Kevin Regner Lab

Kevin R. Regner, MD, MS, FASN

Interim Chief and Associate Professor, Department of Medicine
kregner@mcw.edu

The primary goal of the Regner laboratory is to investigate the cellular, molecular, and genetic mechanisms involved in ischemic acute kidney injury (AKI) and kidney repair.

Current projects include:

1. Activator of G Protein Signaling 3 in Ischemic Renal Injury. The objective of this study is to characterize the role of Activator of G protein signaling 3 (AGS3), a novel non-receptor regulator of G-protein function, in renal tubular regeneration following ischemic AKI.

2. Genetic mapping and gene identification for acute kidney injury in outbred rats. The objective of this study is to identify novel genes that modulate susceptibility or resistance to AKI using a novel genetic resource, heterogeneous stock rats.

Bohan Xing, BS

Research Technologist I
bxing@mcw.edu

Utilizing the murine model of renal ischemia-reperfusion injury, Bohan characterizes renal injury using molecular and biochemical assays and histological analysis.

MicroRNA-214-3p in the Kidney Contributes to the Development of Hypertension.

(Liu Y, Usa K, Wang F, Liu P, Geurts AM, Li J, Williams AM, Regner KR, Kong Y, Liu H, Nie J, Liang M.) J Am Soc Nephrol. 2018 10;29(10):2518-2528.
Urinary exosomal expression of activator of G protein signaling 3 in polycystic kidney disease.

(Keri KC, Regner KR, Dall AT, Park F.) BMC Res Notes. 2018 Jun 07;11(1):359.
Artificial intelligence, physiological genomics, and precision medicine.

(Williams AM, Liu Y, Regner KR, Jotterand F, Liu P, Liang M.) Physiol Genomics. 2018 04 01;50(4):237-243.
Tissue-Specific MicroRNA Expression Patterns in Four Types of Kidney Disease.

(Baker MA, Davis SJ, Liu P, Pan X, Williams AM, Iczkowski KA, Gallagher ST, Bishop K, Regner KR, Liu Y, Liang M.) J Am Soc Nephrol. 2017 Oct;28(10):2985-2992.
Outcome analysis of continuous intraoperative renal replacement therapy in the highest acuity liver transplant recipients: A single-center experience.

(Zimmerman MA, Selim M, Kim J, Regner K, Saeian K, Zanowski S, Martin A, Connolly LA, Lauer KK, Woehlck HJ, Hong JC.) Surgery. 2017 05;161(5):1279-1286.
TRIP13-deficient tubular epithelial cells are susceptible to apoptosis following acute kidney injury.

(Pressly JD, Hama T, Brien SO, Regner KR, Park F.) Sci Rep. 2017 03 03;7:43196.
Kidney Injury in Liver Disease.

(Regner KR, Singbartl K.) Crit Care Clin. 2016 Jul;32(3):343-55.
Activator of G-protein Signaling 3 Controls Renal Epithelial Cell Survival and ERK5 Activation.

(Rasmussen SA, Kwon M, Pressly JD, Blumer JB, Regner KR, Park F.) J Mol Signal. 2015 Nov 27;10:6.
Deficiency in the Formation of 20-Hydroxyeicosatetraenoic Acid Enhances Renal Ischemia-Reperfusion Injury.

(Muroya Y, Fan F, Regner KR, Falck JR, Garrett MR, Juncos LA, Roman RJ.) J Am Soc Nephrol. 2015 Oct;26(10):2460-9.
Localization and expression profile of Group I and II Activators of G-protein Signaling in the kidney.

(Lenarczyk M, Pressly JD, Arnett J, Regner KR, Park F.) J Mol Histol. 2015 Apr;46(2):123-36.
G-protein βγ subunit dimers modulate kidney repair after ischemia-reperfusion injury in rats.

(White SM, North LM, Haines E, Goldberg M, Sullivan LM, Pressly JD, Weber DS, Park F, Regner KR.) Mol Pharmacol. 2014 Oct;86(4):369-77.
De novo expression of sodium-glucose cotransporter SGLT2 in Bowman's capsule coincides with replacement of parietal epithelial cell layer with proximal tubule-like epithelium.

(Tabatabai NM, North PE, Regner KR, Kumar SN, Duris CB, Blodgett AB.) J Membr Biol. 2014 Aug;247(8):675-83.

Cardiovascular Center

Kevin Regner Lab

Kevin R. Regner, MD, MS, FASN

Bohan Xing, BS

Recent Publications