Guanylyl cyclase-C receptor mRNA distribution along the rat nephron

Carrithers, Stephen L.; Taylor, Bradley K.; Cai, Weiyan; Johnson, Brett; Ott, Cobern E.; Greenberg, Richard N.; Jackson, Brian A.

doi:10.1016/s0167-0115(00)00139-7

Cited by 44 publications

(34 citation statements)

References 34 publications

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“…In the human kidney, we detected GC-C again only in the kidney cortex and specifically in proximal tubules ( Figure 6) (60,61). In contrary to these findings in mouse and human, in rat kidney, Carrithers et al (58) found mRNA for GC-C in all nephron segments, suggesting differences in tissue distribution of GC-C in different species. A few years ago, it became evident that proximal tubules are targets of guanylin peptides.…”

Section: Signaling Mechanisms Of Guanylin Peptides In the Kidneymentioning

confidence: 84%

“…However, another possible source of cGMP in the urine could be the activation of other members of the guanylate cyclase family, such as the orphan receptor GC-G, which is present in the luminal membrane of principal cells of rat and mouse CCD (21,57). The source of guanylin peptides in the tubular lumen besides glomerular filtration from the circulation could also be tubular cells because mRNA for GN and UGN is also expressed in kidney epithelial cells (54,58,59). Similar to the difference in the axial expression along the intestine, GN and UGN are not expressed equally along the different nephron segments (Figure 5).…”

Section: Signaling Mechanisms Of Guanylin Peptides In the Kidneymentioning

confidence: 99%

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Cellular Effects of Guanylin and Uroguanylin

Sinđić

Schlatter

2006

Journal of the American Society of Nephrology

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Ingestion of a salty meal induces secretion of guanylin (GN) and uroguanylin (UGN) into the intestinal lumen, where they inhibit Na ؉ absorption and induce Cl ؊ , HCO 3 ؊ , and water secretion. Simultaneously, these hormones stimulate renal electrolyte excretion by inducing natriuresis, kaliuresis, and diuresis. GN and UGN therefore participate in the prevention of hypernatremia and hypervolemia after salty meals. The signaling pathway of GN and UGN in the intestine is well known. They activate enterocytes via guanylate cyclase C (GC-C), which leads to cGMP-dependent inhibition of Na ؉ /H ؉ exchange and activation of the cystic fibrosis transmembrane regulator. In GC-C-deficient mice, GN and UGN still produce renal natriuresis, kaliuresis, and diuresis, suggesting different signaling pathways in the kidney compared with the intestine. Signaling pathways for GN and UGN in the kidney differ along the various nephron segments. In proximal tubule cells, a cGMP-and GC-C-dependent signaling was demonstrated for both peptides. In addition, UGN activates a pertussis toxinsensitive G-protein-coupled receptor. A similar dual signaling pathway is also known for atrial natriuretic peptide. Recently, a cGMP-independent signaling pathway for GN and UGN was also shown in principal cells of the human and mouse cortical collecting duct. Because GN and UGN activate different signaling pathways in specific organs and even within the kidney, this review focuses on more recent findings on cellular effects and signaling mechanisms of these peptides and their pathophysiologic implications in the intestine and the kidney.

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Section: Signaling Mechanisms Of Guanylin Peptides In the Kidneymentioning

confidence: 84%

Section: Signaling Mechanisms Of Guanylin Peptides In the Kidneymentioning

confidence: 99%

Cellular Effects of Guanylin and Uroguanylin

Sinđić

Schlatter

2006

Journal of the American Society of Nephrology

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“…For example, uroguanylin mRNA levels are upregulated in the intestine and kidney when freshwateradapted eels are exposed to the considerably higher NaCl concentration of seawater (16,17). This finding suggests that uroguanylin may function in fish to regulate body sodium levels in a fashion similar to the physiological role that Lorenz et al (7) suggest for uroguanylin in the mouse, where the expression of uroguanylin mRNAs may also be under the influence of NaCl in the diet (14,15). Might uroguanylin serve to regulate body sodium balance in mammals by some common regulatory mechanism(s) similar to those involved in the complicated physiology underlying osmoregulation in fish?…”

Section: Uroguanylin and Osmoregulationmentioning

confidence: 84%

“…Such an intestine-kidney axis will likely be an oversimplification of the physiological mechanism that operates in vivo because uroguanylin is also produced in the kidney where it may act locally. Increases in dietary NaCl raise uroguanylin mRNA levels in the intestine and kidney, suggesting that both endocrine and paracrine/autocrine actions of uroguanylin could participate in tubular signaling mechanisms that govern renal sodium transport (14,15).…”

Section: Uroguanylin Deficiency Impairs Sodium Excretionmentioning

confidence: 99%

A novel role for uroguanylin in the regulation of sodium balance

Forte¹

2003

J. Clin. Invest.

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Uroguanylin is a peptide hormone that regulates sodium excretion by the kidney when excess NaCl is consumed. A new study demonstrates that mice deficient in uroguanylin have blunted urinary sodium excretion responses to oral sodium loads in addition to elevated blood pressure (see related article beginning on page 1244). A physiological role for uroguanylin is discussed, linking the intestine and kidney in an endocrine axis for the maintenance of sodium balance.

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“…OK-GC expressed in COS-1 or HEK-293 cells generates cGMP when stimulated by guanylin/uroguanylin/STa and the deduced amino acid sequence of the extracellular ligand-binding domain shows that OK-GC shares only 55.4^'58.6% identity with rat, human, and porcine GC-Cs, raising the possibility that it is a novel GC-coupled guanylin/uroguanylin/STa receptor [78]. Recently, GC-C mRNA also has been detected in all segments of the rat nephron by RT-PCR [79]. GC-C mRNA is also detected in the regenerating liver [80], and in metastatic tumors of colon cancer [81].…”

Section: -19] Gc-a or Natriuretic Peptide Receptor-a (Npr-a) Is Thmentioning

confidence: 99%