Biochemistry and Molecular Biology
108 N. Greene St, Baltimore, MD, 21201
Education and Training
1994-2000 M.D. General Medicine. School of Medicine, National Autonomous University of Mexico. Mexico.
1999-2000 Internship (Surgery, Internal Medicine and Emergency Medicine) at the Institute of Medical Sciences and Nutrition, Dr. Salvador Zubirán, Mexico.
2001-2007 Ph.D. in Biomedical Sciences, Subject: Physiology and Biophysics, School of Medicine, National Autonomous University of Mexico, Mexico.
2004-2007 Scholar Fellow, Department of Biochemistry and Molecular Biology School of Medicine, University of Maryland, Baltimore, MD, USA. Mentor: Dr. Martin F. Schneider.
2007-2010 Post-doctoral fellow, Department of Biochemistry and Molecular Biology School of Medicine, University of Maryland, Baltimore, MD, USA. Mentor: Dr. Martin F. Schneider.
The knowledge of the physiology and pathophysiology of the human body and mind has been my fascination. Much of my undergraduate, graduate and early postdoctoral research focused on peripheral nervous system physiology and biophysics. This has included the study of the mechanisms of voltage gated calcium channels modulation mediated by G-protein coupled receptors. Voltage gated calcium channels are key mediators of depolarization induced calcium influx into excitable cells, and thereby play pivotal roles in a wide array of physiological responses. In the last 5 years my research has focused on skeletal muscle physiology. I have continued to build on my previous training in electrophysiology and calcium imaging by using experimental paradigms that will allow me to address more clinically relevant questions regarding the regulation of excitation-contraction (e-c) coupling and excitation-transcription (e-t) coupling in skeletal muscle. Because of my clinical background in general medicine, much of my current research has focused on skeletal muscle diseases.
Hernández-Ochoa EO, Contreras M, Cseresnyés Z, Schneider MF. Ca2+ signal summation and NFATc1 nuclear translocation in sympathetic ganglion neurons during repetitive action potentials. Cell Calcium. 2007 Jun;41(6):559-71.
Hernández-Ochoa EO, Schneider MF. Voltage clamp methods for the study of membrane currents and SR Ca(2+) release in adult skeletal muscle fibres. Prog Biophys Mol Biol. 2012 Apr;108(3):98-118.
Hernández-Ochoa EO, Schachter TN, Schneider MF. Elevated nuclear Foxo1 suppresses excitability of skeletal muscle fibers. Am J Physiol Cell Physiol. 2013 Sep 15;305(6):C643-53.
Hernández-Ochoa EO, Robison P, Contreras M, Shen T, Zhao Z, Schneider MF. Elevated extracellular glucose and uncontrolled type 1 diabetes enhance NFAT5 signaling and disrupt the transverse tubular network in mouse skeletal muscle. Exp Biol Med (Maywood). 2012 Sep;237(9):1068-83.
Hernández-Ochoa EO, Pratt SJ, Lovering RM, Schneider MF. Critical Role of Intracellular RyR1 Calcium Release Channels in Skeletal Muscle Function and Disease. Front Physiol. 2016
Garcia, D. E., Li, B.*, Garcia-Ferreiro, R. E.*, Hernandez-Ochoa, E. O.*, Yan, K., Gautam, N., Catterall, W. A., Mackie, K., & Hille, B. G-protein beta-subunit specificity in the fast membrane-delimited inhibition of Ca2+ channels. J Neurosci, 1998. 18(22): p. 9163-70. * Equal authorship contribution.
Garcia-Ferreiro, R.E., Hernandez-Ochoa E.O., and D.E. Garcia, Modulation of N-type Ca2+ channel current kinetics by PMA in rat sympathetic neurons. Pflugers Arch, 2001. 442(6): p. 848-58.
Hernandez-Ochoa, E.O., Rebolledo-Antunez S., Cuellar-Quintero J.L., Garcia-Ferreiro R.E., Farias J.M., Garcia D.E. Canales de Ca2+ neuronales: blanco de autoanticuerpos onconeuronales en el Síndrome de Lambert-Eaton. Archivos de Neurociencia, 2003. 8(3): p. 106-112.
Hernandez-Ochoa, E.O., R.E. Garcia-Ferreiro, and D.E. Garcia, G protein activation inhibits gating charge movement in rat sympathetic neurons. Am J Physiol Cell Physiol, 2007. 292(6): p. C2226-38.
Brown, L.D., Rodney, G.G., Hernandez-Ochoa, E., Ward, C.W., & Schneider, M.F. Ca2+ sparks and T tubule reorganization in dedifferentiating adult mouse skeletal muscle fibers. Am J Physiol Cell Physiol, 2007. 292(3): p. C1156-66.
Prosser, B.L., Wright, N.T., Hernandez-Ochoa, E.O., Varney, K.M., Liu, Y., Olojo, R.O., Zimmer, D.B., Weber, D.J., & Schneider, M.F. S100A1 binds to the calmodulin-binding site of ryanodine receptor and modulates skeletal muscle excitation-contraction coupling. J Biol Chem, 2008. 283(8): p. 5046-57.
Hernandez-Ochoa, E.O., Prosser, B.L., Wright, N.T., Contreras, M., Weber, D.J., & Schneider, M.F. Augmentation of Cav1 channel current and action potential duration after uptake of S100A1 in sympathetic ganglion neurons. Am J Physiol Cell Physiol, 2009. 297(4): p. C955-70.
Prosser, B. L.*, Hernandez-Ochoa, E. O.*, Zimmer, D. B., & Schneider, M. F. The Qgamma component of intra-membrane charge movement is present in mammalian muscle fibres, but suppressed in the absence of S100A1. J Physiol, 2009. 587(Pt 18): p. 4523-41. * Equal authorship contribution.
Prosser, B. L., Hernandez-Ochoa, E. O., Zimmer, D. B., & Schneider, M. F. Simultaneous recording of intramembrane charge movement components and calcium release in wild-type and S100A1-/- muscle fibres. J Physiol, 2009. 587(Pt 18): p. 4543-59.
Prosser, B. L., Hernandez-Ochoa, E.O., Lovering, R. M., Andronache, Z., Zimmer, D. B., Melzer, W., & Schneider, M. F. S100a1 Promotes Action Potential-Initiated Calcium Release Flux and Force Production in Skeletal Muscle. Am J Physiol Cell Physiol, 2010.
Shen T, Liu Y, Contreras M, Hernandez-Ochoa E.O., Randall W.R., and Schneider M.F. DNA binding sites target nuclear NFATc1 to heterochromatin regions in adult skeletal muscle fibers. Histochemistry and Cell Biology, 2010 Oct;134(4):387-402.
Yamaguchi N, Prosser BL, Ghassemi F, Xu L, Pasek DA, Eu JP, Hernandez-Ochoa EO, Cannon BR, Wilder PT, Lovering RM, Weber D, Melzer W, Schneider MF, Meissner G. Modulation of sarcoplasmic reticulum Ca2+ release in skeletal muscle expressing ryanodine receptor impaired in regulation by calmodulin and S100A1. Am J Physiol Cell Physiol, 2011 May;300(5):C998-C1012.
Olojo R.O.*, Hernandez-Ochoa E.O.*, Ikemoto N and Schneider M.F. Effects of conformational peptide probe DP4 on bidirectional signaling between DHPR and RyR1 calcium channels in voltage-clamped skeletal muscle fibers. Biophysical J, 2011. May 18, 100(10):2367-77. *Equal authorship contribution.
Prosser, B. L., Hernandez-Ochoa, E.O. & Schneider, M. F. S100A1 and calmodulin regulation of ryanodine receptor in striated muscle. Cell Calcium 2011. Oct;50(4):323-31. Invited Review.
Robison P, Hernandez-Ochoa E.O.*, and Schneider M.F. Adherent primary cultures of mouse intercostal muscle fibers for isolated fiber studies. J. of Biomedicine and Biotechnology, 2011 2011:393740. doi: 10.1155/2011/393740. Corresponding author*.
Olojo RO, Ziman AP, Hernández-Ochoa EO, Allen PD, Schneider MF, Ward CW. Mice null for calsequestrin 1 exhibit deficits in functional performance and sarcoplasmic reticulum calcium handling. PLoS One. 2011;6(12):e27036.
Hernández-Ochoa EO*, Robison P. Excitation-Contraction Coupling and Excitation-Transcription Coupling in Skeletal Muscle. Biochem Pharmacol 2012, 1:e117. doi:10.4172/2167-0501.1000e117. Corresponding author*.
Liu Y, Hernández-Ochoa EO, Randall WR, Schneider MF. NOX2-dependent ROS is required for HDAC5 nuclear efflux and contributes to HDAC4 nuclear efflux during intense repetitive activity of fast skeletal muscle fibers. Am J Physiol Cell Physiol. 2012 Aug 1;303(3):C334-47.
Wu F, Mi W, Hernández-Ochoa EO, Burns DK, Fu Y, Gray HF, Struyk AF, Schneider MF, Cannon SC. A calcium channel mutant mouse model of hypokalemic periodic paralysis. J Clin Invest. 2012 Dec 3;122(12):4580-91.
Robison P, Hernández-Ochoa EO, Schneider MF. Atypical behavior of NFATc1 in cultured intercostal myofibers. Skelet Muscle. 2014 Jan 3;4(1):1.
Hernández-Ochoa EO, Olojo RO, Rebbeck RT, Dulhunty AF, Schneider MF. β1a490-508, a 19-residue peptide from C-terminal tail of Cav1.1 β1a subunit, potentiates voltage-dependent calcium release in adult skeletal muscle fibers. Biophys J. 2014;106(3):535-47.
Hernández-Ochoa EO, Pratt SJ, Garcia-Pelagio KP, Schneider MF, Lovering RM. Disruption of action potential and calcium signaling properties in malformed myofibers from dystrophin-deficient mice. Physiol Rep. 2015;3(4). pii: e12366. doi: 10.14814/phy2.12366.
Hernández-Ochoa EO*, Vanegas C. Diabetic Myopathy and Mechanisms of Disease. Biochem Pharmacol (Los Angel). 2015;4(5). pii: e179. Epub 2015 Corresponding author*.
Hernández-Ochoa EO, Vanegas C, Iyer SR, Lovering RM, Schneider MF. Alternating bipolar field stimulation identifies muscle fibers with defective excitability but maintained local Ca(2+) signals and contraction. Skelet Muscle. 2016, 5;6:6. doi: 10.1186/s13395-016-0076-8.
Iyer SR, Valencia AP, Hernández-Ochoa EO, Lovering RM. In Vivo Assessment of Muscle Contractility in Animal Studies. Methods Mol Biol. 2016;1460:293-307.
Neuronal and muscular physiology. Calcium signals and voltage-gated ion channels in excitable cells.
Alterations of voltage gated ion channels function and calcium signaling in neurons and muscle.
Pathophysiology of Diabetes, Denervation and Skeletal Muscle diseases.
- One of the major focuses of my research interest is in the function of the sympathetic nervous system. During my PhD studies and eraly during my postdoctoral career, I studied mechanisms of ion channel regulation mediated by neurotransmitters, calcium signaling and the role of extracellular S100A1. I demonstrated that different neurotransmitters and hormones can control the activity of ion channels via the modulation of the voltage sensing apparatus. Our group also discovered that certain patterns of electrical activity control the activation of NFATc1, a transcription factor that regulates a myriad of neuronal functions. I also identified a novel mechanism of regulation of the sympathetic nervous system that innervates the heart when the S100A1 is added extracellularly. This form of regulation may occur during or after a heart attack and the accompanying ischemic damage. My scientific findings from this initial stage of my research career have been cited numerous times in peer-reviewed journals, as well as in book chapters.
- Improving our understanding of skeletal muscle functions constitutes a prerequisite for better treating skeletal muscle diseases. Over the years, myself and colleagues have developed a range of research strategies to allow a greatly improved understanding of muscle physiology and disease conditions.
- My current research and interest involves the application of my expertise in basic muscle research to obtain a better understanding of the pathophysiology of diabetes. Diabetes affects millions of people in the U.S. alone. In uncontrolled diabetes, episodes of acute hyperglycemia often lead to the breakdown of muscle fibers resulting in the release of fiber contents into the bloodstream. This can cause acute kidney damage, and when untreated, can lead to death. My research, hopefully will lead to significant new understandings of the dangerous effects of diabetes on muscle function.
2010 Member, National Researchers System (level 1), granted by The National Council on Science and Technology (CONACYT-Mexico).
2015 Chair, Gordon Research Seminar, preceding Gordon Research Conference: Muscle Excitation/Contraction Coupling.
2015-present Reviewer, Journal of Physiology
2015-present Reviewer, Journal of General Physiology
2015-present Reviewer, Frontiers in Physiology
2015-present Reviewer, Journal of Visual Experimentation
2011-present Editor, Biochemistry and Pharmacology (Los Angeles)
2001-present Member, Biophysical Society
2004-present Member, Latin American Biophysicists Society
2014-present Member, Society of General Physiology
-Primary skeletal muscle cells culture
-In vitro skeletal muscle functional assays
-In vivo muscle gene trasnfer
-Celullar microinjection and micromanipulation