faculty

Thierry Bacro

Jeremy L. Barth, Ph.D.
Research Associate Professor


Room 627, Basic Science Building
Office: (843) 792-9984
Lab: BSB633; (843) 792-2418


Email: barthj@musc.edu

Education:

BS Biochemistry Clemson Univ. 1987
PhD Genetics University of Georgia 1996
Postdoctoral Fellow at Medical University of South Carolina 1997

Links:

   

Research Interests:

Research focuses on understanding how global programs of gene expression influence cell behavior and lineage, whether in normal developmental processes or in pathological states.

My group also operates a shared technology core for conducting transcriptomic and related analyses. Services and instrumentation provided by the core include DNA microarray analysis (Affymetrix), next-generation sequencing analysis (Ion Torrent), real-time PCR analysis (Bio-Rad Cffx96), and RNA quality analysis (Bioanalyzer 2100), together with bioinformatic support needed to apply these technologies.

Research Summary

Mechanisms controlling the production of elastin

Elastin is a connective tissue protein essential for the elastic qualities of numerous tissues, allowing them to regain their shape after stretching or contracting. Although the resilience of these tissues (including skin, blood vessels, lungs and cartilage) is essential for their function, elasticity declines with age and in response to injury and other environmental insults. This is due in part to accumulated damage in elastin fibers and the fact that elastin expression is limited (predominantly) to early development. Understanding how elastin expression is controlled would offer potential for various therapeutic treatments, for example, 1) re-initiating elastin production in conditions of elastin deficiency, and 2) controlling elastin production in tissue replacement constructs to ensure natural biomechanical properties. We are focused on understanding the transcriptional environment necessary for normal elastin synthesis. By mining several datasets, we have identified a group of genes coordinately expressed in elastin-producing systems. Current research is focused on understanding this putative elastogenic gene network using a biofabrication model of elastin synthesis that involves human endothelial cells and vascular smooth muscle cells co-cultured in macroporous gelatin beads.

Understanding the regenerative potential of the auditory system

Injury and/or degeneration of the auditory nerve leads to losses in hearing. This can occur as a function of aging or in response to noise or drug exposure. While hearing losses are generally viewed as permanent, recent studies have pointed to the existence of neural stem/progenitor cells (NSPCs), suggesting that these cells might be used to combat damage to the auditory system. In collaboration with Dr. Hainan Lang (MUSC, Department of Pathology), we are examining the potential for auditory regeneration in response to injury. Our studies highlight that NSPCs exist in the auditory nerve and that injury stimulates their proliferation and differentiation. Furthermore, transcriptional responses following injury evoke a process of de-differentiation, resembling normal development in reverse. Currently we are focusing on identifying the cells that convey neural/stem progenitor function, understanding the transcriptional mechanisms that control their response to injury, and investigating the blockages that limit the full repair of injuries.

Publications

  1. Lang H, Xing Y, Brown LN, Samuvel DJ, Panganiban CH, Havens LT, Balasubramanian S, Wegner M, Krug EL, Barth JL. Neural stem/progenitor cell properties of glial cells in the adult mouse auditory nerve. Sci Rep. 2015 Aug 26;5:13383. doi: 10.1038/srep13383. PubMed PMID: 26307538; PubMed Central PMCID: PMC4549618.
  2. Kang I, Barth JL, Sproul EP, Yoon DW, Workman GA, Braun KR, Argraves WS, Wight TN. Expression of V3 Versican by Rat Arterial Smooth Muscle Cells Promotes Differentiated and Anti-inflammatory Phenotypes. J Biol Chem. 2015 Aug 28;290(35):21629-41. doi: 10.1074/jbc.M115.657486. Epub 2015 Jul 7. PubMed PMID: 26152723.
  3. Harikrishnan K, Cooley MA, Sugi Y, Barth JL, Rasmussen LM, Kern CB, Argraves KM, Argraves WS. Fibulin-1 suppresses endothelial to mesenchymal transition in the proximal outflow tract. Mech Dev. 2015 May;136:123-32. doi: 10.1016/j.mod.2014.12.005. Epub 2015 Jan 6. PubMed PMID: 25575930.
  4. Cooley MA, Harikrishnan K, Oppel JA, Miler SF, Barth JL, Haycraft CJ, Reddy SV, Scott Argraves W. Fibulin-1 is required for bone formation and Bmp-2-mediated induction of Osterix. Bone. 2014 Dec;69:30-8. doi: 10.1016/j.bone.2014.07.038. Epub 2014 Sep 6. PubMed PMID: 25201465; PubMed Central PMCID: PMC4385289.
  5. Zhang YM, Noto JM, Hammond CE, Barth JL, Argraves WS, Backert S, Peek RM Jr, Smolka AJ. Helicobacter pylori-induced posttranscriptional regulation of H-K-ATPase α-subunit gene expression by miRNA. Am J Physiol Gastrointest Liver Physiol. 2014 Apr 1;306(7):G606-13. doi: 10.1152/ajpgi.00333.2013. Epub 2014 Feb 6. PubMed PMID: 24503769; PubMed Central PMCID: PMC4116396.
  6. Aseem O, Barth JL, Klatt SC, Smith BT, Argraves WS. Cubilin expression is monoallelic and epigenetically augmented via PPARs. BMC Genomics. 2013 Jun 18;14:405. doi: 10.1186/1471-2164-14-405. PubMed PMID: 23773363; PubMed Central PMCID: PMC3706236.
  7. Lockhart MM, Wirrig EE, Phelps AL, Ghatnekar AV, Barth JL, Norris RA, Wessels A. Mef2c regulates transcription of the extracellular matrix protein cartilage link protein 1 in the developing murine heart. PLoS One. 2013;8(2):e57073. doi: 10.1371/journal.pone.0057073. Epub 2013 Feb 26. PubMed PMID: 23468913; PubMed Central PMCID: PMC3582617.
  8. Krejčí E, Pesevski Z, DeAlmeida AC, Mrug M, Fresco VM, Argraves WS, Barth JL, Cui X, Sedmera D. Microarray analysis of normal and abnormal chick ventricular myocardial development. Physiol Res. 2012;61 Suppl 1:S137-44. PubMed PMID: 22827870; PubMed Central PMCID: PMC4112186.
  9. Cooley MA, Fresco VM, Dorlon ME, Twal WO, Lee NV, Barth JL, Kern CB, Iruela-Arispe ML, Argraves WS. Fibulin-1 is required during cardiac ventricular morphogenesis for versican cleavage, suppression of ErbB2 and Erk1/2 activation, and to attenuate trabecular cardiomyocyte proliferation. Dev Dyn. 2012 Feb;241(2):303-14. doi: 10.1002/dvdy.23716. Epub 2011 Dec 19. PubMed PMID: 22183742; PubMed Central PMCID: PMC3489172.
  10. Jones JA, Stroud RE, O'Quinn EC, Black LE, Barth JL, Elefteriades JA, Bavaria JE, Gorman JH 3rd, Gorman RC, Spinale FG, Ikonomidis JS. Selective microRNA suppression in human thoracic aneurysms: relationship of miR-29a to aortic size and proteolytic induction. Circ Cardiovasc Genet. 2011 Dec;4(6):605-13. doi:
    10.1161/CIRCGENETICS.111.960419. Epub 2011 Oct 18. PubMed PMID: 22010139; PubMed Central PMCID: PMC3246193.
  11. Embree M, Ono M, Kilts T, Walker D, Langguth J, Mao J, Bi Y, Barth JL, Young M. Role of subchondral bone during early-stage experimental TMJ osteoarthritis. J Dent Res. 2011 Nov;90(11):1331-8. doi: 10.1177/0022034511421930. Epub 2011 Sep 13. PubMed PMID: 21917603; PubMed Central PMCID: PMC3188464.
  12. Argraves KM, Sethi AA, Gazzolo PJ, Wilkerson BA, Remaley AT, Tybjaerg-Hansen A, Nordestgaard BG, Yeatts SD, Nicholas KS, Barth JL, Argraves WS. S1P, dihydro-S1P and C24:1-ceramide levels in the HDL-containing fraction of serum inversely correlate with occurrence of ischemic heart disease. Lipids Health Dis. 2011 May 9;10:70. doi: 10.1186/1476-511X-10-70. PubMed PMID: 21554699; PubMed Central PMCID: PMC3116499.
  13. Gacchina CE, Deb P, Barth JL, Ramamurthi A. Elastogenic inductability of smooth muscle cells from a rat model of late stage abdominal aortic aneurysms. Tissue Eng Part A. 2011 Jul;17(13-14):1699-711. doi: 10.1089/ten.TEA.2010.0526. Epub 2011 May 9. PubMed PMID: 21341992; PubMed Central PMCID: PMC3118732.
Last updated on 23-May-2016
 
 

© 2016  Medical University of South Carolina | Disclaimer