W. Keith Jones, PhD

Molecular Pharmacology and Therapeutics

Professor
Department Chairperson, Molecular Pharmacology and Therapeutics

Languages Spoken

English, French

Biography

Interests
Basketball, Science, collecting vintage fountain pens

Medical Education

Board Certification

American Nurses Credentialing Center
Anesthesiology
American Board of

Research

  • Activation of hERG3 channel stimulates autophagy and promotes cellular senescence in melanoma Perez-Neut, M.; Haar, L.; Rao, V.; Santha, S.; Lansu, K.; Rana, B.; Jones, W. K.; Gentile, S., Oncotarget
  • ACR Appropriateness Criteria(R) Local Excision in Early Stage Rectal Cancer Russo, S.; Blackstock, A. W.; Herman, J. M.; Abdel-Wahab, M.; Azad, N.; Das, P.; Goodman, K. A.; Hong, T. S.; Jabbour, S. K.; Jones, W. E., 3rd; Konski, A. A.; Koong, A. C.; Kumar, R.; Rodriguez-Bigas, M.; Small, W., Jr; Thomas, C. R., Jr; Suh, W. W., American Journal of Clinical Oncology
  • Acute consumption of a high-fat diet prior to ischemia-reperfusion results in cardioprotection through NF-kappaB-dependent regulation of autophagic pathways Haar, L.; Ren, X.; Liu, Y.; Koch, S. E.; Goines, J.; Tranter, M.; Engevik, M. A.; Nieman, M.; Rubinstein, J.; Jones, W. K., American journal of physiology.Heart and circulatory physiology
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  • Azelastine desensitization of transient receptor potential vanilloid 1: A potential mechanism explaining its therapeutic effect in nonallergic rhinitis Singh, U.; Bernstein, J. A.; Haar, L.; Luther, K.; Jones, W. K., American Journal of Rhinology & Allergy
  • Cardiac-specific suppression of NF-kappaB signaling prevents diabetic cardiomyopathy via inhibition of the renin-angiotensin system Thomas, C. M.; Yong, Q. C.; Rosa, R. M.; Seqqat, R.; Gopal, S.; Casarini, D. E.; Jones, W. K.; Gupta, S.; Baker, K. M.; Kumar, R., American journal of physiology.Heart and circulatory physiology
  • Consumption of high fat diet acutely prior to ischemia/reperfusion results in cardioprotection through NF-kappaB dependent regulation of autophagic pathways Haar, L.; Ren, X.; Liu, Y.; Koch, S. E.; Goines, J.; Tranter, M.; Engevik, M. A.; Nieman, M. L.; Rubinstein, J.; Jones, W. K., American journal of physiology.Heart and circulatory physiology
  • Increased fibrosis and progression to heart failure in MRL mice following ischemia/reperfusion injury Smiley, D.; Smith, M. A.; Carreira, V.; Jiang, M.; Koch, S. E.; Kelley, M.; Rubinstein, J.; Jones, W. K.; Tranter, M., Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology
  • Novel role of transient receptor potential vanilloid 2 in the regulation of cardiac performance Rubinstein, J.; Lasko, V. M.; Koch, S. E.; Singh, V. P.; Carreira, V.; Robbins, N.; Patel, A. R.; Jiang, M.; Bidwell, P.; Kranias, E. G.; Jones, W. K.; Lorenz, J. N., American journal of physiology.Heart and circulatory physiology
  • Toward an integrated public health approach for epilepsy in the 21st century Koh, H. K.; Kobau, R.; Whittemore, V. H.; Mann, M. Y.; Johnson, J. G.; Hutter, J. D.; Jones, W. K., Preventing Chronic Disease
  • Age- and gender-related changes in ventricular performance in wild-type FVB/N mice as evaluated by conventional and vector velocity echocardiography imaging: a retrospective study Koch, S. E.; Haworth, K. J.; Robbins, N.; Smith, M. A.; Lather, N.; Anjak, A.; Jiang, M.; Varma, P.; Jones, W. K.; Rubinstein, J., Ultrasound in medicine & biology
  • NF-kappaB mediated miR-26a regulation in cardiac fibrosis Wei, C.; Kim, I. K.; Kumar, S.; Jayasinghe, S.; Hong, N.; Castoldi, G.; Catalucci, D.; Jones, W. K.; Gupta, S., Journal of cellular physiology
  • Novel role of HAX-1 in ischemic injury protection involvement of heat shock protein 90 Lam, C. K.; Zhao, W.; Cai, W.; Vafiadaki, E.; Florea, S. M.; Ren, X.; Liu, Y.; Robbins, N.; Zhang, Z.; Zhou, X.; Jiang, M.; Rubinstein, J.; Jones, W. K.; Kranias, E. G., Circulation research
  • Probenecid as a noninjurious positive inotrope in an ischemic heart disease murine model Koch, S. E.; Tranter, M.; Robbins, N.; Luther, K.; Singh, U.; Jiang, M.; Ren, X.; Tee, T.; Smith, L.; Varma, P.; Jones, W. K.; Rubinstein, J., JOURNAL OF CARDIOVASCULAR PHARMACOLOGY AND THERAPEUTICS
  • Cardiac-specific genetic inhibition of nuclear factor-kappaB prevents right ventricular hypertrophy induced by monocrotaline Kumar, S.; Wei, C.; Thomas, C. M.; Kim, I. K.; Seqqat, R.; Kumar, R.; Baker, K. M.; Jones, W. K.; Gupta, S., American journal of physiology.Heart and circulatory physiology
  • In vivo delivery of nucleic acids via glycopolymer vehicles affords therapeutic infarct size reduction in vivo Tranter, M.; Liu, Y.; He, S.; Gulick, J.; Ren, X.; Robbins, J.; Jones, W. K.; Reineke, T. M., Molecular therapy : the journal of the American Society of Gene Therapy
  • Paracrine effect of Wnt11-overexpressing mesenchymal stem cells on ischemic injury Zuo, S.; Jones, W. K.; Li, H.; He, Z.; Pasha, Z.; Yang, Y.; Wang, Y.; Fan, G. C.; Ashraf, M.; Xu, M., STEM CELLS AND DEVELOPMENT
  • Probenecid: novel use as a non-injurious positive inotrope acting via cardiac TRPV2 stimulation Koch, S. E.; Gao, X.; Haar, L.; Jiang, M.; Lasko, V. M.; Robbins, N.; Cai, W.; Brokamp, C.; Varma, P.; Tranter, M.; Liu, Y.; Ren, X.; Lorenz, J. N.; Wang, H. S.; Jones, W. K.; Rubinstein, J., Journal of Molecular and Cellular Cardiology

Dr. Jones' laboratory studies the molecular basis of cardiovascular disease and molecular interventions designed as therapeutic measures. Cardiovascular disease remains the number one cause of death in developed countries despite decades of research into the environmental and molecular causation.

Previous work in the lab has elucidated a gene network comprised of 238 genes activated or repressed by the transcription factor NF-?B. Interestingly, most of these genes are regulated by a set of only nine microRNAs (mRNAs). miRNAs are small non-coding RNA molecules that regulate gene products primarily at the post-transcriptional. This suggests that these nine miRNAs are important regulatory nodes and play important roles in this gene network. Interestingly, mRNAs can be manipulated by transfection with mimics (gain of function), and antagomirs (loss of function) and such an approach can be used to dissect the role of each miRNA in gene regulation, cardioprotection, and post-myocardial infarction ventricular function and remodeling. Some of the miRNAs may be, or may point towards key players in the genetic pathway that underlie cardioprotection and beneficial ventricular remodeling, and thus development of new therapeutic targets. We are also investigating the possibility that manipulation of these miRNA pathways can be used to extend the life, or modify the reparative properties of stem cells used in the heart after heart attack. RNA therapeutics are also under development, and being investigated as biomarkers. Lately we have shown that miRNAs carried in exosomes and released from stem cells are taken up and affect gene regulation in cardiac recipient cells, with potent effects upon myocardial infarction. We are currently investigating ways to engineer these exosomes as tools for discovery and as therapeutics..

  1. Molecular basis of NF-?B-dependent genes and microRNAs in cardioprotection and in stem cell based tissue repair. Aims,
    1. Elucidate the role of microRNAs in regulating the levels and activity of gene products involved in cardioproteciotn and stem cell repair;
    2. Determine the role of microRNAs from stem cells in mediating cardiac repair after stem cell injection.

  2. Novel diet-induced cardioprotection and connection to GI microflora and adipokine signaling. Aims
    1. Elucidate the role of GI tract microflora in regulating adipokines as initiatiors of cardioprotecion,
    2. Determine the mechanism of adipokine signaling in the heart that results in activation of the NF-?B transcription factor and downstream effects upon autophagy and apoptosis.

  3. microRNAs as paracrine signaling factors and biomarkers. Aims,
    1. Elucidate the microRNAs that are secreted from the heart during cardioprotective maneuvers and where they end up in other tissues and organs,
    2. Determine whether these microRNAs confer remote organ protection.