Dr. Martin Reick Associate Professor Tel: +91 476 2896318/28 Ext: 3109 Email: This e-mail address is being protected from spambots. You need JavaScript enabled to view it

Research Interests:

Impairment of wound healing is one of the most serious secondary complications of diabetes and poor control of serum glucose levels because it can result in sepsis amputation. Several of the processes contributing to normal wound healing are impaired in diabetics. The impaired processes include cell migration and division, angiogenesis and inflammation. Recently the function of the bHLH-PAS transcription factor HIF (consisting of HIF-1alpha and HIF-1beta/ARNT) has been shown to be impaired under hyperglycemic conditions. Inhibition of HIF activation under hyperglycemic is possibly a major cause of impaired wound healing because it controls the expression genes, such as vegf and epo, that are essential regulators of angiogenesis and wound healing. HIF is also known to regulate the expression of other genes such as bFGF and some of the nitric oxide synthase isozymes which have also been implicated in wound healing. Hence we are interested in identifying the molecular mechanisms that inhibit hypoxic activation of HIF under hyperglycemic conditions.

Both insulin and hypoxia induced signaling pathways are affected by hyperglycemic conditions and both pathways control the transcription of an overlapping set of target genes. This has sparked our interest in possible crosstalk between hypoxia induced and insulin induced signaling pathways.

Finally we hope to develop and set up high throughput in vitro and cell based assays of HIF activity as a means to screen natural compounds for their ability to restore hypoxia induced activation of HIF under hyperglycemic conditions.

Publications:

1. Dudley CA, Erbel-Sieler C, Estill SJ, Reick M, Franken P, Pitts S and McKnight SL. Altered patterns of sleep and behavioral adaptability in NPAS2-deficient mice. Science. 2003 Jul 18;301(5631):379-83. Epub 2003 Jul 3.
   
   
2. Rutter J, Reick M and McKnight SL.
   Metabolism and the control of circadian rhythms. Annu Rev Biochem. 2002;71:307-31. Epub 2001 Nov 9. Review.
   
   
3. Shepard J, Reick M, Olson S, and Graveley BR.
   Characterization of U2AF(6), a splicing factor related to U2AF(35). Mol Cell Biol. 2002 Jan;22(1):221-30.
   
   
4. Reick M, Garcia JA, Dudley C and McKnight SL.
   NPAS2: an analog of clock operative in the mammalian forebrain. Science. 2001 Jul 20;293(5529):506-9. Epub 2001 Jul 5.
   
   
5. Rutter J, Reick M, Wu LJ and McKnight SL.
   Regulation of clock and NPAS2 DNA binding by the redox state of NAD cofactors.
   Science. 2001 Jul 20;293(5529):510-4. Epub 2001 Jul 5.
   
   
6. Garcia JA, Zhang D, Estill SJ, Michnoff C, Rutter J, Reick M, Scott K, Diaz-Arrastia R and McKnight SL.
   Impaired cued and contextual memory in NPAS2-deficient mice. Science. 2000 Jun 23;288(5474):2226-30.
   
   
7. Reick M, Robertson RW, Pasco DS and Fagan JB.
   Down-regulation of nuclear aryl hydrocarbon receptor DNA-binding and transactivation functions: requirement for a labile or inducible factor. Mol Cell Biol. 1994 Sep;14(9):5653-60.