Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2019 Oct 30;20(21):5398. doi: 10.3390/ijms20215398

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

PMC Copyright notice

Regulation of lipocalin-2 receptor (SLC22A17) and lipocalin 2 (LCN2) abundance in the renal cortical collecting duct cell line mCCD(cl.1). Several extracellular stimuli control SLC22A17and LCN2 abundance, by acting on Slc22a17 and Lcn2 gene transcription or posttranslational Lcn2 expression. Shown are pathways mediated by arginine vasopressin (AVP), binding to the arginine vasopressin receptor-2 (V2R) (dark blue), hyperosmolarity/-tonicity (light blue) and/or inflammation (magenta). AVP stimulation (dark blue arrow) results from adenylyl cyclase activation, increased intracellular cAMP concentration, and protein kinase A (PKA) activation. PKA, in turn, increases cAMP-responsive element binding protein (CREB) activity. NF-κB activation (magenta arrow) occurs by inflammatory stimuli, such as lipopolysaccharide (LPS) via toll-like receptor 4 (TLR4). After longer periods of hypertonic challenge, the nuclear factor of activated T-cells 5 (NFAT5; also known as TonEBP or OREBP) is activated. Apically expressed SLC22A17 promotes protein endocytosis, possibly to provide amino acids (AA) and/or osmolytes for osmotolerance, but this remains unproven. Cells secrete LCN2 to combat bacterial infections and/or promote proliferation after epithelial damage. ↑ (green) = stimulation; (red) = inhibition. For further details, see text.

Inline graphic — Regulation of lipocalin-2 receptor (SLC22A17) and lipocalin 2 (LCN2) abundance in the renal cortical collecting duct cell line mCCD(cl.1). Several extracellular stimuli control SLC22A17and LCN2 abundance, by acting on Slc22a17 and Lcn2 gene transcription or posttranslational Lcn2 expression. Shown are pathways mediated by arginine vasopressin (AVP), binding to the arginine vasopressin receptor-2 (V2R) (dark blue), hyperosmolarity/-tonicity (light blue) and/or inflammation (magenta). AVP stimulation (dark blue arrow) results from adenylyl cyclase activation, increased intracellular cAMP concentration, and protein kinase A (PKA) activation. PKA, in turn, increases cAMP-responsive element binding protein (CREB) activity. NF-κB activation (magenta arrow) occurs by inflammatory stimuli, such as lipopolysaccharide (LPS) via toll-like receptor 4 (TLR4). After longer periods of hypertonic challenge, the nuclear factor of activated T-cells 5 (NFAT5; also known as TonEBP or OREBP) is activated. Apically expressed SLC22A17 promotes protein endocytosis, possibly to provide amino acids (AA) and/or osmolytes for osmotolerance, but this remains unproven. Cells secrete LCN2 to combat bacterial infections and/or promote proliferation after epithelial damage. ↑ (green) = stimulation; (red) = inhibition. For further details, see text.