Publication Name	World Journal of Cardiology
Manuscript ID	39241
Country	United States

Category	Cardiac & Cardiovascular Systems
Manuscript Type	Basic Study
Article Title	NBCe1 Na+-HCO3- cotransporter ablation causes reduced apoptosis following cardiac ischemia-reperfusion injury in vivo
Manuscript Source	Invited Manuscript
All Author List	Kanimozhi Vairamani, Vikram Prasad, Yigang Wang, Wei Huang, Yinhuai Chen, Mario Medvedovic, John N Lorenz and Gary E Shull
Funding Agency and Grant Number	Funding Agency Grant Number NIH HL061974 (to Gary E Shull) NIH R01HL136025 (to Yigang Wang) NIH P30ES006096 (to Mario Medvedovic) Center for Clinical and Translational Science and Training, University of Cincinnati to Gary E Shull Research Innovation Seed Grant from the University of Cincinnati to Gary E Shull and John N Lorenz
Corresponding Author	Gary E Shull, PhD, Professor, Department of Molecular Genetics, Biochemistry and Microbiology, University of Cincinnati, College of Medicine, 231 Albert Sabin Way, Cincinnati, OH 45267-0524, United States. shullge@ucmail.uc.edu
Key Words	Deep sequencing; Ischemic; Apoptosis; Slc4a4; NBCe1
Core Tip	The NBCe1 Na+-HCO3- cotransporter and NHE1 Na+/H+ exchanger both mediate Na+-loading and intracellular pH regulation in cardiomyocytes. Inhibition of NHE1 protects against ischemia-reperfusion (IR) injury, and evidence suggests that loss of NBCe1 activity could also be cardioprotective. We have developed a conditional NBCe1 knockout mouse model and have used it to determine the effects of NBCe1 ablation in cardiac muscle. These studies demonstrate that loss of NBCe1 does not impair cardiac performance. However, cardiomyocyte apoptosis following IR injury in vivo is much lower in hearts that lack NBCe1, thus indicating that loss of NBCe1 is cardioprotective.
Citation	Vairamani K, Prasad V, Wang Y, Huang W, Chen Y, Medvedovic M, Lorenz JN, Shull GE. NBCe1 Na+-HCO3- cotransporter ablation causes reduced apoptosis following cardiac ischemia-reperfusion injury in vivo. World J Cardiol 2018; 10(9): 97-109

Received	2018-04-06 05:54
Peer-Review Started	2018-04-07 07:01
To Make the First Decision	2018-06-06 07:26
Return for Revision	2018-06-08 00:42
Revised	2018-07-05 18:32
Second Decision	2018-07-13 09:13
Accepted by Journal Editor-in-Chief
Accepted by Company Editor-in-Chief	2018-07-16 05:42
Articles in Press	2018-07-16 05:42
Publication Fee Transferred
Edit the Manuscript by Language Editor	2018-07-26 00:43
Typeset the Manuscript	2018-09-29 01:42

ISSN	1949-8462 (online)
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