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A multi-omics approach to understanding the role of APOL1 in CKD amongst African Ancestry individuals


The Division of Biostatistics at the Department of Preventive Medicine invites you to attend the following seminar. 


Time: Monday, Oct 17, 2:00 PM-3:00 PM CDT 

ZOOM Virtual Room Connection: Register in advance for this meeting 

Seminar Website: https://www.eventcreate.com/e/biostatisticsseminar  

Speaker Bio: https://sph.unc.edu/adv_profile/heather-m-highland-phd/


A multi-omics approach to understanding the role of APOL1 in CKD amongst African Ancestry individuals 


Dr. Heather M. Highland, Associate Professor  
Division of Epidemiology, Gillings School of Global Public Health

The University of North Carolina at Chapel Hill


APOL1 is an integral part of the complement system, a component of innate immunity that serves as the first line of defense against pathogens. The trypanosome that causes African sleeping sickness developed mechanisms to evade the innate immunity system after the migration out of Africa. This created a selective pressure on non-synonymous variants in the APOL1 gene. These variants are only observed in people with recent African ancestry. People carrying two variants in APOL1 are at increased risk of developing a variety of kidney disease. The mechanism by which APOL1 alters kidney function is currently unclear. To investigate potential mechanisms, we have looked at differences in DNA methylation across the genome and metabolomic profiles. Using 1740 African Americans (AA) in the ARIC study and 3886 Hispanic/Latinos in SOL, we did not observe any statistically significant differences in metabolism in preliminary analyses after adjusting for multiple comparisons. In 947 AAs in ARIC, 949 AAs in JHS and 332 AAs in MESA, we identified extensive differences in methylation near the APOL gene family region on chromosome 22 (p=2.7×10-80).  Additional methylation differences were seen near FEZF2, FAM20A, and KIAA0556. The role of these loci in the development of kidney disease in people with two APOL1 risk alleles continues.