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

. 2015 May 1;19(1):200. doi: 10.1186/s13054-015-0919-4

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

© Li et al.; licensee BioMed Central. 2015

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

PMC Copyright notice

Kallistatin treatment enhances suppressor of cytokine signaling-3 (SOCS3) expression through activation of a tyrosine kinase-protein kinase C (PKC)-extracellular signal-regulated kinase (ERK) signaling pathway in RAW264.7 cells. (A) Macrophages were incubated with 0.05 μM wild-type kallistatin (WT-KS), heparin-mutant kallistatin (HM-KS) or active site-mutant kallistatin (AM-KS) for 12 hours. Wild-type or heparin mutant kallistatin, but not active site mutant kallistatin, significantly increased SOCS3 expression (n = 3). (B) The effect of kallistatin on SOCS3 expression in macrophages was blocked by PD98059 (PD; ERK inhibitor), chelerythrine (CHE; PKC inhibitor) and genistein (GEN; tyrosine kinase inhibitor). (C) ERK phosphorylation induced by kallistatin in macrophages was also reversed by PD98059, chelerythrine and genistein (n = 3). *P <0.05 versus control group; ^# P <0.05 versus kallistatin alone.