

Connexin43-dependent mechanism modulates renin secretion and hypertension

Haefliger¹

2006

Journal of Clinical Investigation

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To investigate the function of Cx43 during hypertension, we studied the mouse line Cx43KI32 (KI32), in which the coding region of Cx32 replaces that of Cx43. Within the kidneys of homozygous KI32 mice, Cx32 was expressed in cortical and medullary tubules, as well as in some extra-and intraglomerular vessels, i.e., at sites where Cx32 and Cx43 are found in WT mice. Under such conditions, renin expression was much reduced compared with that observed in the kidneys of WT and heterozygous KI32 littermates. After exposure to a high-salt diet, all mice retained a normal blood pressure. However, whereas the levels of renin were significantly reduced in the kidneys of WT and heterozygous KI32 mice, reaching levels comparable to those observed in homozygous littermates, they were not further affected in the latter animals. Four weeks after the clipping of a renal artery (the 2-kidney, 1-clip [2K1C] model), 2K1C WT and heterozygous mice showed an increase in blood pressure and in the circulating levels of renin, whereas 2K1C homozygous littermates remained normotensive and showed unchanged plasma renin activity. Hypertensive, but not normotensive, mice also developed cardiac hypertrophy. The data indicate that replacement of Cx43 by Cx32 is associated with decreased expression and secretion of renin, thus preventing the renin-dependent hypertension that is normally induced in the 2K1C model.

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“…Transcript levels were determined by hybridization with random primed (Roche Diagnostics) cDNA probes labeled with ␣ 32 P-dCTP (Amersham Bioscience Europe, Otelfingen, Switzerland). Probes were prepared using cDNA clones for rat Cx36 (Serre-Beinier et al, 2000), rat MIF (Waeber et al, 1997), and ␤-actin (Haefliger et al, 2002). Hybridizations were performed overnight at 68°C in Miraclehyb (Stratagene Europe, Amsterdam, Netherlands).…”

Section: Cell-line and Rat-islet Isolationmentioning

confidence: 99%

Glucose represses connexin36 in insulin-secreting cells

Allagnat

Martín

Condorelli

et al. 2005

Journal of Cell Science

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IntroductionThe homeostasis of multicellular organisms depends on many systems allowing the cells to review the functional state of their neighbors (Spray, 1998). Channels located at gap junctions are one way by which vertebrate cells communicate (Meda, 2000). It has been established that this type of intercellular communication permits coordinated cellular activity, including secretion (Meda, 1996). Gap junctions are specific membrane structures consisting of aggregates of intercellular channels that enable the direct exchange of ions and small metabolites such as second messengers. Intercellular channels result from the association of two hemichannels, named connexons, which are separately contributed by two adjacent cells. Each connexon is an assembly of six transmembrane connexins, encoded by a family of genes with more than 20 members (Sohl and Willecke, 2004).We and others have demonstrated that connexin36 (Cx36; 36 kDa) is the sole connexin isoform expressed in insulinproducing ␤-cells of rat and mouse pancreatic islets (SerreBeinier et al., 2000;Theis et al., 2004). In order to evaluate the contribution of Cx36 to the control of insulin secretion, the Cx36 content has been artificially modified in insulin-secreting cells Le Gurun et al., 2003). These experiments provided evidence that Cx36 has to be expressed at a very precise level in order to maintain a normal insulin secretion. Recently, Leite et al. have suggested that, during the maturation process of neonatal islet, the gain of capacity of the islet to secrete insulin was associated with an increase in Cx36 expression levels. Therefore, variations of the endogenous Cx36 expression levels could have major repercussions on ␤-cell function. Considering the fundamental implication of glucose on gene regulation in ␤-cells, we investigated the effect of glucose on the Cx36 levels in insulin-producing cells. Early morphological studies have demonstrated that glucose induces a remodeling of the gap junctions aggregates in pancreatic islets (In't Veld et al., 1986;Meda et al., 1980). Here, we have demonstrated for the first time that glucose induces a time-and dose-dependent decrease of Cx36 mRNA and protein content in several insulin-secreting cell lines and adult pancreatic rat islets.In ␤-cells, glucose metabolism generates fluctuations in the ATP/ADP ratio, leading to oscillations of membrane potential and cytoplasmic calcium concentrations, which then trigger insulin release (Deeney et al., 2000). Thus, ␤-cell stimulation is associated with regular Ca 2+ oscillations (Lenzen et al., 2000). Surprisingly, glucose-induced Ca 2+ oscillations are synchronized among the thousands of ␤-cells that form each pancreatic islet (Jonkers and Henquin, 2001), probably because of a diffusible regulator (Meda, 1996). These oscillations become more regular and prominent in the presence of ␤-cell

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Connexins 43 and 26 Are Differentially Increased after Rat Bladder Outlet Obstruction

Cited by 83 publications

References 40 publications

Detrusor myocyte activity and afferent signaling

Detrusor myocyte activity and afferent signaling

Connexin43-dependent mechanism modulates renin secretion and hypertension

Glucose represses connexin36 in insulin-secreting cells

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