Discipline: Biological Sciences
Subcategory: Cell and Molecular Biology
Nkem Azu - Texas Southern University
Co-Author(s): Shishir Shishodia, Texas Southern University, Houston, TX Selina Hernandez and Ammrutha Immadi, Debakey High School for Health Professionals, Houston, TX
The Platinum Group Metals (PGM), platinum (Pt), Palladium (Pd), and Rhodium (Rh) are released from automobile catalytic converters in the form of nano-sized particles. Significant concentrations of rhodium, palladium, and platinum have been previously reported in tunnel dusts and surface road dusts. Humans can be exposed to these metals through inhalation of airborne particulate matter (PM) that may provoke respiratory diseases and other adverse effects. Exposure to atmospheric PM is known to induce many respiratory diseases especially in susceptible populations such as children. It is however not clear which constituents of atmospheric PM are responsible for the observed health effects. Platinum like other transition metals exist in several different forms having different oxidation states and are chemically inert. Hypoxia is suggested to drive pathophysiological lung processes in infant lung, pulmonary hypertension, asthma and chronic obstructive pulmonary disease. However, very little is known about the mechanism in which environmental contaminants like PGMs have on pulmonary function. Our preliminary findings showed increased activation of MAPK proteins. It has been previously suggested that the increased expression of MAPK protein ERK 1/2, JNK and P38 play a role in the activation of hypoxia inducible factor (HIF). We hypothesized that exposure to PGM will affect the hypoxia pathway which is essential in the development of pulmonary diseases. To test this hypothesis, we examined the expression of 80 different hypoxia genes using real-time PCR in non-cancer lung cells exposed to platinum group metals and compared expression in lung cells not exposed to PGM salts. In the present study, we demonstrate mRNA level PGM salt stimulation led to an induction of the positive acute phase genes alpha 1-antitrypsin (SERPINA1), TLR2 (Toll-like receptor 2), ADAM17 (A disintegrin and metalloproteinase 17), EGLN3 (hypoxia-inducible factor prolyl hydroxylase), PRKCB (protein kinase C beta), PRKCD (protein kinase C delta), and PGF (placental growth factor). All of which have been implicated in the development of asthma and COPD. To our knowledge, links between PGM exposure and potential development of pulmonary diseases has not been reported. Future studies will be directed towards understanding the hypoxic response induced following road dust exposure.
Funder Acknowledgement(s): Funding was provided by NSF/RISE grant to S. Shishodia
Faculty Advisor: Shishir Shishodia, email@example.com
Role: Preliminary data used on which our current research is based on were carried out by NSF-RISE student summer interns and analyzed by myself, and my mentor Dr. Shishodia. Amrutha Immadi worked on the preliminary data which included MTT assay to determine the adequate road dust and PGM salt concentrations in cancer and non-cancer cells to be used for future experiments, while Selena Hernandez performed cell treatments, whole-cell protein extractions and western blot. Gene expression studies (RNA extraction, cDNA synthesis, RT-PCR detection) were performed by myself. Experiments were designed and analyzed by Dr. Shishir Shishodia.