John J. Reiners, Ph.D.

Wayne State University
Professor, Institute of Environmental Health Sciences
Core Leader, Cell Signaling and Function Research Core, EHS Center for Molecular & Cellular Toxicology

Principal Investigator, Training Program in Molecular and Cellular Toxicology

Tel.

(313) 963-7661

Fax.

(313) 577- 0082

Email:

john.reiners.jr@wayne.edu

Address:

Institute of Environmental Health Sciences

Wayne State University
2727 Second Avenue, Room 4000
Detroit, MI 48201-2654

     
Research Interests:    

The aryl hydrocarbon receptor (AhR) is a ubiquitously expressed, ligand-activated transcription factor. Its’ ligand-dependent activities influence processes involved in xenobiotic metabolism, immune function, development, cell cycle progression, and cell death. The Reiners laboratory is interested in: 1) the signaling processes that regulate AhR function; 2) AhR regulation of cholesterol trafficking and homeostasis; and the 3) ligand-independent functions of the AhR. With regards to the latter, particular attention is focused on how the AhR regulates lysosome fragility, and susceptibilities to subclasses of cytotoxic agents.

Although the term ‘death’ has negative connotations, it is a normal physiological process and necessary for maintenance of homeostasis. Indeed, cancer is often a consequence of defective cell death pathways. The Reiners laboratory is interested in understanding the processes of programmed cell death, and determining how insults to specific organelles (lysosomes, endoplasmic reticulum, nucleus, mitochondria) initiate death pathways. Such information has significant therapeutic application.

     
Select Publications:    

Caruso JA, Mathieu PA, Reiners Jr JJ. Sphingomyelins suppress the targeted disruption of lysosomes / endosomes and the induction of apoptosis by the lysosomal photosensitizer NPe6 in photodynamic therapy protocols. Biochem J. 2005 June 8; [Epub ahead of print] PMID: 15943580

Kessel D., Conley M, Vincete MG, Reiners Jr JJ. Studies on the subcellular localization of the porphycene CPO. Photochem. Photbiol. 2005 May-Jun;81(3):153-63. PMID 15745423

Reiners JJ Jr, Kessel D. Susceptibility of myelomonocytic leukemia U937 cells to the induction of apoptosis by the non-peptidic Bcl-2 ligand HA14-1 is cell cycle phase-dependent. Cancer Lett. 2005 Apr 28;221(2):153-63. PMID: 15808401

Kessel D, Castelli M, Reiners JJ. Ruthenium red-mediated suppression of Bcl-2 loss and Ca(2+) release initiated by photodamage to the endoplasmic reticulum: scavenging of reactive oxygen species. Cell Death Differ. 2005 May;12(5):502-11. PMID: 15719027

Joiakim A, Mathieu PA, Elliott AA, Reiners JJ Jr. Superinduction of CYP1A1 in MCF10A cultures by cycloheximide, anisomycin, and puromycin: a process independent of effects on protein translation and unrelated to suppression of aryl hydrocarbon receptor proteolysis by the proteasome. Mol Pharmacol. 2004 Oct;66(4):936-47. PMID: 15385644

Castelli M, Reiners JJ, Kessel D. A mechanism for the proapoptotic activity of ursodeoxycholic acid: effects on Bcl-2 conformation. Cell Death Differ. 2004 Aug;11(8):906-14. PMID: 15258617

Caruso JA, Mathieu PA, Joiakim A, Leeson B, Kessel D, Sloane BF, Reiners JJ Jr. Differential susceptibilities of murine hepatoma 1c1c7 and Tao cells to the lysosomal photosensitizer NPe6: influence of aryl hydrocarbon receptor on lysosomal fragility and protease contents. Mol Pharmacol. 2004 Apr;65(4):1016-28. PMID: 15044632

Joiakim A, Mathieu PA, Palermo C, Gasiewicz TA, Reiners JJ Jr.  The Jun N-terminal kinase inhibitor SP600125 is a ligand and antagonist of the aryl hydrocarbon receptor. Drug Metab Dispos. 2003 Nov;31(11):1279-82. PMID: 14570754

Mattingly RR, Gibbs RA, Menard RE, Reiners JJ Jr. Potent suppression of proliferation of a10 vascular smooth muscle cells by combined treatment with lovastatin and 3-allylfarnesol, an inhibitor of protein farnesyltransferase. J Pharmacol Exp Ther. 2002 Oct;303(1):74-81. PMID: 12235235

Reiners JJ Jr, Caruso JA, Mathieu P, Chelladurai B, Yin XM, Kessel D. Release of cytochrome c and activation of pro-caspase-9 following lysosomal photodamage involves Bid cleavage. Cell Death Differ. 2002 Sep;9(9):934-44. PMID: 12181744