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Review
. 2010 Jul;19(4):366-71.
doi: 10.1097/MNH.0b013e32833aff32.

The renin phenotype: roles and regulation in the kidney

Maria L S Sequeira Lopez  1 , R Ariel Gomez
Affiliations
Review

The renin phenotype: roles and regulation in the kidney

Maria L S Sequeira Lopez et al. Curr Opin Nephrol Hypertens. 2010 Jul.

Abstract

Purpose of review: Renin cells are fundamental for the control of blood pressure, fluid electrolyte homeostasis and kidney development. This review discusses recent discoveries regarding the mechanisms that control the identity and fate of renin cells and their role in the maintenance of kidney architecture and function.

Recent findings: It is now established that cyclic AMP is a crucial factor for the regulation of the renin phenotype. Furthermore, additional factors such as microRNAs and gap junctions have recently emerged as key regulators for the maintenance and proper functioning of renin cells.

Summary: Experiments described in this review will hopefully raise new questions regarding the mechanisms that control the identity, plasticity and function of renin cells.

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Figures

Figure 1
Figure 1. Major events in renin expression
Activation of a G protein-coupled Rc by its ligand leads to conformational change transmitted to a G protein complex. The Gsα subunit is released from the complex after conversion of GTP to GDP and activates the AC, which in turn converts ATP in the second messenger cAMP. cAMP activates PKA that phosphorylates the CREB in the nucleus. Phosphorylated CREB recruits CBP and p300 and binds to the CRE in the enhancer region of the renin promoter, switching on renin mRNA transcription. At the proximal promoter, Hox and Pbx 1b paralogs bind to the HOX–PBX site and also initiate renin transcription. Posttranscriptional regulation at the 3’UTR occurs by binding proteins that increase renin mRNA stability (not depicted) and by miRNA, which repress renin translation, degrade renin mRNA or both. cAMP also stimulates renin release (not depicted). For ease of reading most of the binding sites and their interactions along the promoter are not depicted. AC, adenylyl cyclase; cAMP, cyclic AMP; CRE, cAMP responsive element; CREB, cAMP responsive element binding protein; GJ, gap junction; miRNA, microRNA; PKA, protein kinase A; Pol II, polymerase II; Rc, receptor; UTR, untranslated region.
See this image and copyright information in PMC

References

    1. Reddi V, Zaglul A, Pentz ES, Gomez RA. Renin-expressing cells are associated with branching of the developing kidney vasculature. J Am Soc Nephrol. 1998;9:63–71. - PubMed
    1. Sequeira Lopez ML, Gomez RA. The role of angiotensin II in kidney embryogenesis and kidney abnormalities. Curr Opin Nephrol Hypertens. 2004;13:117–122. - PubMed
    1. Gomez RA, Chevalier RL, Sturgill BC, et al. Maturation of the intrarenal renin distribution in Wistar–Kyoto rats. J Hypertens. 1986;4:s31–s33.
    1. Sequeira Lopez ML, Pentz ES, Robert B, et al. Embryonic origin and lineage of juxtaglomerular cells. Am J Physiol Renal Physiol. 2001;281:F345–F356. - PubMed
    1. Sequeira Lopez ML, Pentz ES, Nomasa T, et al. Renin cells are precursors for multiple cell types that switch to the renin phenotype when homeostasis is threatened. Dev Cell. 2004;6:719–728. - PubMed

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